Mixed Topics

This article is part of a series of articles on the Home Improvements and Structural Alterations program (HISA), a home modification (HM) program within the Veterans Health Administration (VHA). HISA is a benefit awarded to veterans with disabilities (VWDs) and is instrumental in affording physical accessibility and structural alterations to veterans’ homes.¹ The overarching goals of this project are to describe and understand HISA use by VWDs. Previous work has shown geographical variation in the number of HISA prescriptions across counties in the US (Figure 1).¹ The current work seeks to describe and predict the county-level rates of HISA use. Information about what predicts HISA utilization at the county level is important because it enhances understanding of program utilization at a national level. The long-term goal of the series is to provide knowledge about HM services within VHA to improve community-based independent living of VWDs by increasing awareness and utilization of HM services. 

Background

A health care professional (HCP) approves a HM support award by evaluating the practicality of the support to improve the built environment of a given veteran’s disability.^1,2 Previously we detailed some of the preliminary research into the HISA program, including HISA user demographic and clinical characteristics, types of HMs received, user suggestions for improvement, and geospatial analysis of HISA prescriptions concentration.^1-4

The geospatial analyses of HISA prescriptions revealed clusters of high numbers of HISA users (hot spots) and low numbers of HISA users (cold spots), indicating that HISA is either not prescribed or uniformly used across the US. The previous research prompted investigation into county-level variables that may impact HISA utilization rates. This inquiry focuses on county characteristics associated with HISA use rates, such as measures of clinical care and quality of care (eg, access to health services variables, lack of insurance, preventable hospital stays), physical environment, and sociodemographic characteristics. Clinical care and quality of care measures promote the interaction with HCPs. Moreover, access to health care is an important indicator of health outcomes.^5,6 An individual’s capacity to access health services, such as a HM program, greatly impacts well-being, safety, independence, and health.^2,4 Well-being, safety, independence, and health become compromised if individuals cannot access care, if needed care is lacking in their area, if HCPs are not available, or are unwilling to provide care due to lack of insurance coverage.^7-12 In locations where health care services are minimal due to lack of specialists or health care facilities, the quality of (or access to) care may be compromised, resulting in preventable conditions becoming problematic.^13,14 These conditions may result in unnecessary hospitalizations for conditions that could have been treated during routine care. Financial barriers to care particularly among low-income people and the uninsured have proven detrimental to health.^15,16 On the other hand, preventable hospital stays are a quality of care measure (ie, a proxy for poor quality of care). HISA operates within a health care system; thus, it is imperative to include these measures impacting health. 

In this study, we sought to identify county-level predictors—in particular, county-level proxies for access to care—that may be associated with county-level HISA use. We define HISA utilization rate as the percentage of a county’s VHA patients who have received a HISA award.

Methods

This study used data from the National Prosthetics Patient Database (NPPD), US Department of Veterans Affairs (VA) medical database inpatient and outpatient datasets, VHA Support Service Center (VSSC) data cubes, and the County Health Rankings database (CHRD). First, the study cohort was identified from NPPD users who have obtained a HISA award from fiscal years (FY) 2015 to 2018. Analysis started with FY 2015 following new regulations (38 CFR § 17) governing the operations of the HISA program.² The study cohort was matched with records from NPPD and VA inpatient and outpatient datasets to obtain information about the veterans’ demographic characteristics and their HM characteristics and costs. The number of VHA end-of-year (EOY) patients per county was extracted from the VSSC Current Enrollment Cube, which was used in calculation of the county-level HISA utilization rate.¹⁷ Finally, zip code–based locational data were used to calculate approximate drive time and distance from the HISA user’s approximate location to the facility where they received their HM prescription. Drive times and drive distances were calculated with Esri ArcGIS Pro (v2.6.3) by placing zip code centroid and VHA facilities on a nationwide road network that contains both road speeds and distances.

Calculations

Patient-level data were aggregated up to county-level variables by calculating the sum, mean, or percent per county. HISA user sample characteristics, including sex, race, rurality (urban, rural), marital status, and Class 1 vs Class 2 disability-related eligibility groups, were aggregated to the county level by calculating percentages of HISA users of the given characteristics out of total HISA users in the county. Disability-related eligibility groups (Class 1 vs Class 2 HISA users) determines the maximum lifetime award dollar amount. Specifically, those with service-connected disabilities or those with a ≥ 50% disability rating (regardless of whether or not their disability is service connected) are classified as Class 1 HISA users and are eligible to receive a maximum lifetime award of $6800. Those with a recorded disability that is not connected to their military service, and who have a disability rating of < 50% are classified as Class 2 HISA users and are eligible to receive a lifetime maximum award of $2000.

The county-level number of HISA users was used as the numerator for calculation of county-level HISA utilization rate. Counties with zero HISA users were excluded. The number of EOY VHA patients per county in FY 2018 was divided by 1000 and used as the denominator in the calculation of county-level HISA utilization rate. Thus, the outcome variable is HISA utilization rate per 1000 VHA patients in FY 2018 (HISA utilization rate).

County-Level Variables

County-level variables were downloaded from the 2020 CHRD.^5,6 An explanation of the CHRD model and the factors used in this study are shown in the eAppendix (available at doi: 10.12788/fp.0279).⁶ County-level aggregated HISA user data and the CHRD data were matched using county Federal Information Processing Standards codes. Access to care measures collected from CHRD included percentages uninsured and ratios of population to primary care physicians, dentists, mental health professionals, and other primary care professionals. Other CHRD measures included those for quality of care (rate of preventable hospital stay) and housing quality (percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, percent of homeownership). Of secondary interest was county population rurality, as previous research findings showed the annual average of HISA users who are from rural areas ranged from 30 to 35%.

Analysis Methods

SAS (v9.4), R (v4.0.2), and RStudio (v1.3.1093) were used for data preparation and analysis.¹⁸ Multiple regression analysis was used to predict county-level utilization rate from county-level variables. Sociodemographic characteristics from CHRD and HISA data were included as important control predictors in the regression model, though our focus for this paper are the access to care and housing quality predictors.

Model diagnostics (examination of model residuals, Breusch-Godfrey test, Breusch-Pagan test) revealed significant heteroskedasticity of the model; thus, robust standard errors and associated P values were computed using the R estimatr package (v0.30.2).¹⁹ Some predictor variables of interest (eg, ratio of mental health professionals) were removed during the model building process either due to problems of multicollinearity or excessive missingness that would have resulted in listwise deletion.

Results

County-level HISA utilization rate per 1000 EOY VHA patients ranged from 0.09 to 59.7%, with a 6.6% mean and 5% median (Figure 2). The data were highly positively skewed. The final model included 33 total predictor variables (Table 1). The final regression model was a significantly better predictor of county-level HISA utilization rate than a null model (F[33-2184], 10.18; P < .001). The adjusted model R² showed that the overall model accounted for approximately 23% of variance in county-level HISA utilization rate (Table 2).

Among the primary variables of interest, percent uninsured adults and rate of preventable hospital stays emerged as significant predictors of county-level HISA utilization rate. Specifically, county percentage of uninsured adults was negatively related to county-level HISA utilization rate (b = -8.99, P = .005), indicating that the higher the proportion of uninsured adults—with all other predictors held constant—the lower the HISA utilization rate. Percent uninsured adults ranged from 2.7 to 42.4% across counties, with a mean (SD) of 12.7% (5.8%) and 11.4% median.

Discussion

This study examined whether county-level characteristics, specifically variables for access to care, quality of care, and housing quality, were predictive of a county’s HISA utilization rate. Given that this series of work on the HISA program is (to our knowledge) the first of its kind, and given the exploratory nature of this analysis, we did not have specific predictions for the effects of any one given variable. Nevertheless, some of the results were surprising, and we believe they warrant additional study. In particular, the opposing direction of effects for access to care and quality of care variables were hard to reconcile.

The county percent of uninsured adults (an access to care variable, specifically, a proxy for poor access to care) was negatively associated with county-level HISA utilization rate, whereas the county rate of preventable hospital stays (a quality of care variable, but also potentially an access to care variable, and specifically, proxies for poor quality of care or poor access to care) was positively associated with county-level HISA utilization rate. To describe the relationships more generally, one coefficient in the regression model indicated that the poorer the access to care, the lower the HISA utilization rate (higher percent of uninsured adults predicts lower HISA utilization rate), while another coefficient in the regression model indicated the poorer the quality of and access to care, the higher the HISA utilization rate (higher rate of preventable hospital stays predicts higher HISA utilization rate). Future study is warranted to disentangle and reconcile the various community-level predictors of this service.

Housing quality measures (eg, percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, and percent of homeownership) are important in the consideration of whether a HM will be performed or should be performed. For example, if a person is cost burdened by the amount of expenditure spent in housing there will be little discretionary funds to perform a HM. Individuals who do not own their home may experience complications in obtaining permission from landlords to perform a HM. County-level predictors of housing quality (percent of households with high housing costs, overcrowding, and lack of kitchen or plumbing) were not significantly associated with county-level HISA utilization rate but are also nevertheless relevant to the discussion of home modifications. Of particular interest is the percent of households with lack of kitchen or plumbing variable, which was positively related to county-level HISA utilization rate although not statistically significant. HM elements related to the kitchen (eg, heighten countertop) add to the accessibility of the home allowing for the performing of activities of daily living such as cooking. Between FY 2015 and FY 2018, we discovered 131 prescriptions for kitchen (n = 90) and plumbing (n = 41) HMs, which is a very small proportion of the 30,780 total HMs (there were 24,397 bathroom HMs). The nonsignificant coefficient for this variable may reflect the small number of veterans that obtained these HM.

Limitations

The potentially conflicting direction of effects for a significant access to care variable (percent uninsured adults) and a significant access to care and quality of care variable (preventable hospital stays) are interesting and warrant additional study, but the inability to interpret or explain this apparent inconsistency constitutes a limitation of the current data and analyses presented here. Another limitation is that this analysis uses county-level predictors for what is ultimately an individual-level outcome. It would have been ideal to have both individual- and county-level data to conduct a multilevel analysis; in particular, individual-level data within counties of individuals (both veterans and nonveterans) who did not receive a HISA award (including both those who applied and were denied, and who did not apply) would be highly valuable.

Conclusions

Our continuing research into veterans’ use of HM fills a gap in the literature about the characteristics of HISA users, the impact of county-level variables on the use of HISA, and the geographic distribution and use of HISA within the VHA. While it is important to examine the influence of broader systems on individual outcomes, there could be myriad other factors that are more proximal and more closely related to whether any one individual applies for, let alone receives, a HISA award. Indeed, a low overall adjusted model R² indicates that there is considerable variability in county-level HISA utilization rate that was not accounted for by the current model; this further speaks to warranted additional study.

More research is needed to understand and account for geographical variation in HISA utilization rate across the US. However, this work serves as an exploratory first step at quantifying and predicting HISA utilization rate at a broad level, with the ultimate goal of increasing access to HMs for veterans with disabilities.

Acknowledgments

This research was supported by grant 15521 from the US Department of Veterans Affairs, Office of Rural Health. Furthermore, the research was supported in part by grant K12 HD055929 from the National Institutes of Health. We want to acknowledge Cheri E. Knecht, Project Coordinator, for her assistance throughout all aspects of our research study and for her thoughtful contributions during the writing of this manuscript.

This article is part of a series of articles on the Home Improvements and Structural Alterations program (HISA), a home modification (HM) program within the Veterans Health Administration (VHA). HISA is a benefit awarded to veterans with disabilities (VWDs) and is instrumental in affording physical accessibility and structural alterations to veterans’ homes.¹ The overarching goals of this project are to describe and understand HISA use by VWDs. Previous work has shown geographical variation in the number of HISA prescriptions across counties in the US (Figure 1).¹ The current work seeks to describe and predict the county-level rates of HISA use. Information about what predicts HISA utilization at the county level is important because it enhances understanding of program utilization at a national level. The long-term goal of the series is to provide knowledge about HM services within VHA to improve community-based independent living of VWDs by increasing awareness and utilization of HM services. 

Background

A health care professional (HCP) approves a HM support award by evaluating the practicality of the support to improve the built environment of a given veteran’s disability.^1,2 Previously we detailed some of the preliminary research into the HISA program, including HISA user demographic and clinical characteristics, types of HMs received, user suggestions for improvement, and geospatial analysis of HISA prescriptions concentration.^1-4

The geospatial analyses of HISA prescriptions revealed clusters of high numbers of HISA users (hot spots) and low numbers of HISA users (cold spots), indicating that HISA is either not prescribed or uniformly used across the US. The previous research prompted investigation into county-level variables that may impact HISA utilization rates. This inquiry focuses on county characteristics associated with HISA use rates, such as measures of clinical care and quality of care (eg, access to health services variables, lack of insurance, preventable hospital stays), physical environment, and sociodemographic characteristics. Clinical care and quality of care measures promote the interaction with HCPs. Moreover, access to health care is an important indicator of health outcomes.^5,6 An individual’s capacity to access health services, such as a HM program, greatly impacts well-being, safety, independence, and health.^2,4 Well-being, safety, independence, and health become compromised if individuals cannot access care, if needed care is lacking in their area, if HCPs are not available, or are unwilling to provide care due to lack of insurance coverage.^7-12 In locations where health care services are minimal due to lack of specialists or health care facilities, the quality of (or access to) care may be compromised, resulting in preventable conditions becoming problematic.^13,14 These conditions may result in unnecessary hospitalizations for conditions that could have been treated during routine care. Financial barriers to care particularly among low-income people and the uninsured have proven detrimental to health.^15,16 On the other hand, preventable hospital stays are a quality of care measure (ie, a proxy for poor quality of care). HISA operates within a health care system; thus, it is imperative to include these measures impacting health. 

In this study, we sought to identify county-level predictors—in particular, county-level proxies for access to care—that may be associated with county-level HISA use. We define HISA utilization rate as the percentage of a county’s VHA patients who have received a HISA award.

Methods

This study used data from the National Prosthetics Patient Database (NPPD), US Department of Veterans Affairs (VA) medical database inpatient and outpatient datasets, VHA Support Service Center (VSSC) data cubes, and the County Health Rankings database (CHRD). First, the study cohort was identified from NPPD users who have obtained a HISA award from fiscal years (FY) 2015 to 2018. Analysis started with FY 2015 following new regulations (38 CFR § 17) governing the operations of the HISA program.² The study cohort was matched with records from NPPD and VA inpatient and outpatient datasets to obtain information about the veterans’ demographic characteristics and their HM characteristics and costs. The number of VHA end-of-year (EOY) patients per county was extracted from the VSSC Current Enrollment Cube, which was used in calculation of the county-level HISA utilization rate.¹⁷ Finally, zip code–based locational data were used to calculate approximate drive time and distance from the HISA user’s approximate location to the facility where they received their HM prescription. Drive times and drive distances were calculated with Esri ArcGIS Pro (v2.6.3) by placing zip code centroid and VHA facilities on a nationwide road network that contains both road speeds and distances.

Calculations

Patient-level data were aggregated up to county-level variables by calculating the sum, mean, or percent per county. HISA user sample characteristics, including sex, race, rurality (urban, rural), marital status, and Class 1 vs Class 2 disability-related eligibility groups, were aggregated to the county level by calculating percentages of HISA users of the given characteristics out of total HISA users in the county. Disability-related eligibility groups (Class 1 vs Class 2 HISA users) determines the maximum lifetime award dollar amount. Specifically, those with service-connected disabilities or those with a ≥ 50% disability rating (regardless of whether or not their disability is service connected) are classified as Class 1 HISA users and are eligible to receive a maximum lifetime award of $6800. Those with a recorded disability that is not connected to their military service, and who have a disability rating of < 50% are classified as Class 2 HISA users and are eligible to receive a lifetime maximum award of $2000.

The county-level number of HISA users was used as the numerator for calculation of county-level HISA utilization rate. Counties with zero HISA users were excluded. The number of EOY VHA patients per county in FY 2018 was divided by 1000 and used as the denominator in the calculation of county-level HISA utilization rate. Thus, the outcome variable is HISA utilization rate per 1000 VHA patients in FY 2018 (HISA utilization rate).

County-Level Variables

County-level variables were downloaded from the 2020 CHRD.^5,6 An explanation of the CHRD model and the factors used in this study are shown in the eAppendix (available at doi: 10.12788/fp.0279).⁶ County-level aggregated HISA user data and the CHRD data were matched using county Federal Information Processing Standards codes. Access to care measures collected from CHRD included percentages uninsured and ratios of population to primary care physicians, dentists, mental health professionals, and other primary care professionals. Other CHRD measures included those for quality of care (rate of preventable hospital stay) and housing quality (percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, percent of homeownership). Of secondary interest was county population rurality, as previous research findings showed the annual average of HISA users who are from rural areas ranged from 30 to 35%.

Analysis Methods

SAS (v9.4), R (v4.0.2), and RStudio (v1.3.1093) were used for data preparation and analysis.¹⁸ Multiple regression analysis was used to predict county-level utilization rate from county-level variables. Sociodemographic characteristics from CHRD and HISA data were included as important control predictors in the regression model, though our focus for this paper are the access to care and housing quality predictors.

Model diagnostics (examination of model residuals, Breusch-Godfrey test, Breusch-Pagan test) revealed significant heteroskedasticity of the model; thus, robust standard errors and associated P values were computed using the R estimatr package (v0.30.2).¹⁹ Some predictor variables of interest (eg, ratio of mental health professionals) were removed during the model building process either due to problems of multicollinearity or excessive missingness that would have resulted in listwise deletion.

Results

County-level HISA utilization rate per 1000 EOY VHA patients ranged from 0.09 to 59.7%, with a 6.6% mean and 5% median (Figure 2). The data were highly positively skewed. The final model included 33 total predictor variables (Table 1). The final regression model was a significantly better predictor of county-level HISA utilization rate than a null model (F[33-2184], 10.18; P < .001). The adjusted model R² showed that the overall model accounted for approximately 23% of variance in county-level HISA utilization rate (Table 2).

Among the primary variables of interest, percent uninsured adults and rate of preventable hospital stays emerged as significant predictors of county-level HISA utilization rate. Specifically, county percentage of uninsured adults was negatively related to county-level HISA utilization rate (b = -8.99, P = .005), indicating that the higher the proportion of uninsured adults—with all other predictors held constant—the lower the HISA utilization rate. Percent uninsured adults ranged from 2.7 to 42.4% across counties, with a mean (SD) of 12.7% (5.8%) and 11.4% median.

Discussion

This study examined whether county-level characteristics, specifically variables for access to care, quality of care, and housing quality, were predictive of a county’s HISA utilization rate. Given that this series of work on the HISA program is (to our knowledge) the first of its kind, and given the exploratory nature of this analysis, we did not have specific predictions for the effects of any one given variable. Nevertheless, some of the results were surprising, and we believe they warrant additional study. In particular, the opposing direction of effects for access to care and quality of care variables were hard to reconcile.

The county percent of uninsured adults (an access to care variable, specifically, a proxy for poor access to care) was negatively associated with county-level HISA utilization rate, whereas the county rate of preventable hospital stays (a quality of care variable, but also potentially an access to care variable, and specifically, proxies for poor quality of care or poor access to care) was positively associated with county-level HISA utilization rate. To describe the relationships more generally, one coefficient in the regression model indicated that the poorer the access to care, the lower the HISA utilization rate (higher percent of uninsured adults predicts lower HISA utilization rate), while another coefficient in the regression model indicated the poorer the quality of and access to care, the higher the HISA utilization rate (higher rate of preventable hospital stays predicts higher HISA utilization rate). Future study is warranted to disentangle and reconcile the various community-level predictors of this service.

Housing quality measures (eg, percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, and percent of homeownership) are important in the consideration of whether a HM will be performed or should be performed. For example, if a person is cost burdened by the amount of expenditure spent in housing there will be little discretionary funds to perform a HM. Individuals who do not own their home may experience complications in obtaining permission from landlords to perform a HM. County-level predictors of housing quality (percent of households with high housing costs, overcrowding, and lack of kitchen or plumbing) were not significantly associated with county-level HISA utilization rate but are also nevertheless relevant to the discussion of home modifications. Of particular interest is the percent of households with lack of kitchen or plumbing variable, which was positively related to county-level HISA utilization rate although not statistically significant. HM elements related to the kitchen (eg, heighten countertop) add to the accessibility of the home allowing for the performing of activities of daily living such as cooking. Between FY 2015 and FY 2018, we discovered 131 prescriptions for kitchen (n = 90) and plumbing (n = 41) HMs, which is a very small proportion of the 30,780 total HMs (there were 24,397 bathroom HMs). The nonsignificant coefficient for this variable may reflect the small number of veterans that obtained these HM.

Limitations

The potentially conflicting direction of effects for a significant access to care variable (percent uninsured adults) and a significant access to care and quality of care variable (preventable hospital stays) are interesting and warrant additional study, but the inability to interpret or explain this apparent inconsistency constitutes a limitation of the current data and analyses presented here. Another limitation is that this analysis uses county-level predictors for what is ultimately an individual-level outcome. It would have been ideal to have both individual- and county-level data to conduct a multilevel analysis; in particular, individual-level data within counties of individuals (both veterans and nonveterans) who did not receive a HISA award (including both those who applied and were denied, and who did not apply) would be highly valuable.

Conclusions

Our continuing research into veterans’ use of HM fills a gap in the literature about the characteristics of HISA users, the impact of county-level variables on the use of HISA, and the geographic distribution and use of HISA within the VHA. While it is important to examine the influence of broader systems on individual outcomes, there could be myriad other factors that are more proximal and more closely related to whether any one individual applies for, let alone receives, a HISA award. Indeed, a low overall adjusted model R² indicates that there is considerable variability in county-level HISA utilization rate that was not accounted for by the current model; this further speaks to warranted additional study.

More research is needed to understand and account for geographical variation in HISA utilization rate across the US. However, this work serves as an exploratory first step at quantifying and predicting HISA utilization rate at a broad level, with the ultimate goal of increasing access to HMs for veterans with disabilities.

Acknowledgments

This research was supported by grant 15521 from the US Department of Veterans Affairs, Office of Rural Health. Furthermore, the research was supported in part by grant K12 HD055929 from the National Institutes of Health. We want to acknowledge Cheri E. Knecht, Project Coordinator, for her assistance throughout all aspects of our research study and for her thoughtful contributions during the writing of this manuscript.

This article is part of a series of articles on the Home Improvements and Structural Alterations program (HISA), a home modification (HM) program within the Veterans Health Administration (VHA). HISA is a benefit awarded to veterans with disabilities (VWDs) and is instrumental in affording physical accessibility and structural alterations to veterans’ homes.¹ The overarching goals of this project are to describe and understand HISA use by VWDs. Previous work has shown geographical variation in the number of HISA prescriptions across counties in the US (Figure 1).¹ The current work seeks to describe and predict the county-level rates of HISA use. Information about what predicts HISA utilization at the county level is important because it enhances understanding of program utilization at a national level. The long-term goal of the series is to provide knowledge about HM services within VHA to improve community-based independent living of VWDs by increasing awareness and utilization of HM services. 

Background

A health care professional (HCP) approves a HM support award by evaluating the practicality of the support to improve the built environment of a given veteran’s disability.^1,2 Previously we detailed some of the preliminary research into the HISA program, including HISA user demographic and clinical characteristics, types of HMs received, user suggestions for improvement, and geospatial analysis of HISA prescriptions concentration.^1-4

The geospatial analyses of HISA prescriptions revealed clusters of high numbers of HISA users (hot spots) and low numbers of HISA users (cold spots), indicating that HISA is either not prescribed or uniformly used across the US. The previous research prompted investigation into county-level variables that may impact HISA utilization rates. This inquiry focuses on county characteristics associated with HISA use rates, such as measures of clinical care and quality of care (eg, access to health services variables, lack of insurance, preventable hospital stays), physical environment, and sociodemographic characteristics. Clinical care and quality of care measures promote the interaction with HCPs. Moreover, access to health care is an important indicator of health outcomes.^5,6 An individual’s capacity to access health services, such as a HM program, greatly impacts well-being, safety, independence, and health.^2,4 Well-being, safety, independence, and health become compromised if individuals cannot access care, if needed care is lacking in their area, if HCPs are not available, or are unwilling to provide care due to lack of insurance coverage.^7-12 In locations where health care services are minimal due to lack of specialists or health care facilities, the quality of (or access to) care may be compromised, resulting in preventable conditions becoming problematic.^13,14 These conditions may result in unnecessary hospitalizations for conditions that could have been treated during routine care. Financial barriers to care particularly among low-income people and the uninsured have proven detrimental to health.^15,16 On the other hand, preventable hospital stays are a quality of care measure (ie, a proxy for poor quality of care). HISA operates within a health care system; thus, it is imperative to include these measures impacting health. 

In this study, we sought to identify county-level predictors—in particular, county-level proxies for access to care—that may be associated with county-level HISA use. We define HISA utilization rate as the percentage of a county’s VHA patients who have received a HISA award.

Methods

This study used data from the National Prosthetics Patient Database (NPPD), US Department of Veterans Affairs (VA) medical database inpatient and outpatient datasets, VHA Support Service Center (VSSC) data cubes, and the County Health Rankings database (CHRD). First, the study cohort was identified from NPPD users who have obtained a HISA award from fiscal years (FY) 2015 to 2018. Analysis started with FY 2015 following new regulations (38 CFR § 17) governing the operations of the HISA program.² The study cohort was matched with records from NPPD and VA inpatient and outpatient datasets to obtain information about the veterans’ demographic characteristics and their HM characteristics and costs. The number of VHA end-of-year (EOY) patients per county was extracted from the VSSC Current Enrollment Cube, which was used in calculation of the county-level HISA utilization rate.¹⁷ Finally, zip code–based locational data were used to calculate approximate drive time and distance from the HISA user’s approximate location to the facility where they received their HM prescription. Drive times and drive distances were calculated with Esri ArcGIS Pro (v2.6.3) by placing zip code centroid and VHA facilities on a nationwide road network that contains both road speeds and distances.

Calculations

Patient-level data were aggregated up to county-level variables by calculating the sum, mean, or percent per county. HISA user sample characteristics, including sex, race, rurality (urban, rural), marital status, and Class 1 vs Class 2 disability-related eligibility groups, were aggregated to the county level by calculating percentages of HISA users of the given characteristics out of total HISA users in the county. Disability-related eligibility groups (Class 1 vs Class 2 HISA users) determines the maximum lifetime award dollar amount. Specifically, those with service-connected disabilities or those with a ≥ 50% disability rating (regardless of whether or not their disability is service connected) are classified as Class 1 HISA users and are eligible to receive a maximum lifetime award of $6800. Those with a recorded disability that is not connected to their military service, and who have a disability rating of < 50% are classified as Class 2 HISA users and are eligible to receive a lifetime maximum award of $2000.

The county-level number of HISA users was used as the numerator for calculation of county-level HISA utilization rate. Counties with zero HISA users were excluded. The number of EOY VHA patients per county in FY 2018 was divided by 1000 and used as the denominator in the calculation of county-level HISA utilization rate. Thus, the outcome variable is HISA utilization rate per 1000 VHA patients in FY 2018 (HISA utilization rate).

County-Level Variables

County-level variables were downloaded from the 2020 CHRD.^5,6 An explanation of the CHRD model and the factors used in this study are shown in the eAppendix (available at doi: 10.12788/fp.0279).⁶ County-level aggregated HISA user data and the CHRD data were matched using county Federal Information Processing Standards codes. Access to care measures collected from CHRD included percentages uninsured and ratios of population to primary care physicians, dentists, mental health professionals, and other primary care professionals. Other CHRD measures included those for quality of care (rate of preventable hospital stay) and housing quality (percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, percent of homeownership). Of secondary interest was county population rurality, as previous research findings showed the annual average of HISA users who are from rural areas ranged from 30 to 35%.

Analysis Methods

SAS (v9.4), R (v4.0.2), and RStudio (v1.3.1093) were used for data preparation and analysis.¹⁸ Multiple regression analysis was used to predict county-level utilization rate from county-level variables. Sociodemographic characteristics from CHRD and HISA data were included as important control predictors in the regression model, though our focus for this paper are the access to care and housing quality predictors.

Model diagnostics (examination of model residuals, Breusch-Godfrey test, Breusch-Pagan test) revealed significant heteroskedasticity of the model; thus, robust standard errors and associated P values were computed using the R estimatr package (v0.30.2).¹⁹ Some predictor variables of interest (eg, ratio of mental health professionals) were removed during the model building process either due to problems of multicollinearity or excessive missingness that would have resulted in listwise deletion.

Results

County-level HISA utilization rate per 1000 EOY VHA patients ranged from 0.09 to 59.7%, with a 6.6% mean and 5% median (Figure 2). The data were highly positively skewed. The final model included 33 total predictor variables (Table 1). The final regression model was a significantly better predictor of county-level HISA utilization rate than a null model (F[33-2184], 10.18; P < .001). The adjusted model R² showed that the overall model accounted for approximately 23% of variance in county-level HISA utilization rate (Table 2).

Among the primary variables of interest, percent uninsured adults and rate of preventable hospital stays emerged as significant predictors of county-level HISA utilization rate. Specifically, county percentage of uninsured adults was negatively related to county-level HISA utilization rate (b = -8.99, P = .005), indicating that the higher the proportion of uninsured adults—with all other predictors held constant—the lower the HISA utilization rate. Percent uninsured adults ranged from 2.7 to 42.4% across counties, with a mean (SD) of 12.7% (5.8%) and 11.4% median.

Discussion

This study examined whether county-level characteristics, specifically variables for access to care, quality of care, and housing quality, were predictive of a county’s HISA utilization rate. Given that this series of work on the HISA program is (to our knowledge) the first of its kind, and given the exploratory nature of this analysis, we did not have specific predictions for the effects of any one given variable. Nevertheless, some of the results were surprising, and we believe they warrant additional study. In particular, the opposing direction of effects for access to care and quality of care variables were hard to reconcile.

The county percent of uninsured adults (an access to care variable, specifically, a proxy for poor access to care) was negatively associated with county-level HISA utilization rate, whereas the county rate of preventable hospital stays (a quality of care variable, but also potentially an access to care variable, and specifically, proxies for poor quality of care or poor access to care) was positively associated with county-level HISA utilization rate. To describe the relationships more generally, one coefficient in the regression model indicated that the poorer the access to care, the lower the HISA utilization rate (higher percent of uninsured adults predicts lower HISA utilization rate), while another coefficient in the regression model indicated the poorer the quality of and access to care, the higher the HISA utilization rate (higher rate of preventable hospital stays predicts higher HISA utilization rate). Future study is warranted to disentangle and reconcile the various community-level predictors of this service.

Housing quality measures (eg, percent of households with high housing costs, percent of households with overcrowding, percent of households with lack of kitchen or plumbing, percent of households with severe housing cost burden, and percent of homeownership) are important in the consideration of whether a HM will be performed or should be performed. For example, if a person is cost burdened by the amount of expenditure spent in housing there will be little discretionary funds to perform a HM. Individuals who do not own their home may experience complications in obtaining permission from landlords to perform a HM. County-level predictors of housing quality (percent of households with high housing costs, overcrowding, and lack of kitchen or plumbing) were not significantly associated with county-level HISA utilization rate but are also nevertheless relevant to the discussion of home modifications. Of particular interest is the percent of households with lack of kitchen or plumbing variable, which was positively related to county-level HISA utilization rate although not statistically significant. HM elements related to the kitchen (eg, heighten countertop) add to the accessibility of the home allowing for the performing of activities of daily living such as cooking. Between FY 2015 and FY 2018, we discovered 131 prescriptions for kitchen (n = 90) and plumbing (n = 41) HMs, which is a very small proportion of the 30,780 total HMs (there were 24,397 bathroom HMs). The nonsignificant coefficient for this variable may reflect the small number of veterans that obtained these HM.

Limitations

The potentially conflicting direction of effects for a significant access to care variable (percent uninsured adults) and a significant access to care and quality of care variable (preventable hospital stays) are interesting and warrant additional study, but the inability to interpret or explain this apparent inconsistency constitutes a limitation of the current data and analyses presented here. Another limitation is that this analysis uses county-level predictors for what is ultimately an individual-level outcome. It would have been ideal to have both individual- and county-level data to conduct a multilevel analysis; in particular, individual-level data within counties of individuals (both veterans and nonveterans) who did not receive a HISA award (including both those who applied and were denied, and who did not apply) would be highly valuable.

Conclusions

Our continuing research into veterans’ use of HM fills a gap in the literature about the characteristics of HISA users, the impact of county-level variables on the use of HISA, and the geographic distribution and use of HISA within the VHA. While it is important to examine the influence of broader systems on individual outcomes, there could be myriad other factors that are more proximal and more closely related to whether any one individual applies for, let alone receives, a HISA award. Indeed, a low overall adjusted model R² indicates that there is considerable variability in county-level HISA utilization rate that was not accounted for by the current model; this further speaks to warranted additional study.

More research is needed to understand and account for geographical variation in HISA utilization rate across the US. However, this work serves as an exploratory first step at quantifying and predicting HISA utilization rate at a broad level, with the ultimate goal of increasing access to HMs for veterans with disabilities.

Acknowledgments

This research was supported by grant 15521 from the US Department of Veterans Affairs, Office of Rural Health. Furthermore, the research was supported in part by grant K12 HD055929 from the National Institutes of Health. We want to acknowledge Cheri E. Knecht, Project Coordinator, for her assistance throughout all aspects of our research study and for her thoughtful contributions during the writing of this manuscript.

I still remember the woman who came to my office that day, years ago. She was struggling and uncomfortable, and she wanted “something” for stress. She described her life, and to me, it sounded stressful. She lived in a blended family and she described the chaos that one might expect to find in a household with four teens, their friends, their activities, and all it took to keep the household going. I spent 2 hours evaluating the patient, and I could not find a diagnosis that fit this problem nor – I believed – a pill that would fix it. She didn’t “meet criteria” for a psychiatric disorder, but she insisted she was uncomfortable and she wanted to try medication. I admit, I relented and I gave her a prescription for fluoxetine.

When she returned a few weeks later, my patient said she felt better, and what I remember decades later was her statement: “Now I can see dishes in the sink and be okay with it.” Perhaps she had downplayed her anxiety during our first meeting, but what I took from this was that some people are uncomfortable in ways that our lexicon does not capture, and sometimes medication helps with this discomfort.

The APA’s Diagnostic and Statistical Manual of Mental Disorders attempts to capture the problems of emotional and behavioral distress and classify them into discrete syndromes that can be validated and reliably diagnosed by different evaluators. Our disorders are syndromic; they are defined by clusters of symptoms that occur together, and not by a single symptom, lab value, or radiologic finding. The DSM is rewritten periodically so that what is or is not a disorder can bend with new discoveries and with a changing culture. And for better or for worse, when there is an available medication that can alleviate a problem, this may influence what once was a variant of normal into becoming a disorder.

Our illnesses often lie along a spectrum, so there is no precise point where someone who is easily distracted is a person with attention deficit disorder as opposed to being a mentally healthy person who is easily distracted, or a shy person is someone with social anxiety disorder. At the extremes, pathology and dysfunction are obvious, but sometimes we are left to let patients define whether they are suffering, whether they want to address this with medications, and whether their distress warrants taking a chance that they might have side effects or an adverse reaction to a medication.

When we look at our criteria, sometimes we fall short. One needs to have at least five symptoms out of nine options, to be present for 2 weeks to be diagnosed with major depression, yet I don’t know a single psychiatrist who would not offer medication to a patient who ascribed to feeling profoundly sad with thoughts of suicide in the absence of other symptoms of depression. These issues have come to the forefront with the recent inclusion of prolonged grief in the DSM, as a disorder that is distinct from both normal grieving and from major depression.

In recent weeks, mass murder has been on everyone’s mind as we mourn those lost in Uvalde, Buffalo, and unfortunately, in so many other places. Absolutely no one thinks that someone who shoots strangers is “normal” or emotionally well. Yet psychiatry is often tasked with figuring out if someone is mad (mentally ill), bad (evil), or both. We don’t have a clear path for how to treat and manage people who commit horrendous acts of violence unless they meet criteria for another illness. Yet no one would argue that a person who informs others that he is thinking of killing strangers is in need of some type of intervention, regardless of his motive. We struggle too, with how to manage people who have more regular angry outbursts or emotional dysregulation. Perhaps we diagnose intermittent explosive disorder, or irritability caused by a mood disorder, but we don’t always know how to help people to control their tempers and modulate their emotions. And our semantics to describe psychic pain and anguish are surprisingly limited – sometimes we can only assume that someone who lashes out must be in turmoil.

Psychiatry continues to struggle with our relationship with human suffering. Suffering is part of life, not necessarily a sign of illness, and in his iconic memoir, “Man’s Search for Meaning,” psychiatrist Viktor Frankl, MD, wrote of the atrocities he endured in a Nazi concentration camp. It was through his suffering that Dr. Frankl found meaning and he used these harrowing experiences to fuel positive emotions later in life. Dr. Frankl wrote: “If there is a meaning in life at all, then there must be a meaning in suffering. Suffering is an ineradicable part of life, even as fate and death. Without suffering and death, human life cannot be complete.”

Suffering may be the kindling for acts of violence, or for profound creativity. Would we have music, art, cinema, poetry, or fiction if no one ever suffered? Yet suffering and emotional torment are often what leads people to seek treatment, and what leads us, as healers, to offer any range of therapies. For years, suicide rates have been rising, as have overdose death. And now, in addition to these “deaths of despair,” we are hearing about skyrocketing rates of depression and anxiety in our world that is so full of reasons to be sad and anxious. Access to treatment is limited by so many things, and it is not always clear when one needs psychiatric interventions or when problems will heal on their own, leaving scars or not.

I wrote this article in response to the hundreds of comments that were placed on an article I wrote after the horrors at Uvalde and Buffalo: “Don’t Equate Mass Shootings with Mental Illness.” Many of the commenters suggested I believe the shooter was perfectly sane, and that I am naive (or worse). Many wrote in with their own thoughts about what causes people to become mass murderers. One commenter wrote: “To suggest that random killers do not have mental health issues and their behavior is normal is ridiculous.” I don’t believe that I ever suggested that such behavior was normal, but – for many of these crimes – we as a society have decided to treat the behavior as criminal and not as the product of our current concept of mental disorders. Obviously, people who are well, who are emotionally at peace and comfortable in their own skin, don’t kill strangers.

Dr. Miller is a coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore.

I still remember the woman who came to my office that day, years ago. She was struggling and uncomfortable, and she wanted “something” for stress. She described her life, and to me, it sounded stressful. She lived in a blended family and she described the chaos that one might expect to find in a household with four teens, their friends, their activities, and all it took to keep the household going. I spent 2 hours evaluating the patient, and I could not find a diagnosis that fit this problem nor – I believed – a pill that would fix it. She didn’t “meet criteria” for a psychiatric disorder, but she insisted she was uncomfortable and she wanted to try medication. I admit, I relented and I gave her a prescription for fluoxetine.

When she returned a few weeks later, my patient said she felt better, and what I remember decades later was her statement: “Now I can see dishes in the sink and be okay with it.” Perhaps she had downplayed her anxiety during our first meeting, but what I took from this was that some people are uncomfortable in ways that our lexicon does not capture, and sometimes medication helps with this discomfort.

The APA’s Diagnostic and Statistical Manual of Mental Disorders attempts to capture the problems of emotional and behavioral distress and classify them into discrete syndromes that can be validated and reliably diagnosed by different evaluators. Our disorders are syndromic; they are defined by clusters of symptoms that occur together, and not by a single symptom, lab value, or radiologic finding. The DSM is rewritten periodically so that what is or is not a disorder can bend with new discoveries and with a changing culture. And for better or for worse, when there is an available medication that can alleviate a problem, this may influence what once was a variant of normal into becoming a disorder.

Our illnesses often lie along a spectrum, so there is no precise point where someone who is easily distracted is a person with attention deficit disorder as opposed to being a mentally healthy person who is easily distracted, or a shy person is someone with social anxiety disorder. At the extremes, pathology and dysfunction are obvious, but sometimes we are left to let patients define whether they are suffering, whether they want to address this with medications, and whether their distress warrants taking a chance that they might have side effects or an adverse reaction to a medication.

When we look at our criteria, sometimes we fall short. One needs to have at least five symptoms out of nine options, to be present for 2 weeks to be diagnosed with major depression, yet I don’t know a single psychiatrist who would not offer medication to a patient who ascribed to feeling profoundly sad with thoughts of suicide in the absence of other symptoms of depression. These issues have come to the forefront with the recent inclusion of prolonged grief in the DSM, as a disorder that is distinct from both normal grieving and from major depression.

In recent weeks, mass murder has been on everyone’s mind as we mourn those lost in Uvalde, Buffalo, and unfortunately, in so many other places. Absolutely no one thinks that someone who shoots strangers is “normal” or emotionally well. Yet psychiatry is often tasked with figuring out if someone is mad (mentally ill), bad (evil), or both. We don’t have a clear path for how to treat and manage people who commit horrendous acts of violence unless they meet criteria for another illness. Yet no one would argue that a person who informs others that he is thinking of killing strangers is in need of some type of intervention, regardless of his motive. We struggle too, with how to manage people who have more regular angry outbursts or emotional dysregulation. Perhaps we diagnose intermittent explosive disorder, or irritability caused by a mood disorder, but we don’t always know how to help people to control their tempers and modulate their emotions. And our semantics to describe psychic pain and anguish are surprisingly limited – sometimes we can only assume that someone who lashes out must be in turmoil.

Psychiatry continues to struggle with our relationship with human suffering. Suffering is part of life, not necessarily a sign of illness, and in his iconic memoir, “Man’s Search for Meaning,” psychiatrist Viktor Frankl, MD, wrote of the atrocities he endured in a Nazi concentration camp. It was through his suffering that Dr. Frankl found meaning and he used these harrowing experiences to fuel positive emotions later in life. Dr. Frankl wrote: “If there is a meaning in life at all, then there must be a meaning in suffering. Suffering is an ineradicable part of life, even as fate and death. Without suffering and death, human life cannot be complete.”

Suffering may be the kindling for acts of violence, or for profound creativity. Would we have music, art, cinema, poetry, or fiction if no one ever suffered? Yet suffering and emotional torment are often what leads people to seek treatment, and what leads us, as healers, to offer any range of therapies. For years, suicide rates have been rising, as have overdose death. And now, in addition to these “deaths of despair,” we are hearing about skyrocketing rates of depression and anxiety in our world that is so full of reasons to be sad and anxious. Access to treatment is limited by so many things, and it is not always clear when one needs psychiatric interventions or when problems will heal on their own, leaving scars or not.

I wrote this article in response to the hundreds of comments that were placed on an article I wrote after the horrors at Uvalde and Buffalo: “Don’t Equate Mass Shootings with Mental Illness.” Many of the commenters suggested I believe the shooter was perfectly sane, and that I am naive (or worse). Many wrote in with their own thoughts about what causes people to become mass murderers. One commenter wrote: “To suggest that random killers do not have mental health issues and their behavior is normal is ridiculous.” I don’t believe that I ever suggested that such behavior was normal, but – for many of these crimes – we as a society have decided to treat the behavior as criminal and not as the product of our current concept of mental disorders. Obviously, people who are well, who are emotionally at peace and comfortable in their own skin, don’t kill strangers.

Dr. Miller is a coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore.

I still remember the woman who came to my office that day, years ago. She was struggling and uncomfortable, and she wanted “something” for stress. She described her life, and to me, it sounded stressful. She lived in a blended family and she described the chaos that one might expect to find in a household with four teens, their friends, their activities, and all it took to keep the household going. I spent 2 hours evaluating the patient, and I could not find a diagnosis that fit this problem nor – I believed – a pill that would fix it. She didn’t “meet criteria” for a psychiatric disorder, but she insisted she was uncomfortable and she wanted to try medication. I admit, I relented and I gave her a prescription for fluoxetine.

When she returned a few weeks later, my patient said she felt better, and what I remember decades later was her statement: “Now I can see dishes in the sink and be okay with it.” Perhaps she had downplayed her anxiety during our first meeting, but what I took from this was that some people are uncomfortable in ways that our lexicon does not capture, and sometimes medication helps with this discomfort.

The APA’s Diagnostic and Statistical Manual of Mental Disorders attempts to capture the problems of emotional and behavioral distress and classify them into discrete syndromes that can be validated and reliably diagnosed by different evaluators. Our disorders are syndromic; they are defined by clusters of symptoms that occur together, and not by a single symptom, lab value, or radiologic finding. The DSM is rewritten periodically so that what is or is not a disorder can bend with new discoveries and with a changing culture. And for better or for worse, when there is an available medication that can alleviate a problem, this may influence what once was a variant of normal into becoming a disorder.

Our illnesses often lie along a spectrum, so there is no precise point where someone who is easily distracted is a person with attention deficit disorder as opposed to being a mentally healthy person who is easily distracted, or a shy person is someone with social anxiety disorder. At the extremes, pathology and dysfunction are obvious, but sometimes we are left to let patients define whether they are suffering, whether they want to address this with medications, and whether their distress warrants taking a chance that they might have side effects or an adverse reaction to a medication.

When we look at our criteria, sometimes we fall short. One needs to have at least five symptoms out of nine options, to be present for 2 weeks to be diagnosed with major depression, yet I don’t know a single psychiatrist who would not offer medication to a patient who ascribed to feeling profoundly sad with thoughts of suicide in the absence of other symptoms of depression. These issues have come to the forefront with the recent inclusion of prolonged grief in the DSM, as a disorder that is distinct from both normal grieving and from major depression.

In recent weeks, mass murder has been on everyone’s mind as we mourn those lost in Uvalde, Buffalo, and unfortunately, in so many other places. Absolutely no one thinks that someone who shoots strangers is “normal” or emotionally well. Yet psychiatry is often tasked with figuring out if someone is mad (mentally ill), bad (evil), or both. We don’t have a clear path for how to treat and manage people who commit horrendous acts of violence unless they meet criteria for another illness. Yet no one would argue that a person who informs others that he is thinking of killing strangers is in need of some type of intervention, regardless of his motive. We struggle too, with how to manage people who have more regular angry outbursts or emotional dysregulation. Perhaps we diagnose intermittent explosive disorder, or irritability caused by a mood disorder, but we don’t always know how to help people to control their tempers and modulate their emotions. And our semantics to describe psychic pain and anguish are surprisingly limited – sometimes we can only assume that someone who lashes out must be in turmoil.

Psychiatry continues to struggle with our relationship with human suffering. Suffering is part of life, not necessarily a sign of illness, and in his iconic memoir, “Man’s Search for Meaning,” psychiatrist Viktor Frankl, MD, wrote of the atrocities he endured in a Nazi concentration camp. It was through his suffering that Dr. Frankl found meaning and he used these harrowing experiences to fuel positive emotions later in life. Dr. Frankl wrote: “If there is a meaning in life at all, then there must be a meaning in suffering. Suffering is an ineradicable part of life, even as fate and death. Without suffering and death, human life cannot be complete.”

Suffering may be the kindling for acts of violence, or for profound creativity. Would we have music, art, cinema, poetry, or fiction if no one ever suffered? Yet suffering and emotional torment are often what leads people to seek treatment, and what leads us, as healers, to offer any range of therapies. For years, suicide rates have been rising, as have overdose death. And now, in addition to these “deaths of despair,” we are hearing about skyrocketing rates of depression and anxiety in our world that is so full of reasons to be sad and anxious. Access to treatment is limited by so many things, and it is not always clear when one needs psychiatric interventions or when problems will heal on their own, leaving scars or not.

I wrote this article in response to the hundreds of comments that were placed on an article I wrote after the horrors at Uvalde and Buffalo: “Don’t Equate Mass Shootings with Mental Illness.” Many of the commenters suggested I believe the shooter was perfectly sane, and that I am naive (or worse). Many wrote in with their own thoughts about what causes people to become mass murderers. One commenter wrote: “To suggest that random killers do not have mental health issues and their behavior is normal is ridiculous.” I don’t believe that I ever suggested that such behavior was normal, but – for many of these crimes – we as a society have decided to treat the behavior as criminal and not as the product of our current concept of mental disorders. Obviously, people who are well, who are emotionally at peace and comfortable in their own skin, don’t kill strangers.

Dr. Miller is a coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore.

The U.S. Food and Drug Administration approved baricitinib oral tablets on June 13 as the first systemic treatment for adult patients with severe alopecia areata.

The disorder with the hallmark signs of patchy baldness affects more than 300,000 people in the United States each year. In patients with the autoimmune disorder, the body attacks its own hair follicles and hair falls out, often in clumps. In February, the FDA granted priority review for baricitinib in adults with severe AA.

Baricitinib (Olumiant) is a Janus kinase (JAK) inhibitor, which blocks the activity of one or more enzymes, interfering with the pathway that leads to inflammation.

The FDA reports the most common side effects include upper respiratory tract infections, headache, acne, hyperlipidemia, increase of creatinine phosphokinase, urinary tract infection, elevated liver enzymes, inflammation of hair follicles, fatigue, lower respiratory tract infections, nausea, Candida infections, anemia, neutropenia, abdominal pain, herpes zoster (shingles), and weight gain. The labeling for baricitinib includes a boxed warning for serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis.
 

Evidence from two trials led to announcement

The decision came after review of the results from two randomized, double-blind, placebo-controlled trials (BRAVE AA-1 and BRAVE AA-2) with patients who had at least 50% scalp hair loss as measured by the Severity of Alopecia Tool (SALT score) for more than 6 months.

Patients in these trials got either a placebo, 2 mg of baricitinib, or 4 mg of baricitinib every day. The primary endpoint for both trials was the proportion of patients who achieved at least 80% scalp hair coverage at week 36.

In BRAVE AA-1, 22% of the 184 patients who received 2 mg of baricitinib and 35% of the 281 patients who received 4 mg of baricitinib achieved at least 80% scalp hair coverage, compared with 5% of the 189 patients in the placebo group.

In BRAVE AA-2, 17% of the 156 patients who received 2 mg of baricitinib and 32% of the 234 patients who received 4 mg achieved at least 80% scalp hair coverage, compared with 3% of the 156 patients in the placebo group.

The results were reported at the annual meeting of the American Academy of Dermatology meeting in March.

Baricitinib was originally approved in 2018 as a treatment for adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response to one or more tumor necrosis factor (TNF)–blockers. It is also approved for treating COVID-19 in certain hospitalized adults. 

Two other companies, Pfizer and Concert Pharmaceuticals, have JAK inhibitors in late-stage development for AA. The drugs are already on the market for treating rheumatoid arthritis and other autoimmune diseases. FDA approval is important for insurance coverage of the drugs, which have a list price of nearly $2,500 a month, according to The New York Times.

Until now, the only treatments for moderate to severe AA approved by the FDA have been intralesional steroid injections, contact sensitization, and systemic immunosuppressants, but they have demonstrated limited efficacy, are inconvenient for patients to take, and have been unsuitable for use long term.

“Today’s approval will help fulfill a significant unmet need for patients with severe alopecia areata,” Kendall Marcus, MD, director of the Division of Dermatology and Dentistry in the FDA’s Center for Drug Evaluation and Research, said in the press release.

As Medscape reported last month, The European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) has recommended approval of baricitinib for adults with severe AA.

AA received widespread international attention earlier this year at the Academy Awards ceremony, when actor Will Smith walked from the audience up onto the stage and slapped comedian Chris Rock in the face after he directed a joke at Mr. Smith’s wife, Jada Pinkett Smith, about her shaved head. Mrs. Pinkett Smith has AA and has been public about her struggles with the disease.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration approved baricitinib oral tablets on June 13 as the first systemic treatment for adult patients with severe alopecia areata.

The disorder with the hallmark signs of patchy baldness affects more than 300,000 people in the United States each year. In patients with the autoimmune disorder, the body attacks its own hair follicles and hair falls out, often in clumps. In February, the FDA granted priority review for baricitinib in adults with severe AA.

Baricitinib (Olumiant) is a Janus kinase (JAK) inhibitor, which blocks the activity of one or more enzymes, interfering with the pathway that leads to inflammation.

The FDA reports the most common side effects include upper respiratory tract infections, headache, acne, hyperlipidemia, increase of creatinine phosphokinase, urinary tract infection, elevated liver enzymes, inflammation of hair follicles, fatigue, lower respiratory tract infections, nausea, Candida infections, anemia, neutropenia, abdominal pain, herpes zoster (shingles), and weight gain. The labeling for baricitinib includes a boxed warning for serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis.
 

Evidence from two trials led to announcement

The decision came after review of the results from two randomized, double-blind, placebo-controlled trials (BRAVE AA-1 and BRAVE AA-2) with patients who had at least 50% scalp hair loss as measured by the Severity of Alopecia Tool (SALT score) for more than 6 months.

Patients in these trials got either a placebo, 2 mg of baricitinib, or 4 mg of baricitinib every day. The primary endpoint for both trials was the proportion of patients who achieved at least 80% scalp hair coverage at week 36.

In BRAVE AA-1, 22% of the 184 patients who received 2 mg of baricitinib and 35% of the 281 patients who received 4 mg of baricitinib achieved at least 80% scalp hair coverage, compared with 5% of the 189 patients in the placebo group.

In BRAVE AA-2, 17% of the 156 patients who received 2 mg of baricitinib and 32% of the 234 patients who received 4 mg achieved at least 80% scalp hair coverage, compared with 3% of the 156 patients in the placebo group.

The results were reported at the annual meeting of the American Academy of Dermatology meeting in March.

Baricitinib was originally approved in 2018 as a treatment for adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response to one or more tumor necrosis factor (TNF)–blockers. It is also approved for treating COVID-19 in certain hospitalized adults. 

Two other companies, Pfizer and Concert Pharmaceuticals, have JAK inhibitors in late-stage development for AA. The drugs are already on the market for treating rheumatoid arthritis and other autoimmune diseases. FDA approval is important for insurance coverage of the drugs, which have a list price of nearly $2,500 a month, according to The New York Times.

Until now, the only treatments for moderate to severe AA approved by the FDA have been intralesional steroid injections, contact sensitization, and systemic immunosuppressants, but they have demonstrated limited efficacy, are inconvenient for patients to take, and have been unsuitable for use long term.

“Today’s approval will help fulfill a significant unmet need for patients with severe alopecia areata,” Kendall Marcus, MD, director of the Division of Dermatology and Dentistry in the FDA’s Center for Drug Evaluation and Research, said in the press release.

As Medscape reported last month, The European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) has recommended approval of baricitinib for adults with severe AA.

AA received widespread international attention earlier this year at the Academy Awards ceremony, when actor Will Smith walked from the audience up onto the stage and slapped comedian Chris Rock in the face after he directed a joke at Mr. Smith’s wife, Jada Pinkett Smith, about her shaved head. Mrs. Pinkett Smith has AA and has been public about her struggles with the disease.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration approved baricitinib oral tablets on June 13 as the first systemic treatment for adult patients with severe alopecia areata.

The disorder with the hallmark signs of patchy baldness affects more than 300,000 people in the United States each year. In patients with the autoimmune disorder, the body attacks its own hair follicles and hair falls out, often in clumps. In February, the FDA granted priority review for baricitinib in adults with severe AA.

Baricitinib (Olumiant) is a Janus kinase (JAK) inhibitor, which blocks the activity of one or more enzymes, interfering with the pathway that leads to inflammation.

The FDA reports the most common side effects include upper respiratory tract infections, headache, acne, hyperlipidemia, increase of creatinine phosphokinase, urinary tract infection, elevated liver enzymes, inflammation of hair follicles, fatigue, lower respiratory tract infections, nausea, Candida infections, anemia, neutropenia, abdominal pain, herpes zoster (shingles), and weight gain. The labeling for baricitinib includes a boxed warning for serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis.
 

Evidence from two trials led to announcement

The decision came after review of the results from two randomized, double-blind, placebo-controlled trials (BRAVE AA-1 and BRAVE AA-2) with patients who had at least 50% scalp hair loss as measured by the Severity of Alopecia Tool (SALT score) for more than 6 months.

Patients in these trials got either a placebo, 2 mg of baricitinib, or 4 mg of baricitinib every day. The primary endpoint for both trials was the proportion of patients who achieved at least 80% scalp hair coverage at week 36.

In BRAVE AA-1, 22% of the 184 patients who received 2 mg of baricitinib and 35% of the 281 patients who received 4 mg of baricitinib achieved at least 80% scalp hair coverage, compared with 5% of the 189 patients in the placebo group.

In BRAVE AA-2, 17% of the 156 patients who received 2 mg of baricitinib and 32% of the 234 patients who received 4 mg achieved at least 80% scalp hair coverage, compared with 3% of the 156 patients in the placebo group.

The results were reported at the annual meeting of the American Academy of Dermatology meeting in March.

Baricitinib was originally approved in 2018 as a treatment for adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response to one or more tumor necrosis factor (TNF)–blockers. It is also approved for treating COVID-19 in certain hospitalized adults. 

Two other companies, Pfizer and Concert Pharmaceuticals, have JAK inhibitors in late-stage development for AA. The drugs are already on the market for treating rheumatoid arthritis and other autoimmune diseases. FDA approval is important for insurance coverage of the drugs, which have a list price of nearly $2,500 a month, according to The New York Times.

Until now, the only treatments for moderate to severe AA approved by the FDA have been intralesional steroid injections, contact sensitization, and systemic immunosuppressants, but they have demonstrated limited efficacy, are inconvenient for patients to take, and have been unsuitable for use long term.

“Today’s approval will help fulfill a significant unmet need for patients with severe alopecia areata,” Kendall Marcus, MD, director of the Division of Dermatology and Dentistry in the FDA’s Center for Drug Evaluation and Research, said in the press release.

As Medscape reported last month, The European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) has recommended approval of baricitinib for adults with severe AA.

AA received widespread international attention earlier this year at the Academy Awards ceremony, when actor Will Smith walked from the audience up onto the stage and slapped comedian Chris Rock in the face after he directed a joke at Mr. Smith’s wife, Jada Pinkett Smith, about her shaved head. Mrs. Pinkett Smith has AA and has been public about her struggles with the disease.

A version of this article first appeared on Medscape.com.

The investigational drug momelotinib has shown benefits in myelofibrosis in a new phase 3 trial, which could now lead to a Food and Drug Administration approval.

This drug had previously shown mixed results in a phase 3 trial funded by Gilead, which stopped development of the product; it was acquired by Sierra Oncology, which conducted the latest positive phase 3 trial and now plans to use it to apply for FDA approval.

Momelotinib, an oral Janus kinase 1 and JAK2 inhibitor, significantly outperformed danazol on symptoms, spleen size, and anemia in adults with anemic myelofibrosis in the randomized trial of 195 patients from 21 countries presented at the annual meeting of the American Society of Clinical Oncology.

“The current state for the treatment of myelofibrosis relies on JAK2,” said Ruben Mesa, MD, of the Mays Cancer Center at the UT Health San Antonio MD Anderson Cancer Center.

“Momelotinib is a JAK1 and JAK2 inhibitor.” However, in the early days of studying momelotinib,“it became clear that there was also potentially an improvement in anemia,” which may be related to the additional inhibition of ACVR1, he explained.

Data suggest that the ability to curb anemia in anemic myelofibrosis patients prolongs their lives for up to 8 years, Dr. Mesa added.

Previous studies, notably the phase 3 SIMPLIFY study, showed that momelotinib was associated with comparable effects on spleen volume, transfusion, and total symptom scores from baseline that were similar to ruxolitinib.

In the current study, known as MOMENTUM, a daily dose of momelotinib was compared to danazol for treatment of symptomatic and anemic myelofibrosis (MF) patients who had previously received standard JAK-inhibitor therapy.

In the study, the researchers randomized 130 patients to momelotinib and 65 to danazol. After 24 weeks, those in the danazol group were allowed to cross over to momelotinib. The primary endpoint of the study was total symptom score (TSS) response after 24 weeks. Secondary endpoints included transfusion independence and splenic response at 24 weeks. The median age of the patients in the momelotinib group was 71 years, 60.8% were male, and 82% were white. The baseline demographics were not significantly different in the danazol group.

Overall, 24.6% of momelotinib patients responded with improved total symptom scores at 24 weeks vs. 9.2% of the danazol group. Spleen response also was significantly higher in the momelotinib group; 40% of patients showed a 25% reduction and 23% showed a 35% reduction, compared with 6.2% and 3.1%, respectively, of patients in the danazol group. Transfusion independence at week 24 also was higher for momelotinib patients, compared with danazol patients (31% vs. 20%, respectively, P = 0064).

Adverse events of grade 3 or higher occurred in 53.8% of momelotinib patients and 64.6% of danazol patients, and serious adverse events occurred in 34.6% and 40.0%, respectively. Nearly all patients had anemia, but only 27.7% and 26.2% of the momelotinib and danazol groups, respectively, had thrombocytopenia of grade 3 or higher. The most common nonhematologic adverse events were diarrhea, nausea, and increased blood creatinine. A total of 27.7% of the patients in the momelotinib group discontinued treatment; 16 of whom did so because of an adverse event.

Also, at 24 weeks, patients in the momelotinib group showed a trend towards increased overall survival, compared with danazol (HR, 0.506, P = 0.719).

With momelotinib, there is a consistent thrombocytopenic profile across subgroups, the data on which were presented separately at ASCO (poster 7061), Dr. Mesa added.

“We feel that these findings support the future use of momelotinib as an effective treatment in MF patients, especially those with anemia,” he concluded.
 

Cytopenia data are exciting

The key finding in the current study is that “momelotinib leads to important endpoints including significant improvement in symptoms and spleen reduction,” said Dr. Gabriela Hobbs of Harvard Medical School, Boston, who served as the discussant for the study.

“I think a novel finding of momelotinib that is definitely exciting from the treatment perspective is that momelotinib can also lead to improvement in cytopenias,” she said. “We often have to decide between treating the symptoms of the spleen at the expense of blood counts,” in MF patients, she noted.

The study was sponsored by Sierra Oncology. Dr. Mesa disclosed relationships with companies including Constellation Pharmaceutical, La Jolla Pharma, and study sponsor Sierra Oncology, as well as funding from AbbVie, Celgene, Constellation Pharmaceuticals, CTI, Genentech, Incyte, Mays Cancer Center, NCI, Promedior, and Samus. Dr. Hobbs had no financial conflicts to disclose.

This article was updated 06/14/2022.

The investigational drug momelotinib has shown benefits in myelofibrosis in a new phase 3 trial, which could now lead to a Food and Drug Administration approval.

This drug had previously shown mixed results in a phase 3 trial funded by Gilead, which stopped development of the product; it was acquired by Sierra Oncology, which conducted the latest positive phase 3 trial and now plans to use it to apply for FDA approval.

Momelotinib, an oral Janus kinase 1 and JAK2 inhibitor, significantly outperformed danazol on symptoms, spleen size, and anemia in adults with anemic myelofibrosis in the randomized trial of 195 patients from 21 countries presented at the annual meeting of the American Society of Clinical Oncology.

“The current state for the treatment of myelofibrosis relies on JAK2,” said Ruben Mesa, MD, of the Mays Cancer Center at the UT Health San Antonio MD Anderson Cancer Center.

“Momelotinib is a JAK1 and JAK2 inhibitor.” However, in the early days of studying momelotinib,“it became clear that there was also potentially an improvement in anemia,” which may be related to the additional inhibition of ACVR1, he explained.

Data suggest that the ability to curb anemia in anemic myelofibrosis patients prolongs their lives for up to 8 years, Dr. Mesa added.

Previous studies, notably the phase 3 SIMPLIFY study, showed that momelotinib was associated with comparable effects on spleen volume, transfusion, and total symptom scores from baseline that were similar to ruxolitinib.

In the current study, known as MOMENTUM, a daily dose of momelotinib was compared to danazol for treatment of symptomatic and anemic myelofibrosis (MF) patients who had previously received standard JAK-inhibitor therapy.

In the study, the researchers randomized 130 patients to momelotinib and 65 to danazol. After 24 weeks, those in the danazol group were allowed to cross over to momelotinib. The primary endpoint of the study was total symptom score (TSS) response after 24 weeks. Secondary endpoints included transfusion independence and splenic response at 24 weeks. The median age of the patients in the momelotinib group was 71 years, 60.8% were male, and 82% were white. The baseline demographics were not significantly different in the danazol group.

Overall, 24.6% of momelotinib patients responded with improved total symptom scores at 24 weeks vs. 9.2% of the danazol group. Spleen response also was significantly higher in the momelotinib group; 40% of patients showed a 25% reduction and 23% showed a 35% reduction, compared with 6.2% and 3.1%, respectively, of patients in the danazol group. Transfusion independence at week 24 also was higher for momelotinib patients, compared with danazol patients (31% vs. 20%, respectively, P = 0064).

Adverse events of grade 3 or higher occurred in 53.8% of momelotinib patients and 64.6% of danazol patients, and serious adverse events occurred in 34.6% and 40.0%, respectively. Nearly all patients had anemia, but only 27.7% and 26.2% of the momelotinib and danazol groups, respectively, had thrombocytopenia of grade 3 or higher. The most common nonhematologic adverse events were diarrhea, nausea, and increased blood creatinine. A total of 27.7% of the patients in the momelotinib group discontinued treatment; 16 of whom did so because of an adverse event.

Also, at 24 weeks, patients in the momelotinib group showed a trend towards increased overall survival, compared with danazol (HR, 0.506, P = 0.719).

With momelotinib, there is a consistent thrombocytopenic profile across subgroups, the data on which were presented separately at ASCO (poster 7061), Dr. Mesa added.

“We feel that these findings support the future use of momelotinib as an effective treatment in MF patients, especially those with anemia,” he concluded.
 

Cytopenia data are exciting

The key finding in the current study is that “momelotinib leads to important endpoints including significant improvement in symptoms and spleen reduction,” said Dr. Gabriela Hobbs of Harvard Medical School, Boston, who served as the discussant for the study.

“I think a novel finding of momelotinib that is definitely exciting from the treatment perspective is that momelotinib can also lead to improvement in cytopenias,” she said. “We often have to decide between treating the symptoms of the spleen at the expense of blood counts,” in MF patients, she noted.

The study was sponsored by Sierra Oncology. Dr. Mesa disclosed relationships with companies including Constellation Pharmaceutical, La Jolla Pharma, and study sponsor Sierra Oncology, as well as funding from AbbVie, Celgene, Constellation Pharmaceuticals, CTI, Genentech, Incyte, Mays Cancer Center, NCI, Promedior, and Samus. Dr. Hobbs had no financial conflicts to disclose.

This article was updated 06/14/2022.

The investigational drug momelotinib has shown benefits in myelofibrosis in a new phase 3 trial, which could now lead to a Food and Drug Administration approval.

This drug had previously shown mixed results in a phase 3 trial funded by Gilead, which stopped development of the product; it was acquired by Sierra Oncology, which conducted the latest positive phase 3 trial and now plans to use it to apply for FDA approval.

Momelotinib, an oral Janus kinase 1 and JAK2 inhibitor, significantly outperformed danazol on symptoms, spleen size, and anemia in adults with anemic myelofibrosis in the randomized trial of 195 patients from 21 countries presented at the annual meeting of the American Society of Clinical Oncology.

“The current state for the treatment of myelofibrosis relies on JAK2,” said Ruben Mesa, MD, of the Mays Cancer Center at the UT Health San Antonio MD Anderson Cancer Center.

“Momelotinib is a JAK1 and JAK2 inhibitor.” However, in the early days of studying momelotinib,“it became clear that there was also potentially an improvement in anemia,” which may be related to the additional inhibition of ACVR1, he explained.

Data suggest that the ability to curb anemia in anemic myelofibrosis patients prolongs their lives for up to 8 years, Dr. Mesa added.

Previous studies, notably the phase 3 SIMPLIFY study, showed that momelotinib was associated with comparable effects on spleen volume, transfusion, and total symptom scores from baseline that were similar to ruxolitinib.

In the current study, known as MOMENTUM, a daily dose of momelotinib was compared to danazol for treatment of symptomatic and anemic myelofibrosis (MF) patients who had previously received standard JAK-inhibitor therapy.

In the study, the researchers randomized 130 patients to momelotinib and 65 to danazol. After 24 weeks, those in the danazol group were allowed to cross over to momelotinib. The primary endpoint of the study was total symptom score (TSS) response after 24 weeks. Secondary endpoints included transfusion independence and splenic response at 24 weeks. The median age of the patients in the momelotinib group was 71 years, 60.8% were male, and 82% were white. The baseline demographics were not significantly different in the danazol group.

Overall, 24.6% of momelotinib patients responded with improved total symptom scores at 24 weeks vs. 9.2% of the danazol group. Spleen response also was significantly higher in the momelotinib group; 40% of patients showed a 25% reduction and 23% showed a 35% reduction, compared with 6.2% and 3.1%, respectively, of patients in the danazol group. Transfusion independence at week 24 also was higher for momelotinib patients, compared with danazol patients (31% vs. 20%, respectively, P = 0064).

Adverse events of grade 3 or higher occurred in 53.8% of momelotinib patients and 64.6% of danazol patients, and serious adverse events occurred in 34.6% and 40.0%, respectively. Nearly all patients had anemia, but only 27.7% and 26.2% of the momelotinib and danazol groups, respectively, had thrombocytopenia of grade 3 or higher. The most common nonhematologic adverse events were diarrhea, nausea, and increased blood creatinine. A total of 27.7% of the patients in the momelotinib group discontinued treatment; 16 of whom did so because of an adverse event.

Also, at 24 weeks, patients in the momelotinib group showed a trend towards increased overall survival, compared with danazol (HR, 0.506, P = 0.719).

With momelotinib, there is a consistent thrombocytopenic profile across subgroups, the data on which were presented separately at ASCO (poster 7061), Dr. Mesa added.

“We feel that these findings support the future use of momelotinib as an effective treatment in MF patients, especially those with anemia,” he concluded.
 

Cytopenia data are exciting

The key finding in the current study is that “momelotinib leads to important endpoints including significant improvement in symptoms and spleen reduction,” said Dr. Gabriela Hobbs of Harvard Medical School, Boston, who served as the discussant for the study.

“I think a novel finding of momelotinib that is definitely exciting from the treatment perspective is that momelotinib can also lead to improvement in cytopenias,” she said. “We often have to decide between treating the symptoms of the spleen at the expense of blood counts,” in MF patients, she noted.

The study was sponsored by Sierra Oncology. Dr. Mesa disclosed relationships with companies including Constellation Pharmaceutical, La Jolla Pharma, and study sponsor Sierra Oncology, as well as funding from AbbVie, Celgene, Constellation Pharmaceuticals, CTI, Genentech, Incyte, Mays Cancer Center, NCI, Promedior, and Samus. Dr. Hobbs had no financial conflicts to disclose.

This article was updated 06/14/2022.

In 2016, Gupta and Cahill challenged the field of psychiatry to reexamine prescribing patterns.¹ They warned against the use of polypharmacy when not attached to improved patient functioning. They were concerned with the limited evidence for polypharmacy as well as DSM diagnostic criteria. In their inspiring article, they described a process of deprescribing.

In an effort to study and practice their recommendations, we have noticed a lack of literature examining the elimination of diagnostic labels. While there have been some studies looking at comorbidity, especially with substance use disorders,² there is a paucity of scientific evidence on patients with numerous diagnoses. Yet our practices are filled with patients who have been labeled with multiple conflicting or redundant diagnoses throughout their lives depending on the setting or the orientation of the practitioner.

The DSM-5 warns against diagnosing disorders when “the occurrence … is not better explained by” another disorder.³ A mix of diagnoses creates confusion for patients as well as clinicians trying to sort through their reported psychiatric histories.

A routine example would include a patient presenting for an initial evaluation and stating “I’ve been diagnosed as manic-depressive, high anxiety, split personality, posttraumatic stress, insomnia, ADD, and depression.” A review of the medical record will reveal a list of diagnoses, including bipolar II, generalized anxiety disorder, borderline personality disorder, posttraumatic stress disorder, unspecified insomnia, attention-deficit/hyperactivity disorder, and major depressive disorder. The medication list includes lamotrigine, valproic acid, citalopram, bupropion, buspirone, prazosin, methylphenidate, clonazepam, hydroxyzine, and low-dose quetiapine at night as needed.

This is an example of polypharmacy treating multiple, and at times conflicting, diagnoses. While an extreme case, in our experience, cases like this are not uncommon. It was actually in our efforts to examine deprescribing that we noticed this quandary. When inquiring about patients on many psychotropic medications, we often receive this retort: the patient is only prescribed one medication per disorder. Some providers have the belief that multiple disorders justify multiple medications, and that this tautological thinking legitimizes polypharmacy.

A patient who has varying moods, some fears, a fluctuating temperament, past traumas, occasional difficulty sleeping, intermittent inattention, and some sadness may be given all the diagnoses listed above and the resulting medication list. The multiplication of diagnoses, “polydiagnosing,” is a convenient justification for future polypharmacy. A lack of careful assessment and thinking in the application of new diagnoses permits the use of increasing numbers of pharmacological agents. A constellation of symptoms of anxiety, concentration deficits, affective dysregulation, and psychosis may justify the combination of benzodiazepines, stimulants, mood stabilizers, and antipsychotics, while a patient with “just” schizophrenia who is sometimes sad, scared, or distracted is more likely to be kept on just one medication, likely an antipsychotic.

Contrary to most medical disorders (for example, tuberculosis) but similar to others (for example, chronic pain), psychiatric disorders are based on the opinion of a “modest number of ‘expert’ classifications.”⁴ While the broad categories of disorders are justifiable, individual diagnoses are burdened with high rates of comorbidity; lack of treatment specificity; and evidence that distinct syndromes share a genetic basis. Those concerns were exemplified in the study examining the inter-rater reliability of DSM-5 diagnoses, where many disorders were found to have questionable validity.⁵

A psychiatric diagnosis should be based on biological, psychological, and social factors, which align with our understanding of the natural course of an illness. A patient presenting with transient symptoms of sadness in the context of significant social factors like homelessness and/or significant biological factors associated with schizophrenia should not reflexively receive an additional diagnosis of a depressive disorder. A patient reporting poor concentration in the context of a manic episode should not receive an additional diagnosis of attention-deficit disorder. An older patient with depression on multiple antipsychotics for adjunctive treatment should not necessarily receive a diagnosis of cognitive disorder at the first sign of memory problems.

The cavalier and inconsistent use of diagnoses renders the patients with no clear narrative of who they are. They end up integrating the varying providers’ opinions as a cacophony of labels of unclear significance. Many patients have contradictory diagnoses like major depressive disorder and bipolar disorder, or schizophrenia and schizoaffective disorder. Those inaccurate diagnoses could not only lead to treatment mistakes, but also psychological harm.⁶

A clearer diagnostic picture is not only more scientifically sound but also more coherent to the patient. This in turn can lead to an improved treatment alliance and buy-in from the patient. Assisting a patient in sorting out and understanding the vast arrays of diagnostic labels they may hear throughout their treatment can serve as a tool for psychoeducation, empowerment, and control over their own care and themselves.

How should a provider practice de-diagnosing? Based on the work of Reeve, et al.,⁷ on the principles crucial to deprescribing, and subsequent research by Gupta and Cahill,⁸ we compiled a list of considerations for practitioners wishing to engage in this type of work with their patients.
 

Choose the right time. While insurance companies require diagnostic findings from the first visit, abrupt de-diagnosing for the sake of simplifying the record from that first visit could be detrimental. Patients can become attached to and find meaning in their diagnostic labels. This was exemplified with the removal of Asperger’s syndrome from the DSM-5.⁹ Acute symptomatology may be an opportune time to revisit the core pathology of a patient, or a poor time for a patient to have this discussion.

Compile a list of all the patient’s diagnoses. Our initial visits are often illuminated when patients enumerate the vast number of diagnoses they have been given by different providers. Patients will often list half a dozen diagnoses. The patterns often follow life courses with ADHD, conduct disorder, and learning disability in childhood; with anxiety, depression, and/or bipolar disorder in early adulthood; to complicated grief, depression with pseudodementia, and neurocognitive disorders in older adults. Yet patients rarely appreciate the temporary or episodic nature of mental disorders and instead accumulate diagnoses at each change of provider.

Initiate discussion with the patient. It is meaningful to see if patients resonate with the question, “Do you ever feel like every psychiatrist you have seen has given you a different diagnosis?” In our experience, patients’ reactions to this question usually exemplify the problematic nature of the vast array of diagnoses our patients are given. The majority of them are unable to confidently explain the meaning of those diagnoses, the context in which they were given, or their significance. This simple exercise has a powerful effect on raising awareness to patients of the problematic nature of polydiagnosing.

Introduce de-diagnosing. The engagement of patients in the diagnostic process has a significant effect. Reviewing not only diagnostic criteria but also nosology and debates in our understanding of diagnoses can provide patients with further engagement in their care. A simple review of the debate of the bereavement exclusion may permit a patient to not only understand the complexity, but also the changing nature of diagnoses. Suddenly, they are no longer bystanders, but informed participants in their care.

Identify diagnoses most appropriate for removal. Contradictory diagnoses are common in the clinical settings we work in. We routinely see patients carrying multiple mood diagnoses, despite our diagnostic systems not permitting one to have both unipolar and bipolar depression. Superfluous diagnoses are also frequent, with patients receiving depressive, or anxious labels when in an acute state of psychosis or mania. This is exemplified by patients suffering from thought blocking and receiving cognitive or attention-related diagnoses. Concurrent yet different diagnoses are also common in patients with a different list of diagnoses by their primary care provider, their therapist, and their psychiatrist. This is particularly problematic as it forces the patient to alternate their thinking or choose between their providers.

Create a new narrative for the patient. Once diagnoses are explained, clarified, and understood, patients with the help of their providers can reexamine their life story under a new and simplified construct. This process often leads to a less confusing sense of self, an increased dedication to the treatment process, whether behavioral, social, psychological, or pharmacologic.

Consider deprescribing. With a more straightforward and more grounded list of diagnoses (or simply one diagnosis), we find the process of deprescribing to be simpler and more engaging for patients. For example, patients can clearly understand the lack of necessity of an antipsychotic prescription for a resolved substance-induced psychosis. Patients are more engaged in their care, leading to improved medication compliance and less attachment to discontinued medications.

Monitor and adapt. One should of course reevaluate diagnoses as the course of illness provides us with additional information. However, we suggest waiting for a manic episode to emerge prior to diagnosing bipolar rather than suggesting the diagnosis because a patient was wearing red shoes, spoke multiple languages, had multiple degrees and was creative.¹⁰ The contextual basis and progression of the symptoms should lead to continual reassessment of diagnoses.

Physicians are aware of the balance between Occam’s razor, which promotes the simplest single explanation for a problem, versus Hickam’s dictum that reminds us that patients can have as many diseases as they please. However, similarly to polypharmacy, “polydiagnosing” has negative effects. While the field of psychiatry’s advancing knowledge may encourage providers to diagnose their patients with the growing number of diagnoses, patients still need and benefit from a coherent and clear medical narrative. Psychiatry would be wise to recognize this concerning trend, in its attempt at rectifying polypharmacy.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. He has no conflicts of interest. Dr. Lehman is a professor of psychiatry at the University of California, San Diego. He is codirector of all acute and intensive psychiatric treatment at the Veterans Affairs Medical Center in San Diego, where he practices clinical psychiatry. He has no conflicts of interest.

References

1. Gupta S & Cahill JD. A prescription for “deprescribing” in psychiatry. Psychiatr Serv. 2016 Aug 1;67(8):904-7. doi: 10.1176/appi.ps.201500359.

2. Schuckit MA. Comorbidity between substance use disorders and psychiatric conditions. Addiction. 2006 Sep;101 Suppl 1:76-88. doi: 10.1111/j.1360-0443.2006.01592.x.

3. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). American Psychiatric Association, 2022. https://psychiatry.org/psychiatrists/practice/dsm.

4. Kendler KS. An historical framework for psychiatric nosology. Psychol Med. 2009 Dec;39(12):1935-41. doi: 10.1017/S0033291709005753.

5. Regier DA et al. DSM-5 field trials in the United States and Canada. Am J Psychiatry. 2013 Jan;170(1):59-70. doi: 10.1176/appi.ajp.2012.12070999.

6. Bhattacharya R et al. When good news is bad news: psychological impact of false-positive diagnosis of HIV. AIDS Care. 2008 May;20(5):560-4. doi: 10.1080/09540120701867206.

7. Reeve E et al. Review of deprescribing processes and development of an evidence‐based, patient‐centred deprescribing process. Br J Clin Pharmacol. 2014 Oct;78(4):738-47. doi: 10.1111/bcp.12386.

8. Gupta S and Cahill JD. A prescription for “deprescribing” in psychiatry.

9. Solomon M. “On the appearance and disappearance of Asperger’s syndrome” in Kendler and Parnas (eds.) Philosophical Issues in Psychiatry IV: Classification of Psychiatric Illness. Oxford University Press, 2017. doi: 10.1093/med/9780198796022.003.0023.

10. Akiskal HS. Searching for behavioral indicators of bipolar II in patients presenting with major depressive episodes: The “red sign,” the “rule of three,” and other biographic signs of temperamental extravagance, activation, and hypomania. J Affect Disord. 2005 Feb;84(2-3):279-90. doi: 10.1016/j.jad.2004.06.002.

In 2016, Gupta and Cahill challenged the field of psychiatry to reexamine prescribing patterns.¹ They warned against the use of polypharmacy when not attached to improved patient functioning. They were concerned with the limited evidence for polypharmacy as well as DSM diagnostic criteria. In their inspiring article, they described a process of deprescribing.

In an effort to study and practice their recommendations, we have noticed a lack of literature examining the elimination of diagnostic labels. While there have been some studies looking at comorbidity, especially with substance use disorders,² there is a paucity of scientific evidence on patients with numerous diagnoses. Yet our practices are filled with patients who have been labeled with multiple conflicting or redundant diagnoses throughout their lives depending on the setting or the orientation of the practitioner.

The DSM-5 warns against diagnosing disorders when “the occurrence … is not better explained by” another disorder.³ A mix of diagnoses creates confusion for patients as well as clinicians trying to sort through their reported psychiatric histories.

A routine example would include a patient presenting for an initial evaluation and stating “I’ve been diagnosed as manic-depressive, high anxiety, split personality, posttraumatic stress, insomnia, ADD, and depression.” A review of the medical record will reveal a list of diagnoses, including bipolar II, generalized anxiety disorder, borderline personality disorder, posttraumatic stress disorder, unspecified insomnia, attention-deficit/hyperactivity disorder, and major depressive disorder. The medication list includes lamotrigine, valproic acid, citalopram, bupropion, buspirone, prazosin, methylphenidate, clonazepam, hydroxyzine, and low-dose quetiapine at night as needed.

This is an example of polypharmacy treating multiple, and at times conflicting, diagnoses. While an extreme case, in our experience, cases like this are not uncommon. It was actually in our efforts to examine deprescribing that we noticed this quandary. When inquiring about patients on many psychotropic medications, we often receive this retort: the patient is only prescribed one medication per disorder. Some providers have the belief that multiple disorders justify multiple medications, and that this tautological thinking legitimizes polypharmacy.

A patient who has varying moods, some fears, a fluctuating temperament, past traumas, occasional difficulty sleeping, intermittent inattention, and some sadness may be given all the diagnoses listed above and the resulting medication list. The multiplication of diagnoses, “polydiagnosing,” is a convenient justification for future polypharmacy. A lack of careful assessment and thinking in the application of new diagnoses permits the use of increasing numbers of pharmacological agents. A constellation of symptoms of anxiety, concentration deficits, affective dysregulation, and psychosis may justify the combination of benzodiazepines, stimulants, mood stabilizers, and antipsychotics, while a patient with “just” schizophrenia who is sometimes sad, scared, or distracted is more likely to be kept on just one medication, likely an antipsychotic.

Contrary to most medical disorders (for example, tuberculosis) but similar to others (for example, chronic pain), psychiatric disorders are based on the opinion of a “modest number of ‘expert’ classifications.”⁴ While the broad categories of disorders are justifiable, individual diagnoses are burdened with high rates of comorbidity; lack of treatment specificity; and evidence that distinct syndromes share a genetic basis. Those concerns were exemplified in the study examining the inter-rater reliability of DSM-5 diagnoses, where many disorders were found to have questionable validity.⁵

A psychiatric diagnosis should be based on biological, psychological, and social factors, which align with our understanding of the natural course of an illness. A patient presenting with transient symptoms of sadness in the context of significant social factors like homelessness and/or significant biological factors associated with schizophrenia should not reflexively receive an additional diagnosis of a depressive disorder. A patient reporting poor concentration in the context of a manic episode should not receive an additional diagnosis of attention-deficit disorder. An older patient with depression on multiple antipsychotics for adjunctive treatment should not necessarily receive a diagnosis of cognitive disorder at the first sign of memory problems.

The cavalier and inconsistent use of diagnoses renders the patients with no clear narrative of who they are. They end up integrating the varying providers’ opinions as a cacophony of labels of unclear significance. Many patients have contradictory diagnoses like major depressive disorder and bipolar disorder, or schizophrenia and schizoaffective disorder. Those inaccurate diagnoses could not only lead to treatment mistakes, but also psychological harm.⁶

A clearer diagnostic picture is not only more scientifically sound but also more coherent to the patient. This in turn can lead to an improved treatment alliance and buy-in from the patient. Assisting a patient in sorting out and understanding the vast arrays of diagnostic labels they may hear throughout their treatment can serve as a tool for psychoeducation, empowerment, and control over their own care and themselves.

How should a provider practice de-diagnosing? Based on the work of Reeve, et al.,⁷ on the principles crucial to deprescribing, and subsequent research by Gupta and Cahill,⁸ we compiled a list of considerations for practitioners wishing to engage in this type of work with their patients.
 

Choose the right time. While insurance companies require diagnostic findings from the first visit, abrupt de-diagnosing for the sake of simplifying the record from that first visit could be detrimental. Patients can become attached to and find meaning in their diagnostic labels. This was exemplified with the removal of Asperger’s syndrome from the DSM-5.⁹ Acute symptomatology may be an opportune time to revisit the core pathology of a patient, or a poor time for a patient to have this discussion.

Compile a list of all the patient’s diagnoses. Our initial visits are often illuminated when patients enumerate the vast number of diagnoses they have been given by different providers. Patients will often list half a dozen diagnoses. The patterns often follow life courses with ADHD, conduct disorder, and learning disability in childhood; with anxiety, depression, and/or bipolar disorder in early adulthood; to complicated grief, depression with pseudodementia, and neurocognitive disorders in older adults. Yet patients rarely appreciate the temporary or episodic nature of mental disorders and instead accumulate diagnoses at each change of provider.

Initiate discussion with the patient. It is meaningful to see if patients resonate with the question, “Do you ever feel like every psychiatrist you have seen has given you a different diagnosis?” In our experience, patients’ reactions to this question usually exemplify the problematic nature of the vast array of diagnoses our patients are given. The majority of them are unable to confidently explain the meaning of those diagnoses, the context in which they were given, or their significance. This simple exercise has a powerful effect on raising awareness to patients of the problematic nature of polydiagnosing.

Introduce de-diagnosing. The engagement of patients in the diagnostic process has a significant effect. Reviewing not only diagnostic criteria but also nosology and debates in our understanding of diagnoses can provide patients with further engagement in their care. A simple review of the debate of the bereavement exclusion may permit a patient to not only understand the complexity, but also the changing nature of diagnoses. Suddenly, they are no longer bystanders, but informed participants in their care.

Identify diagnoses most appropriate for removal. Contradictory diagnoses are common in the clinical settings we work in. We routinely see patients carrying multiple mood diagnoses, despite our diagnostic systems not permitting one to have both unipolar and bipolar depression. Superfluous diagnoses are also frequent, with patients receiving depressive, or anxious labels when in an acute state of psychosis or mania. This is exemplified by patients suffering from thought blocking and receiving cognitive or attention-related diagnoses. Concurrent yet different diagnoses are also common in patients with a different list of diagnoses by their primary care provider, their therapist, and their psychiatrist. This is particularly problematic as it forces the patient to alternate their thinking or choose between their providers.

Create a new narrative for the patient. Once diagnoses are explained, clarified, and understood, patients with the help of their providers can reexamine their life story under a new and simplified construct. This process often leads to a less confusing sense of self, an increased dedication to the treatment process, whether behavioral, social, psychological, or pharmacologic.

Consider deprescribing. With a more straightforward and more grounded list of diagnoses (or simply one diagnosis), we find the process of deprescribing to be simpler and more engaging for patients. For example, patients can clearly understand the lack of necessity of an antipsychotic prescription for a resolved substance-induced psychosis. Patients are more engaged in their care, leading to improved medication compliance and less attachment to discontinued medications.

Monitor and adapt. One should of course reevaluate diagnoses as the course of illness provides us with additional information. However, we suggest waiting for a manic episode to emerge prior to diagnosing bipolar rather than suggesting the diagnosis because a patient was wearing red shoes, spoke multiple languages, had multiple degrees and was creative.¹⁰ The contextual basis and progression of the symptoms should lead to continual reassessment of diagnoses.

Physicians are aware of the balance between Occam’s razor, which promotes the simplest single explanation for a problem, versus Hickam’s dictum that reminds us that patients can have as many diseases as they please. However, similarly to polypharmacy, “polydiagnosing” has negative effects. While the field of psychiatry’s advancing knowledge may encourage providers to diagnose their patients with the growing number of diagnoses, patients still need and benefit from a coherent and clear medical narrative. Psychiatry would be wise to recognize this concerning trend, in its attempt at rectifying polypharmacy.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. He has no conflicts of interest. Dr. Lehman is a professor of psychiatry at the University of California, San Diego. He is codirector of all acute and intensive psychiatric treatment at the Veterans Affairs Medical Center in San Diego, where he practices clinical psychiatry. He has no conflicts of interest.

References

1. Gupta S & Cahill JD. A prescription for “deprescribing” in psychiatry. Psychiatr Serv. 2016 Aug 1;67(8):904-7. doi: 10.1176/appi.ps.201500359.

2. Schuckit MA. Comorbidity between substance use disorders and psychiatric conditions. Addiction. 2006 Sep;101 Suppl 1:76-88. doi: 10.1111/j.1360-0443.2006.01592.x.

3. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). American Psychiatric Association, 2022. https://psychiatry.org/psychiatrists/practice/dsm.

4. Kendler KS. An historical framework for psychiatric nosology. Psychol Med. 2009 Dec;39(12):1935-41. doi: 10.1017/S0033291709005753.

5. Regier DA et al. DSM-5 field trials in the United States and Canada. Am J Psychiatry. 2013 Jan;170(1):59-70. doi: 10.1176/appi.ajp.2012.12070999.

6. Bhattacharya R et al. When good news is bad news: psychological impact of false-positive diagnosis of HIV. AIDS Care. 2008 May;20(5):560-4. doi: 10.1080/09540120701867206.

7. Reeve E et al. Review of deprescribing processes and development of an evidence‐based, patient‐centred deprescribing process. Br J Clin Pharmacol. 2014 Oct;78(4):738-47. doi: 10.1111/bcp.12386.

8. Gupta S and Cahill JD. A prescription for “deprescribing” in psychiatry.

9. Solomon M. “On the appearance and disappearance of Asperger’s syndrome” in Kendler and Parnas (eds.) Philosophical Issues in Psychiatry IV: Classification of Psychiatric Illness. Oxford University Press, 2017. doi: 10.1093/med/9780198796022.003.0023.

10. Akiskal HS. Searching for behavioral indicators of bipolar II in patients presenting with major depressive episodes: The “red sign,” the “rule of three,” and other biographic signs of temperamental extravagance, activation, and hypomania. J Affect Disord. 2005 Feb;84(2-3):279-90. doi: 10.1016/j.jad.2004.06.002.

In 2016, Gupta and Cahill challenged the field of psychiatry to reexamine prescribing patterns.¹ They warned against the use of polypharmacy when not attached to improved patient functioning. They were concerned with the limited evidence for polypharmacy as well as DSM diagnostic criteria. In their inspiring article, they described a process of deprescribing.

In an effort to study and practice their recommendations, we have noticed a lack of literature examining the elimination of diagnostic labels. While there have been some studies looking at comorbidity, especially with substance use disorders,² there is a paucity of scientific evidence on patients with numerous diagnoses. Yet our practices are filled with patients who have been labeled with multiple conflicting or redundant diagnoses throughout their lives depending on the setting or the orientation of the practitioner.

The DSM-5 warns against diagnosing disorders when “the occurrence … is not better explained by” another disorder.³ A mix of diagnoses creates confusion for patients as well as clinicians trying to sort through their reported psychiatric histories.

A routine example would include a patient presenting for an initial evaluation and stating “I’ve been diagnosed as manic-depressive, high anxiety, split personality, posttraumatic stress, insomnia, ADD, and depression.” A review of the medical record will reveal a list of diagnoses, including bipolar II, generalized anxiety disorder, borderline personality disorder, posttraumatic stress disorder, unspecified insomnia, attention-deficit/hyperactivity disorder, and major depressive disorder. The medication list includes lamotrigine, valproic acid, citalopram, bupropion, buspirone, prazosin, methylphenidate, clonazepam, hydroxyzine, and low-dose quetiapine at night as needed.

This is an example of polypharmacy treating multiple, and at times conflicting, diagnoses. While an extreme case, in our experience, cases like this are not uncommon. It was actually in our efforts to examine deprescribing that we noticed this quandary. When inquiring about patients on many psychotropic medications, we often receive this retort: the patient is only prescribed one medication per disorder. Some providers have the belief that multiple disorders justify multiple medications, and that this tautological thinking legitimizes polypharmacy.

A patient who has varying moods, some fears, a fluctuating temperament, past traumas, occasional difficulty sleeping, intermittent inattention, and some sadness may be given all the diagnoses listed above and the resulting medication list. The multiplication of diagnoses, “polydiagnosing,” is a convenient justification for future polypharmacy. A lack of careful assessment and thinking in the application of new diagnoses permits the use of increasing numbers of pharmacological agents. A constellation of symptoms of anxiety, concentration deficits, affective dysregulation, and psychosis may justify the combination of benzodiazepines, stimulants, mood stabilizers, and antipsychotics, while a patient with “just” schizophrenia who is sometimes sad, scared, or distracted is more likely to be kept on just one medication, likely an antipsychotic.

Contrary to most medical disorders (for example, tuberculosis) but similar to others (for example, chronic pain), psychiatric disorders are based on the opinion of a “modest number of ‘expert’ classifications.”⁴ While the broad categories of disorders are justifiable, individual diagnoses are burdened with high rates of comorbidity; lack of treatment specificity; and evidence that distinct syndromes share a genetic basis. Those concerns were exemplified in the study examining the inter-rater reliability of DSM-5 diagnoses, where many disorders were found to have questionable validity.⁵

A psychiatric diagnosis should be based on biological, psychological, and social factors, which align with our understanding of the natural course of an illness. A patient presenting with transient symptoms of sadness in the context of significant social factors like homelessness and/or significant biological factors associated with schizophrenia should not reflexively receive an additional diagnosis of a depressive disorder. A patient reporting poor concentration in the context of a manic episode should not receive an additional diagnosis of attention-deficit disorder. An older patient with depression on multiple antipsychotics for adjunctive treatment should not necessarily receive a diagnosis of cognitive disorder at the first sign of memory problems.

The cavalier and inconsistent use of diagnoses renders the patients with no clear narrative of who they are. They end up integrating the varying providers’ opinions as a cacophony of labels of unclear significance. Many patients have contradictory diagnoses like major depressive disorder and bipolar disorder, or schizophrenia and schizoaffective disorder. Those inaccurate diagnoses could not only lead to treatment mistakes, but also psychological harm.⁶

A clearer diagnostic picture is not only more scientifically sound but also more coherent to the patient. This in turn can lead to an improved treatment alliance and buy-in from the patient. Assisting a patient in sorting out and understanding the vast arrays of diagnostic labels they may hear throughout their treatment can serve as a tool for psychoeducation, empowerment, and control over their own care and themselves.

How should a provider practice de-diagnosing? Based on the work of Reeve, et al.,⁷ on the principles crucial to deprescribing, and subsequent research by Gupta and Cahill,⁸ we compiled a list of considerations for practitioners wishing to engage in this type of work with their patients.
 

Choose the right time. While insurance companies require diagnostic findings from the first visit, abrupt de-diagnosing for the sake of simplifying the record from that first visit could be detrimental. Patients can become attached to and find meaning in their diagnostic labels. This was exemplified with the removal of Asperger’s syndrome from the DSM-5.⁹ Acute symptomatology may be an opportune time to revisit the core pathology of a patient, or a poor time for a patient to have this discussion.

Compile a list of all the patient’s diagnoses. Our initial visits are often illuminated when patients enumerate the vast number of diagnoses they have been given by different providers. Patients will often list half a dozen diagnoses. The patterns often follow life courses with ADHD, conduct disorder, and learning disability in childhood; with anxiety, depression, and/or bipolar disorder in early adulthood; to complicated grief, depression with pseudodementia, and neurocognitive disorders in older adults. Yet patients rarely appreciate the temporary or episodic nature of mental disorders and instead accumulate diagnoses at each change of provider.

Initiate discussion with the patient. It is meaningful to see if patients resonate with the question, “Do you ever feel like every psychiatrist you have seen has given you a different diagnosis?” In our experience, patients’ reactions to this question usually exemplify the problematic nature of the vast array of diagnoses our patients are given. The majority of them are unable to confidently explain the meaning of those diagnoses, the context in which they were given, or their significance. This simple exercise has a powerful effect on raising awareness to patients of the problematic nature of polydiagnosing.

Introduce de-diagnosing. The engagement of patients in the diagnostic process has a significant effect. Reviewing not only diagnostic criteria but also nosology and debates in our understanding of diagnoses can provide patients with further engagement in their care. A simple review of the debate of the bereavement exclusion may permit a patient to not only understand the complexity, but also the changing nature of diagnoses. Suddenly, they are no longer bystanders, but informed participants in their care.

Identify diagnoses most appropriate for removal. Contradictory diagnoses are common in the clinical settings we work in. We routinely see patients carrying multiple mood diagnoses, despite our diagnostic systems not permitting one to have both unipolar and bipolar depression. Superfluous diagnoses are also frequent, with patients receiving depressive, or anxious labels when in an acute state of psychosis or mania. This is exemplified by patients suffering from thought blocking and receiving cognitive or attention-related diagnoses. Concurrent yet different diagnoses are also common in patients with a different list of diagnoses by their primary care provider, their therapist, and their psychiatrist. This is particularly problematic as it forces the patient to alternate their thinking or choose between their providers.

Create a new narrative for the patient. Once diagnoses are explained, clarified, and understood, patients with the help of their providers can reexamine their life story under a new and simplified construct. This process often leads to a less confusing sense of self, an increased dedication to the treatment process, whether behavioral, social, psychological, or pharmacologic.

Consider deprescribing. With a more straightforward and more grounded list of diagnoses (or simply one diagnosis), we find the process of deprescribing to be simpler and more engaging for patients. For example, patients can clearly understand the lack of necessity of an antipsychotic prescription for a resolved substance-induced psychosis. Patients are more engaged in their care, leading to improved medication compliance and less attachment to discontinued medications.

Monitor and adapt. One should of course reevaluate diagnoses as the course of illness provides us with additional information. However, we suggest waiting for a manic episode to emerge prior to diagnosing bipolar rather than suggesting the diagnosis because a patient was wearing red shoes, spoke multiple languages, had multiple degrees and was creative.¹⁰ The contextual basis and progression of the symptoms should lead to continual reassessment of diagnoses.

Physicians are aware of the balance between Occam’s razor, which promotes the simplest single explanation for a problem, versus Hickam’s dictum that reminds us that patients can have as many diseases as they please. However, similarly to polypharmacy, “polydiagnosing” has negative effects. While the field of psychiatry’s advancing knowledge may encourage providers to diagnose their patients with the growing number of diagnoses, patients still need and benefit from a coherent and clear medical narrative. Psychiatry would be wise to recognize this concerning trend, in its attempt at rectifying polypharmacy.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. He has no conflicts of interest. Dr. Lehman is a professor of psychiatry at the University of California, San Diego. He is codirector of all acute and intensive psychiatric treatment at the Veterans Affairs Medical Center in San Diego, where he practices clinical psychiatry. He has no conflicts of interest.

References

1. Gupta S & Cahill JD. A prescription for “deprescribing” in psychiatry. Psychiatr Serv. 2016 Aug 1;67(8):904-7. doi: 10.1176/appi.ps.201500359.

2. Schuckit MA. Comorbidity between substance use disorders and psychiatric conditions. Addiction. 2006 Sep;101 Suppl 1:76-88. doi: 10.1111/j.1360-0443.2006.01592.x.

3. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). American Psychiatric Association, 2022. https://psychiatry.org/psychiatrists/practice/dsm.

4. Kendler KS. An historical framework for psychiatric nosology. Psychol Med. 2009 Dec;39(12):1935-41. doi: 10.1017/S0033291709005753.

5. Regier DA et al. DSM-5 field trials in the United States and Canada. Am J Psychiatry. 2013 Jan;170(1):59-70. doi: 10.1176/appi.ajp.2012.12070999.

6. Bhattacharya R et al. When good news is bad news: psychological impact of false-positive diagnosis of HIV. AIDS Care. 2008 May;20(5):560-4. doi: 10.1080/09540120701867206.

7. Reeve E et al. Review of deprescribing processes and development of an evidence‐based, patient‐centred deprescribing process. Br J Clin Pharmacol. 2014 Oct;78(4):738-47. doi: 10.1111/bcp.12386.

8. Gupta S and Cahill JD. A prescription for “deprescribing” in psychiatry.

9. Solomon M. “On the appearance and disappearance of Asperger’s syndrome” in Kendler and Parnas (eds.) Philosophical Issues in Psychiatry IV: Classification of Psychiatric Illness. Oxford University Press, 2017. doi: 10.1093/med/9780198796022.003.0023.

10. Akiskal HS. Searching for behavioral indicators of bipolar II in patients presenting with major depressive episodes: The “red sign,” the “rule of three,” and other biographic signs of temperamental extravagance, activation, and hypomania. J Affect Disord. 2005 Feb;84(2-3):279-90. doi: 10.1016/j.jad.2004.06.002.

Joining Gastroenterology as an editorial fellow is an invaluable experience for the future scientific career. When I joined the fellowship, my main objectives were to learn important aspects about scientific publishing, while improving my editorial and writing skills. Importantly, participating in the fellowship would allow me to determine fields in gastroenterology and hepatology that need more intensive research, evaluate and review manuscripts submitted to a high-impact journal, learn which aspects are important for manuscripts to be considered for publication, and learn how to prepare concise summaries to share with readers. As an editorial fellow, I would not only work with experts on manuscript review and editing, but also be mentored by experts in the field to prepare for a career in scientific publishing.

The application process is easy and straightforward. A curriculum vitae, motivation letter, and conflict of interest form are needed to be considered for the position. Furthermore, a letter of recommendation has to be provided from senior faculty. For the latter, it is beneficial to have worked with someone who is currently active in scientific publishing.

After joining the editorial board, fellows are assigned to associate editors based on their previous experience. Fellows are expected to peer-review manuscripts and discuss their reviews with the associate editors during a brief call or by email, where it is also determined whether additional feedback from the board of editors is needed to move manuscripts forward. If so, fellows are given the opportunity to present manuscripts they reviewed to the editorial board and prepare the decision letter with comments to the authors and editors. This experience teaches which qualities manuscripts need to fulfill to be considered for publication, and how to communicate decisions to authors. During the meetings with the editorial board, fellows are also encouraged to provide feedback for additional manuscripts discussed.

Additionally, fellows have the chance to work on the “Covering the Cover” section of the journal under close mentorship of the responsible editors. Here, they learn to draft short synopses of submitted manuscripts that should be highlighted in the respective sections to give readers a brief overview of important pieces of research with potential clinical applicability. This experience teaches how to write concisely and rephrase the main message of manuscripts without overstating findings and conclusions. Additionally, fellows are invited to write commentaries on recent articles published in other journals and highlight these to Gastroenterology’s readership. This experience teaches how to critically comment on published literature and point out its strengths and limitations. Overall, these learning experiences improve not only editorial and writing skills, but also knowledge in the respective areas of research.

Finally, fellows have the opportunity to write a commentary about a topic of their choice. This experience allows fellows to deepen their expertise in an area of research on an emerging topic they would like to highlight to their readers. Since this type of article is peer reviewed, reviewers’ comments help identify weaknesses of the initially submitted manuscript and increase the awareness about factors that need to be addressed to finally provide a high-quality article that is of value to Gastroenterology’s readership.

Concluding, being an editorial fellow for Gastroenterology is an extremely valuable experience. From an editorial aspect, fellows learn to review, summarize, and comment on submitted manuscripts, as well as which factors need to be addressed by manuscripts to be considered for publication to a high-impact journal. Additionally, fellows network with leaders in the field and expand their knowledge on topics they had not worked on previously. Overall, the fellowship helps improve editorial and writing skills, while staying current in the literature, a skill set that can be applied broadly in the future medical and scientific career.

Dr. Kefalakes is a clinical fellow and research group leader in the department of gastroenterology, hepatology, and endocrinology at Hannover (Germany) Medical School. She has nothing to declare.

Joining Gastroenterology as an editorial fellow is an invaluable experience for the future scientific career. When I joined the fellowship, my main objectives were to learn important aspects about scientific publishing, while improving my editorial and writing skills. Importantly, participating in the fellowship would allow me to determine fields in gastroenterology and hepatology that need more intensive research, evaluate and review manuscripts submitted to a high-impact journal, learn which aspects are important for manuscripts to be considered for publication, and learn how to prepare concise summaries to share with readers. As an editorial fellow, I would not only work with experts on manuscript review and editing, but also be mentored by experts in the field to prepare for a career in scientific publishing.

The application process is easy and straightforward. A curriculum vitae, motivation letter, and conflict of interest form are needed to be considered for the position. Furthermore, a letter of recommendation has to be provided from senior faculty. For the latter, it is beneficial to have worked with someone who is currently active in scientific publishing.

After joining the editorial board, fellows are assigned to associate editors based on their previous experience. Fellows are expected to peer-review manuscripts and discuss their reviews with the associate editors during a brief call or by email, where it is also determined whether additional feedback from the board of editors is needed to move manuscripts forward. If so, fellows are given the opportunity to present manuscripts they reviewed to the editorial board and prepare the decision letter with comments to the authors and editors. This experience teaches which qualities manuscripts need to fulfill to be considered for publication, and how to communicate decisions to authors. During the meetings with the editorial board, fellows are also encouraged to provide feedback for additional manuscripts discussed.

Additionally, fellows have the chance to work on the “Covering the Cover” section of the journal under close mentorship of the responsible editors. Here, they learn to draft short synopses of submitted manuscripts that should be highlighted in the respective sections to give readers a brief overview of important pieces of research with potential clinical applicability. This experience teaches how to write concisely and rephrase the main message of manuscripts without overstating findings and conclusions. Additionally, fellows are invited to write commentaries on recent articles published in other journals and highlight these to Gastroenterology’s readership. This experience teaches how to critically comment on published literature and point out its strengths and limitations. Overall, these learning experiences improve not only editorial and writing skills, but also knowledge in the respective areas of research.

Finally, fellows have the opportunity to write a commentary about a topic of their choice. This experience allows fellows to deepen their expertise in an area of research on an emerging topic they would like to highlight to their readers. Since this type of article is peer reviewed, reviewers’ comments help identify weaknesses of the initially submitted manuscript and increase the awareness about factors that need to be addressed to finally provide a high-quality article that is of value to Gastroenterology’s readership.

Concluding, being an editorial fellow for Gastroenterology is an extremely valuable experience. From an editorial aspect, fellows learn to review, summarize, and comment on submitted manuscripts, as well as which factors need to be addressed by manuscripts to be considered for publication to a high-impact journal. Additionally, fellows network with leaders in the field and expand their knowledge on topics they had not worked on previously. Overall, the fellowship helps improve editorial and writing skills, while staying current in the literature, a skill set that can be applied broadly in the future medical and scientific career.

Dr. Kefalakes is a clinical fellow and research group leader in the department of gastroenterology, hepatology, and endocrinology at Hannover (Germany) Medical School. She has nothing to declare.

Joining Gastroenterology as an editorial fellow is an invaluable experience for the future scientific career. When I joined the fellowship, my main objectives were to learn important aspects about scientific publishing, while improving my editorial and writing skills. Importantly, participating in the fellowship would allow me to determine fields in gastroenterology and hepatology that need more intensive research, evaluate and review manuscripts submitted to a high-impact journal, learn which aspects are important for manuscripts to be considered for publication, and learn how to prepare concise summaries to share with readers. As an editorial fellow, I would not only work with experts on manuscript review and editing, but also be mentored by experts in the field to prepare for a career in scientific publishing.

The application process is easy and straightforward. A curriculum vitae, motivation letter, and conflict of interest form are needed to be considered for the position. Furthermore, a letter of recommendation has to be provided from senior faculty. For the latter, it is beneficial to have worked with someone who is currently active in scientific publishing.

After joining the editorial board, fellows are assigned to associate editors based on their previous experience. Fellows are expected to peer-review manuscripts and discuss their reviews with the associate editors during a brief call or by email, where it is also determined whether additional feedback from the board of editors is needed to move manuscripts forward. If so, fellows are given the opportunity to present manuscripts they reviewed to the editorial board and prepare the decision letter with comments to the authors and editors. This experience teaches which qualities manuscripts need to fulfill to be considered for publication, and how to communicate decisions to authors. During the meetings with the editorial board, fellows are also encouraged to provide feedback for additional manuscripts discussed.

Additionally, fellows have the chance to work on the “Covering the Cover” section of the journal under close mentorship of the responsible editors. Here, they learn to draft short synopses of submitted manuscripts that should be highlighted in the respective sections to give readers a brief overview of important pieces of research with potential clinical applicability. This experience teaches how to write concisely and rephrase the main message of manuscripts without overstating findings and conclusions. Additionally, fellows are invited to write commentaries on recent articles published in other journals and highlight these to Gastroenterology’s readership. This experience teaches how to critically comment on published literature and point out its strengths and limitations. Overall, these learning experiences improve not only editorial and writing skills, but also knowledge in the respective areas of research.

Finally, fellows have the opportunity to write a commentary about a topic of their choice. This experience allows fellows to deepen their expertise in an area of research on an emerging topic they would like to highlight to their readers. Since this type of article is peer reviewed, reviewers’ comments help identify weaknesses of the initially submitted manuscript and increase the awareness about factors that need to be addressed to finally provide a high-quality article that is of value to Gastroenterology’s readership.

Concluding, being an editorial fellow for Gastroenterology is an extremely valuable experience. From an editorial aspect, fellows learn to review, summarize, and comment on submitted manuscripts, as well as which factors need to be addressed by manuscripts to be considered for publication to a high-impact journal. Additionally, fellows network with leaders in the field and expand their knowledge on topics they had not worked on previously. Overall, the fellowship helps improve editorial and writing skills, while staying current in the literature, a skill set that can be applied broadly in the future medical and scientific career.

Dr. Kefalakes is a clinical fellow and research group leader in the department of gastroenterology, hepatology, and endocrinology at Hannover (Germany) Medical School. She has nothing to declare.

Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.

“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.

The study was published online in Neurology.
 

Conflicting findings

Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.

It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.

To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.

Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.

Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).

There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.

However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.

Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.

The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.

They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.

The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.

“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.

The study was published online in Neurology.
 

Conflicting findings

Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.

It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.

To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.

Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.

Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).

There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.

However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.

Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.

The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.

They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.

The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.

“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.

The study was published online in Neurology.
 

Conflicting findings

Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.

It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.

To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.

Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.

Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).

There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.

However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.

Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.

The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.

They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.

The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

On the top left of my desktop is an electronic sticky note entitled, “Apply in Future.” This was where the AGA editorial fellowship was listed when I first started GI fellowship. My interest in the behind-the-scenes of scientific publishing developed early. I wanted to learn not only about the decision-making by the editorial board but also other aspects that impact the process from submission to publication. While waiting for my opportunity to apply, I became a reviewer for several journals and then an associate editor of ACG Case Reports Journal, which gave me some insight.

I applied to the editorial fellowship as a second-year fellow, to start as a third-year fellow. I figured this would give me several chances to apply again if I was not selected! I started off by talking to my program director to ensure that I would have enough time, given other responsibilities. The application consisted of a cover letter, where I expressed why I was interested, particularly focusing on my passion for research and my experience with scientific publishing, a letter of recommendation, and a CV. I was ecstatic when I was selected for the AGA editorial fellowship for Clinical Gastroenterology and Hepatology (CGH), whose editorial board’s mission best aligned with my interests.

Dr. Jonathan Buscaglia was the editorial fellows’ mentor for CGH – he met with us and provided an outline of the year. For the first 6 months, I was a reviewer for submitted manuscripts within my topic of interest – pancreaticobiliary diseases and advanced endoscopy and technology. Dr. Buscaglia gave me feedback on my reviews to improve my critical assessment of study designs and interpreted results. After 6 months as a reviewer, I took on the role of an associate editor. I selected reviewers, evaluated the reviews, and made the decision to accept or reject a manuscript. I presented my assigned manuscript at the weekly board of editors meeting, which was one of the biggest learning experiences. Leading researchers from all over the world gathered at a virtual table and discussed whether each study would have clinical impact on the medical community. Each editor contributed a unique perspective that facilitated a robust and thoughtful discussion of each manuscript brought to the table. I was in awe each week.

What I have learned so far during my year as an AGA editorial fellow with CGH has shaped my approach to personal research and will continue to do so as I develop my research career. It has greatly improved my assessment of the literature and I hope to continue to be involved in the critical review process, especially as a reviewer in my early career, and eventually, a part of an editorial board for a journal that truly impacts clinical medicine, such as Clinical Gastroenterology and Hepatology.
 

Dr. Trieu is a gastroenterology and hepatology fellow at Loyola University Medical Center, Maywood, Ill. She has no conflicts of interest to disclose.

On the top left of my desktop is an electronic sticky note entitled, “Apply in Future.” This was where the AGA editorial fellowship was listed when I first started GI fellowship. My interest in the behind-the-scenes of scientific publishing developed early. I wanted to learn not only about the decision-making by the editorial board but also other aspects that impact the process from submission to publication. While waiting for my opportunity to apply, I became a reviewer for several journals and then an associate editor of ACG Case Reports Journal, which gave me some insight.

I applied to the editorial fellowship as a second-year fellow, to start as a third-year fellow. I figured this would give me several chances to apply again if I was not selected! I started off by talking to my program director to ensure that I would have enough time, given other responsibilities. The application consisted of a cover letter, where I expressed why I was interested, particularly focusing on my passion for research and my experience with scientific publishing, a letter of recommendation, and a CV. I was ecstatic when I was selected for the AGA editorial fellowship for Clinical Gastroenterology and Hepatology (CGH), whose editorial board’s mission best aligned with my interests.

Dr. Jonathan Buscaglia was the editorial fellows’ mentor for CGH – he met with us and provided an outline of the year. For the first 6 months, I was a reviewer for submitted manuscripts within my topic of interest – pancreaticobiliary diseases and advanced endoscopy and technology. Dr. Buscaglia gave me feedback on my reviews to improve my critical assessment of study designs and interpreted results. After 6 months as a reviewer, I took on the role of an associate editor. I selected reviewers, evaluated the reviews, and made the decision to accept or reject a manuscript. I presented my assigned manuscript at the weekly board of editors meeting, which was one of the biggest learning experiences. Leading researchers from all over the world gathered at a virtual table and discussed whether each study would have clinical impact on the medical community. Each editor contributed a unique perspective that facilitated a robust and thoughtful discussion of each manuscript brought to the table. I was in awe each week.

What I have learned so far during my year as an AGA editorial fellow with CGH has shaped my approach to personal research and will continue to do so as I develop my research career. It has greatly improved my assessment of the literature and I hope to continue to be involved in the critical review process, especially as a reviewer in my early career, and eventually, a part of an editorial board for a journal that truly impacts clinical medicine, such as Clinical Gastroenterology and Hepatology.
 

Dr. Trieu is a gastroenterology and hepatology fellow at Loyola University Medical Center, Maywood, Ill. She has no conflicts of interest to disclose.

On the top left of my desktop is an electronic sticky note entitled, “Apply in Future.” This was where the AGA editorial fellowship was listed when I first started GI fellowship. My interest in the behind-the-scenes of scientific publishing developed early. I wanted to learn not only about the decision-making by the editorial board but also other aspects that impact the process from submission to publication. While waiting for my opportunity to apply, I became a reviewer for several journals and then an associate editor of ACG Case Reports Journal, which gave me some insight.

I applied to the editorial fellowship as a second-year fellow, to start as a third-year fellow. I figured this would give me several chances to apply again if I was not selected! I started off by talking to my program director to ensure that I would have enough time, given other responsibilities. The application consisted of a cover letter, where I expressed why I was interested, particularly focusing on my passion for research and my experience with scientific publishing, a letter of recommendation, and a CV. I was ecstatic when I was selected for the AGA editorial fellowship for Clinical Gastroenterology and Hepatology (CGH), whose editorial board’s mission best aligned with my interests.

Dr. Jonathan Buscaglia was the editorial fellows’ mentor for CGH – he met with us and provided an outline of the year. For the first 6 months, I was a reviewer for submitted manuscripts within my topic of interest – pancreaticobiliary diseases and advanced endoscopy and technology. Dr. Buscaglia gave me feedback on my reviews to improve my critical assessment of study designs and interpreted results. After 6 months as a reviewer, I took on the role of an associate editor. I selected reviewers, evaluated the reviews, and made the decision to accept or reject a manuscript. I presented my assigned manuscript at the weekly board of editors meeting, which was one of the biggest learning experiences. Leading researchers from all over the world gathered at a virtual table and discussed whether each study would have clinical impact on the medical community. Each editor contributed a unique perspective that facilitated a robust and thoughtful discussion of each manuscript brought to the table. I was in awe each week.

What I have learned so far during my year as an AGA editorial fellow with CGH has shaped my approach to personal research and will continue to do so as I develop my research career. It has greatly improved my assessment of the literature and I hope to continue to be involved in the critical review process, especially as a reviewer in my early career, and eventually, a part of an editorial board for a journal that truly impacts clinical medicine, such as Clinical Gastroenterology and Hepatology.
 

Dr. Trieu is a gastroenterology and hepatology fellow at Loyola University Medical Center, Maywood, Ill. She has no conflicts of interest to disclose.

ATLANTA – Potential once-daily male oral contraceptives have passed a first clinical hurdle, showing a degree of testosterone suppression that should be sufficient for a contraceptive effect without causing symptomatic hypogonadism, according to phase 1 study results to be presented at the annual meeting of the Endocrine Society.

Credit: Flickr/Marco Verch Professional Photographer/CC by 2.0

There are two pills in development and the studies so far suggest that both or a combination might be able to provide an acceptable balance of efficacy and tolerability, according to Tamar Jacobsohn, a researcher in the Contraceptive Development Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Md.

The two drugs evaluated in this study are dimethandrolone undecanoate (DMAU) and 11b-methyl-19-nortestosterone-17b-dodecylcarbonate (11b-MNTDC). Both are bifunctional prodrugs with androgenic and progestogenic effects. The prodrugs are designed to be cleaved after ingestion so that the active hormones are released over 24 hours, permitting once-daily dosing.

“As potent androgens, these steroids suppress gonadotropin secretion, leading to markedly decreased serum testosterone production,” explained Ms. Jacobsohn in an interview.

However, she noted that there is still a long way to go on this research path. While the phase 1 studies have shown tolerability, the biology involved in suppressing sperm production suggests that men would need to take these pills daily for about 3 months at the very beginning of contraceptive treatment, until adequate sperm suppression is achieved to prevent pregnancy.

“We are working toward a phase 2 trial that will include a contraceptive efficacy endpoint, but there are lots of steps to get there, including more early phase studies,” she noted.

“There is a huge unmet need in terms of male contraceptive methods,” said Arthi Thirumalai, MBBS, an endocrinologist and assistant professor of medicine at the University of Washington School of Medicine in Seattle.

Senior author of a 2020 review article on male contraception, Dr. Thirumalai said in an interview that prodrugs and other hormonal methods to lower testosterone and suppress sperm production are attractive because of convenience, efficacy, and reversibility,

“We hope that oral formulations can be used to address this need,” said Dr. Thirumalai, who has participated in several experimental and clinical studies of male contraception methods. She is, in fact, one of the many coauthors of the data presented by Ms. Jacobsohn.

Ms. Jacobsohn emphasized: “Development of an effective, reversible male contraceptive method will improve reproductive options for men and women, have a major impact on public health by decreasing unintended pregnancy, and allow men to have an increasingly active role in family planning.”

Phase 1 results with DMAU and MNTDC

The work that led to phase 1 studies suggested that each of the drugs — DMAU and MNTDC — might provide adequate hormone suppression to reduce sperm counts without inducing unacceptable symptoms of hypogonadism. To test this potential, dose-ranging phase 1 studies with an endpoint of testosterone suppression were conducted with each one.

In the two placebo-controlled phase 1a studies, which are to be presented in a poster on June 13, healthy male subjects were randomly assigned to two pills of active therapy, four pills of active therapy, or placebo. In the two studies combined, 39 subjects received DMAU, 30 received 11b-MNTDC, and 28 received placebo.

Efficacy was evaluated by measuring testosterone levels. Tolerability was largely based on patient questionnaires.

At the end of 7 days, testosterone levels remained at reference levels (400 to 600 ng/dL) in those who received placebo. The levels fell to less than 100 ng/dL in all subjects assigned to an active agent regardless of which agent or dose was used.

From day 7 to 28, there was less median suppression of testosterone on 200 mg than 400 mg daily (92.7 ng/dL vs. 49.6 ng/dL; P < .001), but both remained below the target of 100 ng/dL, Ms. Jacobsohn reported.

The difference in degree of testosterone suppression did not appear to influence tolerability.

Subjects on four vs. two daily pills “did not report a significant difference in general satisfaction or their willingness to use the pills in the future or recommend them to other men,” said Ms. Jacobson, presenting P values for these outcomes among subjects on active therapy relative to placebo that were not significant, ranging from 0.48 to 0.85.

Overall, there were no serious adverse events. Mild side effects associated with hypogonadism did occur, but “all resolved by the end of the study,” she said.

Zero sperm production is not the goal. Lowering it sufficiently is

Dr. Thirumalai said the need for a male contraceptive is strong. While condoms have a substantial failure rate, vasectomy is not reliably reversible even though the majority of men agree that the responsibility for preventing pregnancy should be shared, she said.

Dr. Thirumalai’s earlier review article found that clinical trials of hormonal suppression to provide male contraception have been conducted for at least 30 years. The challenge has been finding an effective therapy that is well tolerated.

Drugs that combine both androgenic and progestogenic activity might be the answer. By manipulating hormones that lower testosterone, sperm production is reduced without eliminating a man’s ability to ejaculate. Zero sperm production is not the goal, according to data in Dr. Thirumalai’s review article.

Rather, studies suggest that when ejaculate contains less than 1 million sperm per mL (levels typically range from 15 to 200 million sperm/mL), the antipregnancy efficacy is similar to that achieved with female oral contraceptives.

However, clinical trials to demonstrate that this can be achieved safely have yet to be conducted.

Ms. Jacobsohn said that sperm half-life is about 3 months. This means that patients would need to be on hormonal therapy for a period of about this duration before reliable contraception is achieved.

In other words, the efficacy endpoint used in this current study [of 28 days duration] does not ensure effective contraception, but Ms. Jacobsohn suggested this is nevertheless an important step forward in clinical development.

Ms. Jacobsohn and Dr. Thirumalai report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

ATLANTA – Potential once-daily male oral contraceptives have passed a first clinical hurdle, showing a degree of testosterone suppression that should be sufficient for a contraceptive effect without causing symptomatic hypogonadism, according to phase 1 study results to be presented at the annual meeting of the Endocrine Society.

Credit: Flickr/Marco Verch Professional Photographer/CC by 2.0

There are two pills in development and the studies so far suggest that both or a combination might be able to provide an acceptable balance of efficacy and tolerability, according to Tamar Jacobsohn, a researcher in the Contraceptive Development Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Md.

The two drugs evaluated in this study are dimethandrolone undecanoate (DMAU) and 11b-methyl-19-nortestosterone-17b-dodecylcarbonate (11b-MNTDC). Both are bifunctional prodrugs with androgenic and progestogenic effects. The prodrugs are designed to be cleaved after ingestion so that the active hormones are released over 24 hours, permitting once-daily dosing.

“As potent androgens, these steroids suppress gonadotropin secretion, leading to markedly decreased serum testosterone production,” explained Ms. Jacobsohn in an interview.

However, she noted that there is still a long way to go on this research path. While the phase 1 studies have shown tolerability, the biology involved in suppressing sperm production suggests that men would need to take these pills daily for about 3 months at the very beginning of contraceptive treatment, until adequate sperm suppression is achieved to prevent pregnancy.

“We are working toward a phase 2 trial that will include a contraceptive efficacy endpoint, but there are lots of steps to get there, including more early phase studies,” she noted.

“There is a huge unmet need in terms of male contraceptive methods,” said Arthi Thirumalai, MBBS, an endocrinologist and assistant professor of medicine at the University of Washington School of Medicine in Seattle.

Senior author of a 2020 review article on male contraception, Dr. Thirumalai said in an interview that prodrugs and other hormonal methods to lower testosterone and suppress sperm production are attractive because of convenience, efficacy, and reversibility,

“We hope that oral formulations can be used to address this need,” said Dr. Thirumalai, who has participated in several experimental and clinical studies of male contraception methods. She is, in fact, one of the many coauthors of the data presented by Ms. Jacobsohn.

Ms. Jacobsohn emphasized: “Development of an effective, reversible male contraceptive method will improve reproductive options for men and women, have a major impact on public health by decreasing unintended pregnancy, and allow men to have an increasingly active role in family planning.”

Phase 1 results with DMAU and MNTDC

The work that led to phase 1 studies suggested that each of the drugs — DMAU and MNTDC — might provide adequate hormone suppression to reduce sperm counts without inducing unacceptable symptoms of hypogonadism. To test this potential, dose-ranging phase 1 studies with an endpoint of testosterone suppression were conducted with each one.

In the two placebo-controlled phase 1a studies, which are to be presented in a poster on June 13, healthy male subjects were randomly assigned to two pills of active therapy, four pills of active therapy, or placebo. In the two studies combined, 39 subjects received DMAU, 30 received 11b-MNTDC, and 28 received placebo.

Efficacy was evaluated by measuring testosterone levels. Tolerability was largely based on patient questionnaires.

At the end of 7 days, testosterone levels remained at reference levels (400 to 600 ng/dL) in those who received placebo. The levels fell to less than 100 ng/dL in all subjects assigned to an active agent regardless of which agent or dose was used.

From day 7 to 28, there was less median suppression of testosterone on 200 mg than 400 mg daily (92.7 ng/dL vs. 49.6 ng/dL; P < .001), but both remained below the target of 100 ng/dL, Ms. Jacobsohn reported.

The difference in degree of testosterone suppression did not appear to influence tolerability.

Subjects on four vs. two daily pills “did not report a significant difference in general satisfaction or their willingness to use the pills in the future or recommend them to other men,” said Ms. Jacobson, presenting P values for these outcomes among subjects on active therapy relative to placebo that were not significant, ranging from 0.48 to 0.85.

Overall, there were no serious adverse events. Mild side effects associated with hypogonadism did occur, but “all resolved by the end of the study,” she said.

Zero sperm production is not the goal. Lowering it sufficiently is

Dr. Thirumalai said the need for a male contraceptive is strong. While condoms have a substantial failure rate, vasectomy is not reliably reversible even though the majority of men agree that the responsibility for preventing pregnancy should be shared, she said.

Dr. Thirumalai’s earlier review article found that clinical trials of hormonal suppression to provide male contraception have been conducted for at least 30 years. The challenge has been finding an effective therapy that is well tolerated.

Drugs that combine both androgenic and progestogenic activity might be the answer. By manipulating hormones that lower testosterone, sperm production is reduced without eliminating a man’s ability to ejaculate. Zero sperm production is not the goal, according to data in Dr. Thirumalai’s review article.

Rather, studies suggest that when ejaculate contains less than 1 million sperm per mL (levels typically range from 15 to 200 million sperm/mL), the antipregnancy efficacy is similar to that achieved with female oral contraceptives.

However, clinical trials to demonstrate that this can be achieved safely have yet to be conducted.

Ms. Jacobsohn said that sperm half-life is about 3 months. This means that patients would need to be on hormonal therapy for a period of about this duration before reliable contraception is achieved.

In other words, the efficacy endpoint used in this current study [of 28 days duration] does not ensure effective contraception, but Ms. Jacobsohn suggested this is nevertheless an important step forward in clinical development.

Ms. Jacobsohn and Dr. Thirumalai report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

ATLANTA – Potential once-daily male oral contraceptives have passed a first clinical hurdle, showing a degree of testosterone suppression that should be sufficient for a contraceptive effect without causing symptomatic hypogonadism, according to phase 1 study results to be presented at the annual meeting of the Endocrine Society.

Credit: Flickr/Marco Verch Professional Photographer/CC by 2.0

There are two pills in development and the studies so far suggest that both or a combination might be able to provide an acceptable balance of efficacy and tolerability, according to Tamar Jacobsohn, a researcher in the Contraceptive Development Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Md.

The two drugs evaluated in this study are dimethandrolone undecanoate (DMAU) and 11b-methyl-19-nortestosterone-17b-dodecylcarbonate (11b-MNTDC). Both are bifunctional prodrugs with androgenic and progestogenic effects. The prodrugs are designed to be cleaved after ingestion so that the active hormones are released over 24 hours, permitting once-daily dosing.

“As potent androgens, these steroids suppress gonadotropin secretion, leading to markedly decreased serum testosterone production,” explained Ms. Jacobsohn in an interview.

However, she noted that there is still a long way to go on this research path. While the phase 1 studies have shown tolerability, the biology involved in suppressing sperm production suggests that men would need to take these pills daily for about 3 months at the very beginning of contraceptive treatment, until adequate sperm suppression is achieved to prevent pregnancy.

“We are working toward a phase 2 trial that will include a contraceptive efficacy endpoint, but there are lots of steps to get there, including more early phase studies,” she noted.

“There is a huge unmet need in terms of male contraceptive methods,” said Arthi Thirumalai, MBBS, an endocrinologist and assistant professor of medicine at the University of Washington School of Medicine in Seattle.

Senior author of a 2020 review article on male contraception, Dr. Thirumalai said in an interview that prodrugs and other hormonal methods to lower testosterone and suppress sperm production are attractive because of convenience, efficacy, and reversibility,

“We hope that oral formulations can be used to address this need,” said Dr. Thirumalai, who has participated in several experimental and clinical studies of male contraception methods. She is, in fact, one of the many coauthors of the data presented by Ms. Jacobsohn.

Ms. Jacobsohn emphasized: “Development of an effective, reversible male contraceptive method will improve reproductive options for men and women, have a major impact on public health by decreasing unintended pregnancy, and allow men to have an increasingly active role in family planning.”

Phase 1 results with DMAU and MNTDC

The work that led to phase 1 studies suggested that each of the drugs — DMAU and MNTDC — might provide adequate hormone suppression to reduce sperm counts without inducing unacceptable symptoms of hypogonadism. To test this potential, dose-ranging phase 1 studies with an endpoint of testosterone suppression were conducted with each one.

In the two placebo-controlled phase 1a studies, which are to be presented in a poster on June 13, healthy male subjects were randomly assigned to two pills of active therapy, four pills of active therapy, or placebo. In the two studies combined, 39 subjects received DMAU, 30 received 11b-MNTDC, and 28 received placebo.

Efficacy was evaluated by measuring testosterone levels. Tolerability was largely based on patient questionnaires.

At the end of 7 days, testosterone levels remained at reference levels (400 to 600 ng/dL) in those who received placebo. The levels fell to less than 100 ng/dL in all subjects assigned to an active agent regardless of which agent or dose was used.

From day 7 to 28, there was less median suppression of testosterone on 200 mg than 400 mg daily (92.7 ng/dL vs. 49.6 ng/dL; P < .001), but both remained below the target of 100 ng/dL, Ms. Jacobsohn reported.

The difference in degree of testosterone suppression did not appear to influence tolerability.

Subjects on four vs. two daily pills “did not report a significant difference in general satisfaction or their willingness to use the pills in the future or recommend them to other men,” said Ms. Jacobson, presenting P values for these outcomes among subjects on active therapy relative to placebo that were not significant, ranging from 0.48 to 0.85.

Overall, there were no serious adverse events. Mild side effects associated with hypogonadism did occur, but “all resolved by the end of the study,” she said.

Zero sperm production is not the goal. Lowering it sufficiently is

Dr. Thirumalai said the need for a male contraceptive is strong. While condoms have a substantial failure rate, vasectomy is not reliably reversible even though the majority of men agree that the responsibility for preventing pregnancy should be shared, she said.

Dr. Thirumalai’s earlier review article found that clinical trials of hormonal suppression to provide male contraception have been conducted for at least 30 years. The challenge has been finding an effective therapy that is well tolerated.

Drugs that combine both androgenic and progestogenic activity might be the answer. By manipulating hormones that lower testosterone, sperm production is reduced without eliminating a man’s ability to ejaculate. Zero sperm production is not the goal, according to data in Dr. Thirumalai’s review article.

Rather, studies suggest that when ejaculate contains less than 1 million sperm per mL (levels typically range from 15 to 200 million sperm/mL), the antipregnancy efficacy is similar to that achieved with female oral contraceptives.

However, clinical trials to demonstrate that this can be achieved safely have yet to be conducted.

Ms. Jacobsohn said that sperm half-life is about 3 months. This means that patients would need to be on hormonal therapy for a period of about this duration before reliable contraception is achieved.

In other words, the efficacy endpoint used in this current study [of 28 days duration] does not ensure effective contraception, but Ms. Jacobsohn suggested this is nevertheless an important step forward in clinical development.

Ms. Jacobsohn and Dr. Thirumalai report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

When Esther Freeman, MD, PhD, thinks back on what she learned about monkeypox during her training as a dermatologist and an infectious disease epidemiologist, it was widely considered a viral disease with rare outbreaks limited primarily to Central and Western Africa.

“Monkeypox is something we have traditionally only seen very rarely in the U.S.,” Dr. Freeman, director of Global Health Dermatology at Massachusetts General Hospital and Harvard Medical School, Boston, said in an interview. “In the past, outbreaks in the U.S. have been related to international travel or import of exotic pets, which is very different than what we’re seeing as a global community now.”

Courtesy Dr. Ester Freeman

A different clinical presentation

The clinical presentation of monkeypox cases in the current outbreak also differs from that of previous outbreaks. In the past, monkeypox rashes often morphed from a macule to a pustule and commonly affected the face, hands, feet, and trunk, with some patients harboring as many as 200 lesions at once. That pattern still occurs, but increasingly, the presentation is characterized by a more localized spread, especially in the genital region, which Dr. Freeman described as “unusual and not an area we traditionally thought of in the past as a focus for monkeypox.”

Also, affected individuals in the current outbreak may develop fewer lesions, sometimes between 1 and 5 instead of up to 200. “This doesn’t apply to everybody, but it is a bit of a different picture than what we’ve seen in case descriptions and photographs in the past from places like Central Africa,” she said. “What’s being reported out of case clusters from the United Kingdom and Spain is a mix, where some people are having more generalized involvement while others have more localized involvement.” Visual examples of the monkey pox rash can be found in photos from the United Kingdom, the country with the highest number of confirmed cases, on the CDC’s website, and in a report from Spain.

Clusters of monkeypox cases have been reported worldwide in men who have sex with men, “but this is not limited to a particular subgroup of people,” emphasizes Dr. Freeman, who is also a member of the American Academy of Dermatology’s Ad Hoc Task Force to Develop Monkeypox Content, which created an online resource for clinicians. “There are several mechanisms of spread, but direct contact with lesions or infected fluids is one,” she notes.

Moreover, “lesions associated with herpes, syphilis, and molluscum can look similar to a monkeypox lesion. If you have a patient with a new genital lesion and you’re not sure what it is, testing for monkeypox in addition to classic sexually transmitted infections like HSV or syphilis would be reasonable during the current outbreak situation.”

The 2022 monkeypox outbreak may pale in comparison to the spread of COVID-19 in terms of case numbers and societal impact, but dermatologists may be the first point of contact for a person infected with the monkeypox virus. “It’s important for dermatologists to be able to recognize monkeypox, because by recognizing cases, we can stop the outbreak,” Dr. Freeman said. “In theory, an infected person could show up in your clinic, regardless of where you practice in the U.S. But at the same time, it’s important not to panic. This is not COVID-19 all over again; this is different. Yes, it is an outbreak, but we already have a vaccine that works against monkeypox, and while one of the possible modes of transmission for monkeypox is respiratory, it’s much harder to transmit that way than SARS-CoV-2 – it requires closer and longer contact.”

Confirmation of a monkeypox virus infection is based on results of a PCR test based on swabs of a lesion. The AAD task force recommends contacting the local hospital epidemiologist, infection control personnel, and/or state health department about suspected cases, “as different locations will have different regulations on where to send the [PCR] test. If appropriate, the state health department will contact the CDC.”

According to the CDC, current recommendations for personal protective equipment for possible and confirmed monkeypox cases include gown, gloves, a National Institute for Occupational Safety and Health-approved N-95 mask, and eye protection.

 

Topical antiviral an option

If the lesions in a patient with suspected monkeypox have turned into pustules while waiting for the PCR test results, one option is to prescribe 3%-5% topical cidofovir, according to Stephen K. Tyring, MD, PhD, of the departments of dermatology, microbiology & molecular genetics, and internal medicine at the University of Texas Health Science Center, Houston. “That’s the effective antiviral that is most available,” he said. Generic cidofovir is also now available.

Dr. Tyring recommends rapid referral of immunocompromised patients with suspected monkeypox to an infectious disease expert and/or consulting with the CDC. “The pediatric population also seems to be at somewhat more risk, as has been seen in sub-Saharan Africa,” said Dr. Tyring, who is one of the editors of the textbook Tropical Dermatology. “Also, by definition, pregnant women are at more risk because their immune systems aren’t up to par. You also want to make sure that if monkeypox is on a person’s skin that they don’t get it in their eyes, because they could lose their vision.” He added that sub-Saharan Africa has a monkeypox mortality of up to 10%, “which is something we don’t see in the U.S. or Europe. Those of us who grew up in the 20th century got routine smallpox vaccines, and we therefore probably have a degree of immunity to monkeypox. But for the past 40 years or so, unless you are in the military, you are not going to get a routine vaccine to prevent smallpox.”
 

Incubation period, appearance of lesions

Monkeypox has a long incubation period. According to Dr. Freeman, from the point of exposure to the development of symptomatic lesions is typically 7-14 days but can vary from 5-21 days. “It’s important for people to be aware that their exposure may have been in the more distant past, not just a few days ago” she said. “Identifying cases as quickly as possible gives us a window where we can vaccinate close contacts.”

Dr. Freeman and Dr. Tyring reported having no relevant financial disclosures.

CDC guidance on vaccination before and after exposure to monkeypox can be found here . A general Q&A for health care professionals from the CDC can be found here.

When Esther Freeman, MD, PhD, thinks back on what she learned about monkeypox during her training as a dermatologist and an infectious disease epidemiologist, it was widely considered a viral disease with rare outbreaks limited primarily to Central and Western Africa.

“Monkeypox is something we have traditionally only seen very rarely in the U.S.,” Dr. Freeman, director of Global Health Dermatology at Massachusetts General Hospital and Harvard Medical School, Boston, said in an interview. “In the past, outbreaks in the U.S. have been related to international travel or import of exotic pets, which is very different than what we’re seeing as a global community now.”

Courtesy Dr. Ester Freeman

A different clinical presentation

The clinical presentation of monkeypox cases in the current outbreak also differs from that of previous outbreaks. In the past, monkeypox rashes often morphed from a macule to a pustule and commonly affected the face, hands, feet, and trunk, with some patients harboring as many as 200 lesions at once. That pattern still occurs, but increasingly, the presentation is characterized by a more localized spread, especially in the genital region, which Dr. Freeman described as “unusual and not an area we traditionally thought of in the past as a focus for monkeypox.”

Also, affected individuals in the current outbreak may develop fewer lesions, sometimes between 1 and 5 instead of up to 200. “This doesn’t apply to everybody, but it is a bit of a different picture than what we’ve seen in case descriptions and photographs in the past from places like Central Africa,” she said. “What’s being reported out of case clusters from the United Kingdom and Spain is a mix, where some people are having more generalized involvement while others have more localized involvement.” Visual examples of the monkey pox rash can be found in photos from the United Kingdom, the country with the highest number of confirmed cases, on the CDC’s website, and in a report from Spain.

Clusters of monkeypox cases have been reported worldwide in men who have sex with men, “but this is not limited to a particular subgroup of people,” emphasizes Dr. Freeman, who is also a member of the American Academy of Dermatology’s Ad Hoc Task Force to Develop Monkeypox Content, which created an online resource for clinicians. “There are several mechanisms of spread, but direct contact with lesions or infected fluids is one,” she notes.

Moreover, “lesions associated with herpes, syphilis, and molluscum can look similar to a monkeypox lesion. If you have a patient with a new genital lesion and you’re not sure what it is, testing for monkeypox in addition to classic sexually transmitted infections like HSV or syphilis would be reasonable during the current outbreak situation.”

The 2022 monkeypox outbreak may pale in comparison to the spread of COVID-19 in terms of case numbers and societal impact, but dermatologists may be the first point of contact for a person infected with the monkeypox virus. “It’s important for dermatologists to be able to recognize monkeypox, because by recognizing cases, we can stop the outbreak,” Dr. Freeman said. “In theory, an infected person could show up in your clinic, regardless of where you practice in the U.S. But at the same time, it’s important not to panic. This is not COVID-19 all over again; this is different. Yes, it is an outbreak, but we already have a vaccine that works against monkeypox, and while one of the possible modes of transmission for monkeypox is respiratory, it’s much harder to transmit that way than SARS-CoV-2 – it requires closer and longer contact.”

Confirmation of a monkeypox virus infection is based on results of a PCR test based on swabs of a lesion. The AAD task force recommends contacting the local hospital epidemiologist, infection control personnel, and/or state health department about suspected cases, “as different locations will have different regulations on where to send the [PCR] test. If appropriate, the state health department will contact the CDC.”

According to the CDC, current recommendations for personal protective equipment for possible and confirmed monkeypox cases include gown, gloves, a National Institute for Occupational Safety and Health-approved N-95 mask, and eye protection.

 

Topical antiviral an option

If the lesions in a patient with suspected monkeypox have turned into pustules while waiting for the PCR test results, one option is to prescribe 3%-5% topical cidofovir, according to Stephen K. Tyring, MD, PhD, of the departments of dermatology, microbiology & molecular genetics, and internal medicine at the University of Texas Health Science Center, Houston. “That’s the effective antiviral that is most available,” he said. Generic cidofovir is also now available.

Dr. Tyring recommends rapid referral of immunocompromised patients with suspected monkeypox to an infectious disease expert and/or consulting with the CDC. “The pediatric population also seems to be at somewhat more risk, as has been seen in sub-Saharan Africa,” said Dr. Tyring, who is one of the editors of the textbook Tropical Dermatology. “Also, by definition, pregnant women are at more risk because their immune systems aren’t up to par. You also want to make sure that if monkeypox is on a person’s skin that they don’t get it in their eyes, because they could lose their vision.” He added that sub-Saharan Africa has a monkeypox mortality of up to 10%, “which is something we don’t see in the U.S. or Europe. Those of us who grew up in the 20th century got routine smallpox vaccines, and we therefore probably have a degree of immunity to monkeypox. But for the past 40 years or so, unless you are in the military, you are not going to get a routine vaccine to prevent smallpox.”
 

Incubation period, appearance of lesions

Monkeypox has a long incubation period. According to Dr. Freeman, from the point of exposure to the development of symptomatic lesions is typically 7-14 days but can vary from 5-21 days. “It’s important for people to be aware that their exposure may have been in the more distant past, not just a few days ago” she said. “Identifying cases as quickly as possible gives us a window where we can vaccinate close contacts.”

Dr. Freeman and Dr. Tyring reported having no relevant financial disclosures.

CDC guidance on vaccination before and after exposure to monkeypox can be found here . A general Q&A for health care professionals from the CDC can be found here.

When Esther Freeman, MD, PhD, thinks back on what she learned about monkeypox during her training as a dermatologist and an infectious disease epidemiologist, it was widely considered a viral disease with rare outbreaks limited primarily to Central and Western Africa.

“Monkeypox is something we have traditionally only seen very rarely in the U.S.,” Dr. Freeman, director of Global Health Dermatology at Massachusetts General Hospital and Harvard Medical School, Boston, said in an interview. “In the past, outbreaks in the U.S. have been related to international travel or import of exotic pets, which is very different than what we’re seeing as a global community now.”

Courtesy Dr. Ester Freeman

A different clinical presentation

The clinical presentation of monkeypox cases in the current outbreak also differs from that of previous outbreaks. In the past, monkeypox rashes often morphed from a macule to a pustule and commonly affected the face, hands, feet, and trunk, with some patients harboring as many as 200 lesions at once. That pattern still occurs, but increasingly, the presentation is characterized by a more localized spread, especially in the genital region, which Dr. Freeman described as “unusual and not an area we traditionally thought of in the past as a focus for monkeypox.”

Also, affected individuals in the current outbreak may develop fewer lesions, sometimes between 1 and 5 instead of up to 200. “This doesn’t apply to everybody, but it is a bit of a different picture than what we’ve seen in case descriptions and photographs in the past from places like Central Africa,” she said. “What’s being reported out of case clusters from the United Kingdom and Spain is a mix, where some people are having more generalized involvement while others have more localized involvement.” Visual examples of the monkey pox rash can be found in photos from the United Kingdom, the country with the highest number of confirmed cases, on the CDC’s website, and in a report from Spain.

Clusters of monkeypox cases have been reported worldwide in men who have sex with men, “but this is not limited to a particular subgroup of people,” emphasizes Dr. Freeman, who is also a member of the American Academy of Dermatology’s Ad Hoc Task Force to Develop Monkeypox Content, which created an online resource for clinicians. “There are several mechanisms of spread, but direct contact with lesions or infected fluids is one,” she notes.

Moreover, “lesions associated with herpes, syphilis, and molluscum can look similar to a monkeypox lesion. If you have a patient with a new genital lesion and you’re not sure what it is, testing for monkeypox in addition to classic sexually transmitted infections like HSV or syphilis would be reasonable during the current outbreak situation.”

The 2022 monkeypox outbreak may pale in comparison to the spread of COVID-19 in terms of case numbers and societal impact, but dermatologists may be the first point of contact for a person infected with the monkeypox virus. “It’s important for dermatologists to be able to recognize monkeypox, because by recognizing cases, we can stop the outbreak,” Dr. Freeman said. “In theory, an infected person could show up in your clinic, regardless of where you practice in the U.S. But at the same time, it’s important not to panic. This is not COVID-19 all over again; this is different. Yes, it is an outbreak, but we already have a vaccine that works against monkeypox, and while one of the possible modes of transmission for monkeypox is respiratory, it’s much harder to transmit that way than SARS-CoV-2 – it requires closer and longer contact.”

Confirmation of a monkeypox virus infection is based on results of a PCR test based on swabs of a lesion. The AAD task force recommends contacting the local hospital epidemiologist, infection control personnel, and/or state health department about suspected cases, “as different locations will have different regulations on where to send the [PCR] test. If appropriate, the state health department will contact the CDC.”

According to the CDC, current recommendations for personal protective equipment for possible and confirmed monkeypox cases include gown, gloves, a National Institute for Occupational Safety and Health-approved N-95 mask, and eye protection.

 

Topical antiviral an option

If the lesions in a patient with suspected monkeypox have turned into pustules while waiting for the PCR test results, one option is to prescribe 3%-5% topical cidofovir, according to Stephen K. Tyring, MD, PhD, of the departments of dermatology, microbiology & molecular genetics, and internal medicine at the University of Texas Health Science Center, Houston. “That’s the effective antiviral that is most available,” he said. Generic cidofovir is also now available.

Dr. Tyring recommends rapid referral of immunocompromised patients with suspected monkeypox to an infectious disease expert and/or consulting with the CDC. “The pediatric population also seems to be at somewhat more risk, as has been seen in sub-Saharan Africa,” said Dr. Tyring, who is one of the editors of the textbook Tropical Dermatology. “Also, by definition, pregnant women are at more risk because their immune systems aren’t up to par. You also want to make sure that if monkeypox is on a person’s skin that they don’t get it in their eyes, because they could lose their vision.” He added that sub-Saharan Africa has a monkeypox mortality of up to 10%, “which is something we don’t see in the U.S. or Europe. Those of us who grew up in the 20th century got routine smallpox vaccines, and we therefore probably have a degree of immunity to monkeypox. But for the past 40 years or so, unless you are in the military, you are not going to get a routine vaccine to prevent smallpox.”
 

Incubation period, appearance of lesions

Monkeypox has a long incubation period. According to Dr. Freeman, from the point of exposure to the development of symptomatic lesions is typically 7-14 days but can vary from 5-21 days. “It’s important for people to be aware that their exposure may have been in the more distant past, not just a few days ago” she said. “Identifying cases as quickly as possible gives us a window where we can vaccinate close contacts.”

Dr. Freeman and Dr. Tyring reported having no relevant financial disclosures.

CDC guidance on vaccination before and after exposure to monkeypox can be found here . A general Q&A for health care professionals from the CDC can be found here.