Pediatrics

Patients with multisystem inflammatory syndrome caused by COVID-19 typically seem to avoid coronary artery dilation early on, but they may be prone to cardiac injury and dysfunction longer term that requires a more discerning diagnostic approach to sort out.

The findings were revealed in a study of 28 children with COVID-19–related multisystem inflammatory syndrome (MIS-C) at Children’s Hospital of Philadelphia. The study reported that cardiac injury and dysfunction are common in these patients – even those who have preserved ejection fraction – and that diastolic dysfunction is persistent. For comparison, the study also included 20 healthy controls and 20 patients with classic Kawasaki disease (KD).

The study analyzed echocardiography findings in the patients, reporting left ventricular (LV) systolic and diastolic function were worse than in classic Kawasaki disease (KD), which MIS-C mimics. Lead author Daisuke Matsubara, MD, PhD, and colleagues reported that four markers – LV global longitudinal strain, LV circumferential strain rate, right ventricular strain, and left atrial strain – were the strongest predictors of myocardial injury in these patients. After the acute phase, systolic function tended to recover, but diastolic dysfunction persisted.
 

‘Strain’ measurement boosts accuracy

While echocardiography has been reported to be valuable in evaluating coronary artery function in MIS-C patients, Dr. Matsubara of the division of cardiology at CHOP, said in an interview that study is the first to use the newer echocardiography indexes, known as “strain,” to assess heart function.

“Strain is a more sensitive tool than more conventional indexes and can detect subtle decrease in heart function, even when ejection fraction is preserved,” he said. “Numerous publications have reached conclusions that strain improves the prognostic and diagnostic accuracy of echocardiography in a wide variety of cardiac pathologies causing LV dysfunction.”

Dr. Matsubara noted that the coronary arteries were mostly unaffected in the acute stage of MIS-C, as only one patient in their MIS-C cohort had coronary artery involvement, which normalized during early follow-up. “On the other hand, 20% of our classic KD patients had coronary abnormalities, including two with aneurysms.”

By using positive troponin I or elevated brain natriuretic peptide (BNP) to assess cardiac injury, they found a “high” (60%) incidence of myocardial injury in their MIS-C cohort. During early follow-up, most of the MIS-C patients showed normalization of systolic function, although diastolic dysfunction persisted.

When compared with the classic KD group, MIS-C patients had higher rates of mitral regurgitation (46% vs. 15%, P = .06), more pericardial effusion (32% vs. 15%, P = 0.46), and more pleural effusion (39% vs. 0%, P = .004). MIS-C patients with suspected myocardial injury show these findings more frequently than those with actual myocardial injury.

Compared with the healthy controls, the MIS-C patients showed both LV systolic and diastolic dysfunction as well as significantly lower left atrium (LA) strain and peak right ventricle (RV) free-wall longitudinal strain.

“In addition to the left ventricle, two other chambers of the heart, the LA and the RV that are often labeled as the ‘forgotten chambers’ of the heart, were also affected by MIS-C,” Dr. Matsubara said. “Both LA and RV strains were markedly reduced in MIS-C patients, compared to normal and KD patients.”

The study also indicates that elevated troponin I levels may not be as dire in children as they are in adults. Dr. Matsubara cited a study of more than 2,700 adult COVID-19 patients that found that even mild increases in troponin I level were associated with increased death during hospitalization (J Am Coll Cardiol. 2020;76:533-46).

However, most of the patients in the CHOP study, even those with elevated troponin I levels, recovered systolic function quickly. “We speculate that the elevation in cardiac troponins may have less dire implications in children, likely due to a more transient type of cardiac injury and less comorbidities in children,” he said. “Clearly further studies are needed before a definitive statement can be made.”

Dr. Matsubara added that recovered COVID-19 patients may be able to participate in sports as some schools reopen. “We are not saying restrict sport participation, but we are merely urging caution.”

Comprehensive LV evaluation needed

The findings reinforce that myocardial involvement is more frequent and sometimes more severe in MIS-C than previously thought, said Kevin G. Friedman, MD, a pediatrician at Harvard Medical School, Boston, and an attending physician in the department of cardiology at Boston Children’s Hospital. “We are underestimating it by using just traditional measures like ejection fraction. It requires a comprehensive evaluation of left ventricular function; it really affects all aspects of the ventricle, both the systolic function and the diastolic function.”

This study supports that MIS-C patients should have a more detailed analysis than EF on echocardiography, including strain imaging. “Probably these patients should all be followed at centers where they can evaluate a more detailed analysis of the LV and RV function,” he said. Patients with ongoing CA enlargement and LV dysfunction should have follow-up cardiac care indefinitely. Patients who have no cardiac symptoms during the acute phase probably don’t need long-term follow-up.

“We’re just trying to learn more about this disease, and it’s certainly concerning that so many kids are having cardiac involvement,” Dr. Friedman said. “Fortunately they’re getting better; we’re just trying to find out what this means for the long term.”

Dr. Matsubara and Dr. Friedman have no relevant financial disclosures.

SOURCE: Matsubara D et al. J Am Coll Cardiol. 2020 Sep 2. doi: 10.1016/j.jacc.2020.08.056.

Patients with multisystem inflammatory syndrome caused by COVID-19 typically seem to avoid coronary artery dilation early on, but they may be prone to cardiac injury and dysfunction longer term that requires a more discerning diagnostic approach to sort out.

The findings were revealed in a study of 28 children with COVID-19–related multisystem inflammatory syndrome (MIS-C) at Children’s Hospital of Philadelphia. The study reported that cardiac injury and dysfunction are common in these patients – even those who have preserved ejection fraction – and that diastolic dysfunction is persistent. For comparison, the study also included 20 healthy controls and 20 patients with classic Kawasaki disease (KD).

The study analyzed echocardiography findings in the patients, reporting left ventricular (LV) systolic and diastolic function were worse than in classic Kawasaki disease (KD), which MIS-C mimics. Lead author Daisuke Matsubara, MD, PhD, and colleagues reported that four markers – LV global longitudinal strain, LV circumferential strain rate, right ventricular strain, and left atrial strain – were the strongest predictors of myocardial injury in these patients. After the acute phase, systolic function tended to recover, but diastolic dysfunction persisted.
 

‘Strain’ measurement boosts accuracy

While echocardiography has been reported to be valuable in evaluating coronary artery function in MIS-C patients, Dr. Matsubara of the division of cardiology at CHOP, said in an interview that study is the first to use the newer echocardiography indexes, known as “strain,” to assess heart function.

“Strain is a more sensitive tool than more conventional indexes and can detect subtle decrease in heart function, even when ejection fraction is preserved,” he said. “Numerous publications have reached conclusions that strain improves the prognostic and diagnostic accuracy of echocardiography in a wide variety of cardiac pathologies causing LV dysfunction.”

Dr. Matsubara noted that the coronary arteries were mostly unaffected in the acute stage of MIS-C, as only one patient in their MIS-C cohort had coronary artery involvement, which normalized during early follow-up. “On the other hand, 20% of our classic KD patients had coronary abnormalities, including two with aneurysms.”

By using positive troponin I or elevated brain natriuretic peptide (BNP) to assess cardiac injury, they found a “high” (60%) incidence of myocardial injury in their MIS-C cohort. During early follow-up, most of the MIS-C patients showed normalization of systolic function, although diastolic dysfunction persisted.

When compared with the classic KD group, MIS-C patients had higher rates of mitral regurgitation (46% vs. 15%, P = .06), more pericardial effusion (32% vs. 15%, P = 0.46), and more pleural effusion (39% vs. 0%, P = .004). MIS-C patients with suspected myocardial injury show these findings more frequently than those with actual myocardial injury.

Compared with the healthy controls, the MIS-C patients showed both LV systolic and diastolic dysfunction as well as significantly lower left atrium (LA) strain and peak right ventricle (RV) free-wall longitudinal strain.

“In addition to the left ventricle, two other chambers of the heart, the LA and the RV that are often labeled as the ‘forgotten chambers’ of the heart, were also affected by MIS-C,” Dr. Matsubara said. “Both LA and RV strains were markedly reduced in MIS-C patients, compared to normal and KD patients.”

The study also indicates that elevated troponin I levels may not be as dire in children as they are in adults. Dr. Matsubara cited a study of more than 2,700 adult COVID-19 patients that found that even mild increases in troponin I level were associated with increased death during hospitalization (J Am Coll Cardiol. 2020;76:533-46).

However, most of the patients in the CHOP study, even those with elevated troponin I levels, recovered systolic function quickly. “We speculate that the elevation in cardiac troponins may have less dire implications in children, likely due to a more transient type of cardiac injury and less comorbidities in children,” he said. “Clearly further studies are needed before a definitive statement can be made.”

Dr. Matsubara added that recovered COVID-19 patients may be able to participate in sports as some schools reopen. “We are not saying restrict sport participation, but we are merely urging caution.”

Comprehensive LV evaluation needed

The findings reinforce that myocardial involvement is more frequent and sometimes more severe in MIS-C than previously thought, said Kevin G. Friedman, MD, a pediatrician at Harvard Medical School, Boston, and an attending physician in the department of cardiology at Boston Children’s Hospital. “We are underestimating it by using just traditional measures like ejection fraction. It requires a comprehensive evaluation of left ventricular function; it really affects all aspects of the ventricle, both the systolic function and the diastolic function.”

This study supports that MIS-C patients should have a more detailed analysis than EF on echocardiography, including strain imaging. “Probably these patients should all be followed at centers where they can evaluate a more detailed analysis of the LV and RV function,” he said. Patients with ongoing CA enlargement and LV dysfunction should have follow-up cardiac care indefinitely. Patients who have no cardiac symptoms during the acute phase probably don’t need long-term follow-up.

“We’re just trying to learn more about this disease, and it’s certainly concerning that so many kids are having cardiac involvement,” Dr. Friedman said. “Fortunately they’re getting better; we’re just trying to find out what this means for the long term.”

Dr. Matsubara and Dr. Friedman have no relevant financial disclosures.

SOURCE: Matsubara D et al. J Am Coll Cardiol. 2020 Sep 2. doi: 10.1016/j.jacc.2020.08.056.

Patients with multisystem inflammatory syndrome caused by COVID-19 typically seem to avoid coronary artery dilation early on, but they may be prone to cardiac injury and dysfunction longer term that requires a more discerning diagnostic approach to sort out.

The findings were revealed in a study of 28 children with COVID-19–related multisystem inflammatory syndrome (MIS-C) at Children’s Hospital of Philadelphia. The study reported that cardiac injury and dysfunction are common in these patients – even those who have preserved ejection fraction – and that diastolic dysfunction is persistent. For comparison, the study also included 20 healthy controls and 20 patients with classic Kawasaki disease (KD).

The study analyzed echocardiography findings in the patients, reporting left ventricular (LV) systolic and diastolic function were worse than in classic Kawasaki disease (KD), which MIS-C mimics. Lead author Daisuke Matsubara, MD, PhD, and colleagues reported that four markers – LV global longitudinal strain, LV circumferential strain rate, right ventricular strain, and left atrial strain – were the strongest predictors of myocardial injury in these patients. After the acute phase, systolic function tended to recover, but diastolic dysfunction persisted.
 

‘Strain’ measurement boosts accuracy

While echocardiography has been reported to be valuable in evaluating coronary artery function in MIS-C patients, Dr. Matsubara of the division of cardiology at CHOP, said in an interview that study is the first to use the newer echocardiography indexes, known as “strain,” to assess heart function.

“Strain is a more sensitive tool than more conventional indexes and can detect subtle decrease in heart function, even when ejection fraction is preserved,” he said. “Numerous publications have reached conclusions that strain improves the prognostic and diagnostic accuracy of echocardiography in a wide variety of cardiac pathologies causing LV dysfunction.”

Dr. Matsubara noted that the coronary arteries were mostly unaffected in the acute stage of MIS-C, as only one patient in their MIS-C cohort had coronary artery involvement, which normalized during early follow-up. “On the other hand, 20% of our classic KD patients had coronary abnormalities, including two with aneurysms.”

By using positive troponin I or elevated brain natriuretic peptide (BNP) to assess cardiac injury, they found a “high” (60%) incidence of myocardial injury in their MIS-C cohort. During early follow-up, most of the MIS-C patients showed normalization of systolic function, although diastolic dysfunction persisted.

When compared with the classic KD group, MIS-C patients had higher rates of mitral regurgitation (46% vs. 15%, P = .06), more pericardial effusion (32% vs. 15%, P = 0.46), and more pleural effusion (39% vs. 0%, P = .004). MIS-C patients with suspected myocardial injury show these findings more frequently than those with actual myocardial injury.

Compared with the healthy controls, the MIS-C patients showed both LV systolic and diastolic dysfunction as well as significantly lower left atrium (LA) strain and peak right ventricle (RV) free-wall longitudinal strain.

“In addition to the left ventricle, two other chambers of the heart, the LA and the RV that are often labeled as the ‘forgotten chambers’ of the heart, were also affected by MIS-C,” Dr. Matsubara said. “Both LA and RV strains were markedly reduced in MIS-C patients, compared to normal and KD patients.”

The study also indicates that elevated troponin I levels may not be as dire in children as they are in adults. Dr. Matsubara cited a study of more than 2,700 adult COVID-19 patients that found that even mild increases in troponin I level were associated with increased death during hospitalization (J Am Coll Cardiol. 2020;76:533-46).

However, most of the patients in the CHOP study, even those with elevated troponin I levels, recovered systolic function quickly. “We speculate that the elevation in cardiac troponins may have less dire implications in children, likely due to a more transient type of cardiac injury and less comorbidities in children,” he said. “Clearly further studies are needed before a definitive statement can be made.”

Dr. Matsubara added that recovered COVID-19 patients may be able to participate in sports as some schools reopen. “We are not saying restrict sport participation, but we are merely urging caution.”

Comprehensive LV evaluation needed

The findings reinforce that myocardial involvement is more frequent and sometimes more severe in MIS-C than previously thought, said Kevin G. Friedman, MD, a pediatrician at Harvard Medical School, Boston, and an attending physician in the department of cardiology at Boston Children’s Hospital. “We are underestimating it by using just traditional measures like ejection fraction. It requires a comprehensive evaluation of left ventricular function; it really affects all aspects of the ventricle, both the systolic function and the diastolic function.”

This study supports that MIS-C patients should have a more detailed analysis than EF on echocardiography, including strain imaging. “Probably these patients should all be followed at centers where they can evaluate a more detailed analysis of the LV and RV function,” he said. Patients with ongoing CA enlargement and LV dysfunction should have follow-up cardiac care indefinitely. Patients who have no cardiac symptoms during the acute phase probably don’t need long-term follow-up.

“We’re just trying to learn more about this disease, and it’s certainly concerning that so many kids are having cardiac involvement,” Dr. Friedman said. “Fortunately they’re getting better; we’re just trying to find out what this means for the long term.”

Dr. Matsubara and Dr. Friedman have no relevant financial disclosures.

SOURCE: Matsubara D et al. J Am Coll Cardiol. 2020 Sep 2. doi: 10.1016/j.jacc.2020.08.056.

Presenters

Michael Bryant, MD – Children’s Hospital of Los Angeles

Kimberly Manning, MD – Emory University, Atlanta

Kimberly Reynolds, MD – University of Miami

Samir Shah, MD, MSCE, MHM – Cincinnati Children’s Hospital

Ndidi Unaka, MD, MEd – Cincinnati Children’s Hospital

Moderator

Erin Shaughnessy, MD – Phoenix Children’s Hospital

Session summary

This session was devoted to a discussion about how pediatric hospital medicine (PHM) as a field can address racism in medicine. The structural inequity rooted in poverty, housing problems, and differential education represents the essential social determinant of health. No longer can pediatric hospitalists neglect or be in denial of the crucial role that race plays in propagating further inequalities in our society and at our workplace. Historically Black people were exploited in research and still are disproportionately affected when it comes to infant prematurity and mortality, asthma, pain treatments, and so on. The pediatric hospitalist must explore and understand the reasons behind nonadherence and noncompliance among Black patients and always seek to understand before criticizing.

Within learning environments, we must improve how to “autocorrect” and proactively work on our own biases. Dr. Bryant pointed out that each institution has the responsibility to build on the civil rights movement and seize the moment to create a robust response to the inequities manifested during the COVID-19 epidemic, as well as the events following the deaths of George Floyd, Breonna Taylor, Ahmoud Arbery, and many others. Dr. Shah called on the PHM community to take on that obligation by “stepping into the tension,” as Mark Shapiro, MD, has suggested in a conversation/podcast with Dr. Unaka.

As pediatric hospitalists, we will have to show up both individually and as constituents of institutions to address racism by specific projects looking at all data relevant for racism rather than race in quality and safety – thereby amplifying the voices of our Black patients and families, remarked Dr. Unaka. There was a brief reflection on the use of the word “allies” by Dr. Manning and Dr. Reynolds to remind the more than 200 session participants that a bidirectional framework of this process is crucial and that there is a clear need for a partnership to a common goal that should start by “a laydown of privilege of those who have it” to establish equal playing fields once and for all.

Dr. Bryant encouraged a deliberate and early thoughtful process to identify those with opportunities and help young Black people explore journeys in medicine and increase diversity among PHM faculty. Dr. Manning reminded the audience of the power that relationships have and hold in our lives, and not only those of mentors and mentees, but also relationships among all of us as humans. As with those simple situations in which we mess up and have to be able to admit it, apologize for it, and learn to move on, this requires also showing up as a mentee, articulating one’s needs, and learning to break the habits rooted in biases. Dr. Unaka warned against stereotypes and reminded us to look deeper and understand better all of our learners and their blind spots, as well as our own.
 

Key takeaways

• The field of PHM must recognize the role that race plays in propagating inequalities.
• Learning and mentorship environments have to be assessed for the safety of all learners and adjusted to correct (and autocorrect) as many biases as possible.
• Institutions must assume responsibilities to establish a conscious, robust response to injustice and racism in a timely and specific manner.
• Further research efforts must be made to address racism, rather than race.
• The PHM community must show up to create a new, healthy, and deliberate bidirectional framework to endorse and support diversity.

Dr. Giordano is assistant professor of pediatrics at Columbia University and a pediatric hospitalist at NewYork–Presbyterian Morgan Stanley Children’s Hospital, both in New York, with an interest in surgical comanagement. She serves on the Society of Hospital Medicine’s Pediatric Special Interest Group Executive Committee and is the chair of the Education Subcommittee. She is also an advisory board member for the New York/Westchester SHM Chapter.

Presenters

Michael Bryant, MD – Children’s Hospital of Los Angeles

Kimberly Manning, MD – Emory University, Atlanta

Kimberly Reynolds, MD – University of Miami

Samir Shah, MD, MSCE, MHM – Cincinnati Children’s Hospital

Ndidi Unaka, MD, MEd – Cincinnati Children’s Hospital

Moderator

Erin Shaughnessy, MD – Phoenix Children’s Hospital

Session summary

This session was devoted to a discussion about how pediatric hospital medicine (PHM) as a field can address racism in medicine. The structural inequity rooted in poverty, housing problems, and differential education represents the essential social determinant of health. No longer can pediatric hospitalists neglect or be in denial of the crucial role that race plays in propagating further inequalities in our society and at our workplace. Historically Black people were exploited in research and still are disproportionately affected when it comes to infant prematurity and mortality, asthma, pain treatments, and so on. The pediatric hospitalist must explore and understand the reasons behind nonadherence and noncompliance among Black patients and always seek to understand before criticizing.

Within learning environments, we must improve how to “autocorrect” and proactively work on our own biases. Dr. Bryant pointed out that each institution has the responsibility to build on the civil rights movement and seize the moment to create a robust response to the inequities manifested during the COVID-19 epidemic, as well as the events following the deaths of George Floyd, Breonna Taylor, Ahmoud Arbery, and many others. Dr. Shah called on the PHM community to take on that obligation by “stepping into the tension,” as Mark Shapiro, MD, has suggested in a conversation/podcast with Dr. Unaka.

As pediatric hospitalists, we will have to show up both individually and as constituents of institutions to address racism by specific projects looking at all data relevant for racism rather than race in quality and safety – thereby amplifying the voices of our Black patients and families, remarked Dr. Unaka. There was a brief reflection on the use of the word “allies” by Dr. Manning and Dr. Reynolds to remind the more than 200 session participants that a bidirectional framework of this process is crucial and that there is a clear need for a partnership to a common goal that should start by “a laydown of privilege of those who have it” to establish equal playing fields once and for all.

Dr. Bryant encouraged a deliberate and early thoughtful process to identify those with opportunities and help young Black people explore journeys in medicine and increase diversity among PHM faculty. Dr. Manning reminded the audience of the power that relationships have and hold in our lives, and not only those of mentors and mentees, but also relationships among all of us as humans. As with those simple situations in which we mess up and have to be able to admit it, apologize for it, and learn to move on, this requires also showing up as a mentee, articulating one’s needs, and learning to break the habits rooted in biases. Dr. Unaka warned against stereotypes and reminded us to look deeper and understand better all of our learners and their blind spots, as well as our own.
 

Key takeaways

• The field of PHM must recognize the role that race plays in propagating inequalities.
• Learning and mentorship environments have to be assessed for the safety of all learners and adjusted to correct (and autocorrect) as many biases as possible.
• Institutions must assume responsibilities to establish a conscious, robust response to injustice and racism in a timely and specific manner.
• Further research efforts must be made to address racism, rather than race.
• The PHM community must show up to create a new, healthy, and deliberate bidirectional framework to endorse and support diversity.

Dr. Giordano is assistant professor of pediatrics at Columbia University and a pediatric hospitalist at NewYork–Presbyterian Morgan Stanley Children’s Hospital, both in New York, with an interest in surgical comanagement. She serves on the Society of Hospital Medicine’s Pediatric Special Interest Group Executive Committee and is the chair of the Education Subcommittee. She is also an advisory board member for the New York/Westchester SHM Chapter.

Presenters

Michael Bryant, MD – Children’s Hospital of Los Angeles

Kimberly Manning, MD – Emory University, Atlanta

Kimberly Reynolds, MD – University of Miami

Samir Shah, MD, MSCE, MHM – Cincinnati Children’s Hospital

Ndidi Unaka, MD, MEd – Cincinnati Children’s Hospital

Moderator

Erin Shaughnessy, MD – Phoenix Children’s Hospital

Session summary

This session was devoted to a discussion about how pediatric hospital medicine (PHM) as a field can address racism in medicine. The structural inequity rooted in poverty, housing problems, and differential education represents the essential social determinant of health. No longer can pediatric hospitalists neglect or be in denial of the crucial role that race plays in propagating further inequalities in our society and at our workplace. Historically Black people were exploited in research and still are disproportionately affected when it comes to infant prematurity and mortality, asthma, pain treatments, and so on. The pediatric hospitalist must explore and understand the reasons behind nonadherence and noncompliance among Black patients and always seek to understand before criticizing.

Within learning environments, we must improve how to “autocorrect” and proactively work on our own biases. Dr. Bryant pointed out that each institution has the responsibility to build on the civil rights movement and seize the moment to create a robust response to the inequities manifested during the COVID-19 epidemic, as well as the events following the deaths of George Floyd, Breonna Taylor, Ahmoud Arbery, and many others. Dr. Shah called on the PHM community to take on that obligation by “stepping into the tension,” as Mark Shapiro, MD, has suggested in a conversation/podcast with Dr. Unaka.

As pediatric hospitalists, we will have to show up both individually and as constituents of institutions to address racism by specific projects looking at all data relevant for racism rather than race in quality and safety – thereby amplifying the voices of our Black patients and families, remarked Dr. Unaka. There was a brief reflection on the use of the word “allies” by Dr. Manning and Dr. Reynolds to remind the more than 200 session participants that a bidirectional framework of this process is crucial and that there is a clear need for a partnership to a common goal that should start by “a laydown of privilege of those who have it” to establish equal playing fields once and for all.

Dr. Bryant encouraged a deliberate and early thoughtful process to identify those with opportunities and help young Black people explore journeys in medicine and increase diversity among PHM faculty. Dr. Manning reminded the audience of the power that relationships have and hold in our lives, and not only those of mentors and mentees, but also relationships among all of us as humans. As with those simple situations in which we mess up and have to be able to admit it, apologize for it, and learn to move on, this requires also showing up as a mentee, articulating one’s needs, and learning to break the habits rooted in biases. Dr. Unaka warned against stereotypes and reminded us to look deeper and understand better all of our learners and their blind spots, as well as our own.
 

Key takeaways

• The field of PHM must recognize the role that race plays in propagating inequalities.
• Learning and mentorship environments have to be assessed for the safety of all learners and adjusted to correct (and autocorrect) as many biases as possible.
• Institutions must assume responsibilities to establish a conscious, robust response to injustice and racism in a timely and specific manner.
• Further research efforts must be made to address racism, rather than race.
• The PHM community must show up to create a new, healthy, and deliberate bidirectional framework to endorse and support diversity.

Dr. Giordano is assistant professor of pediatrics at Columbia University and a pediatric hospitalist at NewYork–Presbyterian Morgan Stanley Children’s Hospital, both in New York, with an interest in surgical comanagement. She serves on the Society of Hospital Medicine’s Pediatric Special Interest Group Executive Committee and is the chair of the Education Subcommittee. She is also an advisory board member for the New York/Westchester SHM Chapter.

Children and adolescents with cancer report significantly more fatigue than their counterparts without cancer, and cancer-related fatigue (CRF) is “one of the most prevalent and distressing symptoms reported during childhood cancer therapy,” according to Austin L. Brown, PhD, and his colleagues.

Cerebrospinal fluid (CSF) profiles suggest three metabolites are significantly associated with CRF in children with acute lymphoblastic leukemia (ALL), according to a report published in the Journal of Pain and Symptom Management.

The researchers assessed the clinical and demographic characteristics of 171 pediatric ALL patients, who were divided into discovery (n = 86) and replication (n = 85) cohorts.

The entire population had a mean age at diagnosis of 8.48 years; was 56.1% male; and 85.4% had B-lineage ALL. A total of 63.7% received high- or very-high-risk treatment.

CSF samples were obtained and subjected to metabolomic analysis, according to Dr. Brown, an assistant professor at the Baylor College of Medicine, Houston, and colleagues.

The researchers analyzed postinduction CSF from the aforementioned 171 patients as well as diagnostic CSF from 48 patients in an additional replication cohort.
 

Significant metabolites

Analysis of postinduction CSF showed that three metabolites were significantly associated with fatigue in both the discovery and replication cohorts, comprising gamma-glutamylglutamine, dimethylglycine, and asparagine (P < .05).

In diagnostic CSF samples, the abundance of gamma-glutamylglutamine was significantly associated with fatigue (P =.0062).

The metabolites have been implicated in neurotransmitter transportation and glutathione recycling, suggesting glutamatergic pathways or oxidative stress may contribute to ALL-associated CRF, according to the researchers.

“Ultimately, this line of investigation may aid in the development of new prevention and treatment approaches informed by an improved understanding of the etiology and risk factors for cancer-related fatigue,” the researchers concluded.

The study was sponsored by the National Cancer Institute and several nonprofit organizations. The authors reported that they had no conflicts of interest.

mlesney@mdedge.com

SOURCE: Brown AL et al. J Pain Symptom Manage. 2020 Sep 1. doi: 10.1016/j.jpainsymman.2020.08.030.

Children and adolescents with cancer report significantly more fatigue than their counterparts without cancer, and cancer-related fatigue (CRF) is “one of the most prevalent and distressing symptoms reported during childhood cancer therapy,” according to Austin L. Brown, PhD, and his colleagues.

Cerebrospinal fluid (CSF) profiles suggest three metabolites are significantly associated with CRF in children with acute lymphoblastic leukemia (ALL), according to a report published in the Journal of Pain and Symptom Management.

The researchers assessed the clinical and demographic characteristics of 171 pediatric ALL patients, who were divided into discovery (n = 86) and replication (n = 85) cohorts.

The entire population had a mean age at diagnosis of 8.48 years; was 56.1% male; and 85.4% had B-lineage ALL. A total of 63.7% received high- or very-high-risk treatment.

CSF samples were obtained and subjected to metabolomic analysis, according to Dr. Brown, an assistant professor at the Baylor College of Medicine, Houston, and colleagues.

The researchers analyzed postinduction CSF from the aforementioned 171 patients as well as diagnostic CSF from 48 patients in an additional replication cohort.
 

Significant metabolites

Analysis of postinduction CSF showed that three metabolites were significantly associated with fatigue in both the discovery and replication cohorts, comprising gamma-glutamylglutamine, dimethylglycine, and asparagine (P < .05).

In diagnostic CSF samples, the abundance of gamma-glutamylglutamine was significantly associated with fatigue (P =.0062).

The metabolites have been implicated in neurotransmitter transportation and glutathione recycling, suggesting glutamatergic pathways or oxidative stress may contribute to ALL-associated CRF, according to the researchers.

“Ultimately, this line of investigation may aid in the development of new prevention and treatment approaches informed by an improved understanding of the etiology and risk factors for cancer-related fatigue,” the researchers concluded.

The study was sponsored by the National Cancer Institute and several nonprofit organizations. The authors reported that they had no conflicts of interest.

mlesney@mdedge.com

SOURCE: Brown AL et al. J Pain Symptom Manage. 2020 Sep 1. doi: 10.1016/j.jpainsymman.2020.08.030.

Children and adolescents with cancer report significantly more fatigue than their counterparts without cancer, and cancer-related fatigue (CRF) is “one of the most prevalent and distressing symptoms reported during childhood cancer therapy,” according to Austin L. Brown, PhD, and his colleagues.

Cerebrospinal fluid (CSF) profiles suggest three metabolites are significantly associated with CRF in children with acute lymphoblastic leukemia (ALL), according to a report published in the Journal of Pain and Symptom Management.

The researchers assessed the clinical and demographic characteristics of 171 pediatric ALL patients, who were divided into discovery (n = 86) and replication (n = 85) cohorts.

The entire population had a mean age at diagnosis of 8.48 years; was 56.1% male; and 85.4% had B-lineage ALL. A total of 63.7% received high- or very-high-risk treatment.

CSF samples were obtained and subjected to metabolomic analysis, according to Dr. Brown, an assistant professor at the Baylor College of Medicine, Houston, and colleagues.

The researchers analyzed postinduction CSF from the aforementioned 171 patients as well as diagnostic CSF from 48 patients in an additional replication cohort.
 

Significant metabolites

Analysis of postinduction CSF showed that three metabolites were significantly associated with fatigue in both the discovery and replication cohorts, comprising gamma-glutamylglutamine, dimethylglycine, and asparagine (P < .05).

In diagnostic CSF samples, the abundance of gamma-glutamylglutamine was significantly associated with fatigue (P =.0062).

The metabolites have been implicated in neurotransmitter transportation and glutathione recycling, suggesting glutamatergic pathways or oxidative stress may contribute to ALL-associated CRF, according to the researchers.

“Ultimately, this line of investigation may aid in the development of new prevention and treatment approaches informed by an improved understanding of the etiology and risk factors for cancer-related fatigue,” the researchers concluded.

The study was sponsored by the National Cancer Institute and several nonprofit organizations. The authors reported that they had no conflicts of interest.

mlesney@mdedge.com

SOURCE: Brown AL et al. J Pain Symptom Manage. 2020 Sep 1. doi: 10.1016/j.jpainsymman.2020.08.030.

Food allergy is a complex condition that has become a growing concern for parents and an increasing public health problem in the United States. Food allergy affects social interactions, school attendance, and quality of life, especially when associated with comorbid atopic conditions such as asthma, atopic dermatitis, and allergic rhinitis.^1,2 It is the major cause of anaphylaxis in children, accounting for as many as 81% of cases.³ Societal costs of food allergy are great and are spread broadly across the health care system and the family. (See “What is the cost of food allergy?”².)

What a food allergy is—and isn’t

The National Institute of Allergy and Infectious Diseases ­(NIAID) defines food allergy as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food.”⁴ An adverse reaction to food or a food component that lacks an identified immunologic pathophysiology is not considered food allergy but is classified as food intolerance.⁴

The CDC estimates that 4% to 6% of children in the United States have a food allergy. Almost 40% of food-allergic children have a history of severe food-induced reactions.

Food allergy is caused by either immunoglobulin E (IgE)-mediated or non-IgE-mediated immunologic dysfunction. IgE antibodies can trigger an intense inflammatory response to certain allergens. Non-IgE-mediated food allergies are less common and not well understood.

© Joe Gorman

This article focuses only on the diagnosis and management of IgE-mediated food allergy.

The culprits

More than 170 foods have been reported to cause an IgE-­mediated reaction. Table 1^5-8 lists the 8 foods that most commonly cause allergic reactions in the United States and that account for > 50% of allergies to food.⁹ Studies vary in their methodology for estimating the prevalence of allergy to individual foods, but cow’s milk and peanuts appear to be the most common, each affecting as many as 2% to 2.5% of children.^7,8 In general, allergies to cow’s milk and to eggs are more prevalent in very young and preschool children, whereas allergies to peanuts, tree nuts, fish, and shellfish are more prevalent in older children.¹⁰ Labels on all packaged foods regulated by the US Food and Drug Administration must declare if the product contains even a trace of these 8 allergens.

How common is food allergy?

The Centers for Disease Control and Prevention (CDC) estimates that 4% to 6% of children in the United States have a food allergy.^11,12 Almost 40% of food-allergic children have a history of severe food-induced reactions.¹³ Other developed countries cite similar estimates of overall prevalence.^14,15

However, many estimates of the prevalence of food allergy are derived from self-reports, without objective data.⁹ Accurate evaluation of the prevalence of food allergy is challenging because of many factors, including differences in study methodology and the definition of allergy, geographic variation, racial and ethnic variations, and dietary exposure. Parents and children often confuse nonallergic food reactions, such as food intolerance, with food allergy. Precise determination of the prevalence and natural history of food allergy at the population level requires confirmatory oral food challenges of a representative sample of infants and young children with presumed food allergy.¹⁶

Continue to: The CDC concludes that the prevalence...

The CDC concludes that the prevalence of food allergy in children younger than 18 years increased by 18% from 1997 through 2007.^17,18 The cause of this increase is unclear but likely multifactorial; hypotheses include an increase in associated atopic conditions, delayed introduction of allergenic foods, and living in an overly sterile environment with reduced exposure to microbes.¹⁹ A recent population-based study of food allergy among children in Olmsted County, Minnesota, found that the incidence of food allergy increased between 2002 and 2007, stabilized subsequently, and appears to be declining among children 1 to 4 years of age, following a peak in 2006-2007.¹⁹

What are the risk factors?

Proposed risk factors for food allergy include demographics, genetics, a history of atopic disease, and environmental factors. Food allergy might be more common in boys than in girls, and in African Americans and Asians than in Whites.^12,16 A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.²⁰ Infants and children with eczema or asthma are more likely to develop food allergy; the severity of eczema correlates with risk.^12,20 Improvements in hygiene in Western societies have decreased the spread of infection, but this has been accompanied by a rise in atopic disease. In countries where health standards are poor and exposure to pathogens is greater, the prevalence of allergy is low.²¹

A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.

Conversely, increased microbial exposure might help protect against atopy via a pathway in which T-helper cells prevent pro-allergic immune development and keep harmless environmental exposures from becoming allergens.²² Attendance at daycare and exposure to farm animals early in life reduces the likelihood of atopic disease.^16,21 The presence of a dog in the home lessens the probability of egg allergy in infants.²³ Food allergy is less common in younger siblings than in first-born children, possibly due to ­younger siblings’ increased exposure to infection and alterations in the gut microbiome.^23,24

Diagnosis: Established by presentation, positive testing

Onset of symptoms after exposure to a suspected food allergen almost always occurs within 2 hours and, typically, resolves within several hours. Symptoms should occur consistently after ingestion of the food allergen. Subsequent exposures can trigger more severe symptoms, depending on the amount, route, and duration of exposure to the allergen.²⁵ Reactions typically follow ingestion or cutaneous exposures; inhalation rarely triggers a response.²⁶ IgE-mediated release of histamine and other mediators from mast cells and basophils triggers reactions that typically involve one or more organ systems (Table 2).²⁵

Cutaneous symptoms are the most common manifestations of food allergy, occurring in 70% to 80% of childhood reactions. Gastrointestinal and oral or respiratory symptoms occur in, respectively, 40% to 50% and 25% of allergic reactions to food. Cardiovascular symptoms develop in fewer than 10% of allergic reactions.²⁶

Continue to: Anaphylaxis

Anaphylaxis is a serious allergic reaction that develops rapidly and can cause death; diagnosis is based on specific criteria (Table 3).²⁷ Data for rates of anaphylaxis due to food allergy are limited. The incidence of fatal reaction due to food allergy is estimated to be 1 in every 800,000 children annually.³

Clinical suspicion. Food allergy should be suspected in infants and children who present with anaphylaxis or other symptoms (Table 2²⁵) that occur within minutes to hours of ingesting food.⁴ Parental and self-reports alone are insufficient to diagnose food allergy. NIAID guidelines recommend that patient reports of food allergy be confirmed, because multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.⁴ Health care providers must obtain a detailed medical history and pertinent family history, plus perform a physical exam and allergy sensitivity testing. Methods to help diagnose food allergies include skin-prick tests, allergen-specific serum IgE tests, and oral food challenges.⁴

General principles and utility of testing

Before ordering tests, it’s important to distinguish between food sensitization and food allergy and to inform the families of children with suspected food allergy about the limitations of skin-prick tests and serum IgE tests. A child with IgE antibodies specific to a food or with a positive skin-prick test, but without symptoms upon ingestion of the food, is merely sensitized; food allergy indicates the appearance of symptoms following exposure to a specific food, in addition to the detection of specific IgE antibodies or a positive skin-prick test to that same food.²⁸

Skin-prick testing. Skin-prick tests can be performed at any age. The procedure involves pricking or scratching the surface of the skin, usually the volar aspect of the forearm or the back, with a commercial extract. Testing should be performed by a physician or other provider who is properly trained in the technique and in interpreting results. The extract contains specific allergenic proteins that activate mast cells, resulting in a characteristic wheal-and-flare response that is typically measured 15 to 20 minutes after application. Some medications, such as H₁- and H₂-receptor blockers and tricyclic antidepressants, can interfere with results and need to be held for 3 to 5 days before testing.

A positive skin-prick test result is defined as a wheal ≥ 3 mm larger in diameter than the negative control. The larger the size of the wheal, the higher the likelihood of a reaction to the tested food.²⁹ Patients who exhibit dermatographism might experience a wheal-and-flare response from the action of the skin-prick test, rather than from food-specific IgE antibodies. A negative skin-prick test has > 90% negative predictive value, so the test can rule out suspected food allergy.³⁰ However, the skin-prick test alone cannot be used to diagnose food allergy because it has a high false-positive rate.

Continue to: Allergen-specific serum IgE testing

Allergen-specific serum IgE ­testing. Measurement of food-specific serum IgE levels is routinely available and requires only a blood specimen. The test can be used in patients with skin disease, and results are not affected by concurrent medications. The presence of food-specific IgE indicates that the patient is sensitized to that allergen and might react upon exposure; children with a higher level of antibody are more likely to react.²⁹

Food-specific serum IgE tests are sensitive but nonspecific for food allergy.³¹ Broad food-allergy test panels often yield false-positive results that can lead to unnecessary dietary elimination, resulting in years of inconvenience, nutrition problems, and needless health care expense.³²

It is appropriate to order tests of specific serum IgE to foods ingested within the 2 to 3–hour window before onset of symptoms to avoid broad food allergy test panels. Like skin-prick testing, positive allergen-specific serum IgE tests alone cannot diagnose food allergy.

Oral food challenge. The double-blind, placebo-controlled oral food challenge is the gold standard for the diagnosis of food allergy. Because this test is time-consuming and technically difficult, single-blind or open food challenges are more common. Oral food challenges should be performed only by a physician or other provider who can identify and treat anaphylaxis.

The presence of a dog in the home lessens the probability of egg allergy in infants.

The oral challenge starts with a very low dose of suspected food allergen, which is gradually increased every 15 to 30 minutes as vital signs are monitored carefully. Patients are observed for an allergic reaction for 1 hour after the final dose.

Continue to: A retrospective study...

A retrospective study showed that, whereas 19% of patients reacted during an open food challenge, only 2% required epinephrine.³³ Another study showed that 89% of children whose serum IgE testing was positive for specific foods were able to reintroduce those foods into the diet after a reassuring oral food challenge.³⁴

Other diagnostic tests. The basophil activation assay, measurement of total serum IgE, atopy patch tests, and intradermal tests have been used, but are not recommended, for making the diagnosis of food allergy.⁴

How can food allergy be managed?

Medical options are few. No approved treatment exists for food allergy. However, it’s important to appropriately manage acute reactions and reduce the risk of subsequent reactions.¹ Parents or other caregivers can give an H₁ antihistamine, such as diphenhydramine, to infants and children with acute non-life-threatening symptoms. More severe symptoms require rapid administration of epinephrine.¹ Auto-injectable epinephrine should be prescribed for parents and caregivers to use as needed for emergency treatment of anaphylaxis.

Team approach. A multidisciplinary approach to managing food allergy—involving physicians, school nurses, dietitians, and teachers, and using educational materials—is ideal. This strategy expands knowledge about food allergies, enhances correct administration of epinephrine, and reduces allergic reactions.¹

Avoidance of food allergens can be challenging. Parents and caregivers should be taught to interpret the list of ingredients on food packages. Self-recognition of allergic reactions reduces the likelihood of a subsequent severe allergic reaction.³⁵

Continue to: Importance of individualized care

Importance of individualized care. Health care providers should develop personalized management plans for their patients.¹ (A good place to start is with the “Food Allergy & Anaphylaxis Emergency Care Plan”^a developed by Food Allergy Research & Education [FARE]). Keep in mind that children with multiple food allergies consume less calcium and protein, and tend to be shorter⁴; therefore, it’s wise to closely monitor growth in these children and consider referral to a dietitian who is familiar with food allergy.

Potential of immunotherapy. Current research focuses on immunotherapy to induce tolerance to food allergens and protect against life-threatening allergic reactions. The goal of immunotherapy is to lessen adverse reactions to allergenic food proteins; the strategy is to have patients repeatedly ingest small but gradually increasing doses of the food allergen over many months.³⁶ Although immunotherapy has successfully allowed some patients to consume larger quantities of a food without having an allergic reaction, it is unknown whether immunotherapy provides permanent resolution of food allergy. In addition, immunotherapy often causes serious systemic and local reactions.^1,36,37

Is prevention possible?

Maternal diet during pregnancy and lactation does not affect development of food allergy in infants.^38,39 Breastfeeding might prevent development of atopic disease, but evidence is insufficient to determine whether breastfeeding reduces the likelihood of food allergy.³⁹ In nonbreastfed infants at high risk of food allergy, extensively or partially hydrolyzed formula might help protect against food allergy, compared to standard cow’s milk formula.^9,39 Feeding with soy formula rather than cow’s milk formula does not help prevent food allergy.^39,40 Pregnant and breastfeeding women should not restrict their diet as a means of preventing food allergy.³⁹

Diet in infancy. Over the years, physicians have debated the proper timing of the introduction of solid foods into the diet of infants. Traditional teaching advocated delaying introduction of potentially allergenic foods to reduce the risk of food allergy; however, this guideline was based on inconsistent evidence,⁴¹ and the strategy did not reduce the incidence of food allergy. The prevalence of food allergy is lower in developing countries where caregivers introduce foods to infants at an earlier age.²⁰

Multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.

A recent large clinical trial indicates that early introduction of peanut-containing foods can help prevent peanut allergy. The study randomized 4- to 11-month-old infants with severe eczema, egg allergy, or both, to eat or avoid peanut products until 5 years of age. Infants assigned to eat peanuts were 81% less likely to develop peanut allergy than infants in the avoidance group. Absolute risk reduction was 14% (number need to treat = 7).⁴² Another study showed a nonsignificant (20%) lower relative risk of food allergy in breastfed infants who were fed potentially allergenic foods starting at 3 months of age, compared to being exclusively breastfed.⁴³

Continue to: Based on these data...

Based on these data,^42,43 NIAID instituted recommendations in 2017 aimed at preventing peanut allergy⁴⁴:

• In healthy infants without known food allergy and those with mild or moderate eczema, caregivers can introduce peanut-containing foods at home with other solid foods.Parents who are anxious about a possible allergic reaction can introduce peanut products in a physician’s office.
• Infants at high risk of peanut allergy (those with severe eczema or egg allergy, or both) should undergo peanut-specific IgE or skin-prick testing:
  • Negative test: indicates low risk of a reaction to peanuts; the infant should start consuming peanut-containing foods at 4 to 6 months of age, at home or in a physician’s office, depending on the parents’ preference
  • Positive test: Referral to an allergist is recommended.

Do children outgrow food allergy?

Approximately 85% of children who have an allergy to milk, egg, soy, or wheat outgrow their allergy; however, only 15% to 20% who have an allergy to peanuts, tree nuts, fish, or shellfish eventually tolerate these foods. The time to resolution of food allergy varies with the food, and might not occur until adolescence.⁴ No test reliably predicts which children develop tolerance to any given food. A decrease in the food-specific serum IgE level or a decrease in the size of the wheal on skin-prick testing might portend the onset of tolerance to the food.⁴

CORRESPONDENCE
Catherine M. Bettcher, MD, FAAFP, Briarwood Family Medicine, 1801 Briarwood Circle, Building #10, Ann Arbor, MI 48108; cbettche@umich.edu.

Food allergy is a complex condition that has become a growing concern for parents and an increasing public health problem in the United States. Food allergy affects social interactions, school attendance, and quality of life, especially when associated with comorbid atopic conditions such as asthma, atopic dermatitis, and allergic rhinitis.^1,2 It is the major cause of anaphylaxis in children, accounting for as many as 81% of cases.³ Societal costs of food allergy are great and are spread broadly across the health care system and the family. (See “What is the cost of food allergy?”².)

What a food allergy is—and isn’t

The National Institute of Allergy and Infectious Diseases ­(NIAID) defines food allergy as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food.”⁴ An adverse reaction to food or a food component that lacks an identified immunologic pathophysiology is not considered food allergy but is classified as food intolerance.⁴

The CDC estimates that 4% to 6% of children in the United States have a food allergy. Almost 40% of food-allergic children have a history of severe food-induced reactions.

Food allergy is caused by either immunoglobulin E (IgE)-mediated or non-IgE-mediated immunologic dysfunction. IgE antibodies can trigger an intense inflammatory response to certain allergens. Non-IgE-mediated food allergies are less common and not well understood.

© Joe Gorman

This article focuses only on the diagnosis and management of IgE-mediated food allergy.

The culprits

More than 170 foods have been reported to cause an IgE-­mediated reaction. Table 1^5-8 lists the 8 foods that most commonly cause allergic reactions in the United States and that account for > 50% of allergies to food.⁹ Studies vary in their methodology for estimating the prevalence of allergy to individual foods, but cow’s milk and peanuts appear to be the most common, each affecting as many as 2% to 2.5% of children.^7,8 In general, allergies to cow’s milk and to eggs are more prevalent in very young and preschool children, whereas allergies to peanuts, tree nuts, fish, and shellfish are more prevalent in older children.¹⁰ Labels on all packaged foods regulated by the US Food and Drug Administration must declare if the product contains even a trace of these 8 allergens.

How common is food allergy?

The Centers for Disease Control and Prevention (CDC) estimates that 4% to 6% of children in the United States have a food allergy.^11,12 Almost 40% of food-allergic children have a history of severe food-induced reactions.¹³ Other developed countries cite similar estimates of overall prevalence.^14,15

However, many estimates of the prevalence of food allergy are derived from self-reports, without objective data.⁹ Accurate evaluation of the prevalence of food allergy is challenging because of many factors, including differences in study methodology and the definition of allergy, geographic variation, racial and ethnic variations, and dietary exposure. Parents and children often confuse nonallergic food reactions, such as food intolerance, with food allergy. Precise determination of the prevalence and natural history of food allergy at the population level requires confirmatory oral food challenges of a representative sample of infants and young children with presumed food allergy.¹⁶

Continue to: The CDC concludes that the prevalence...

The CDC concludes that the prevalence of food allergy in children younger than 18 years increased by 18% from 1997 through 2007.^17,18 The cause of this increase is unclear but likely multifactorial; hypotheses include an increase in associated atopic conditions, delayed introduction of allergenic foods, and living in an overly sterile environment with reduced exposure to microbes.¹⁹ A recent population-based study of food allergy among children in Olmsted County, Minnesota, found that the incidence of food allergy increased between 2002 and 2007, stabilized subsequently, and appears to be declining among children 1 to 4 years of age, following a peak in 2006-2007.¹⁹

What are the risk factors?

Proposed risk factors for food allergy include demographics, genetics, a history of atopic disease, and environmental factors. Food allergy might be more common in boys than in girls, and in African Americans and Asians than in Whites.^12,16 A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.²⁰ Infants and children with eczema or asthma are more likely to develop food allergy; the severity of eczema correlates with risk.^12,20 Improvements in hygiene in Western societies have decreased the spread of infection, but this has been accompanied by a rise in atopic disease. In countries where health standards are poor and exposure to pathogens is greater, the prevalence of allergy is low.²¹

A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.

Conversely, increased microbial exposure might help protect against atopy via a pathway in which T-helper cells prevent pro-allergic immune development and keep harmless environmental exposures from becoming allergens.²² Attendance at daycare and exposure to farm animals early in life reduces the likelihood of atopic disease.^16,21 The presence of a dog in the home lessens the probability of egg allergy in infants.²³ Food allergy is less common in younger siblings than in first-born children, possibly due to ­younger siblings’ increased exposure to infection and alterations in the gut microbiome.^23,24

Diagnosis: Established by presentation, positive testing

Onset of symptoms after exposure to a suspected food allergen almost always occurs within 2 hours and, typically, resolves within several hours. Symptoms should occur consistently after ingestion of the food allergen. Subsequent exposures can trigger more severe symptoms, depending on the amount, route, and duration of exposure to the allergen.²⁵ Reactions typically follow ingestion or cutaneous exposures; inhalation rarely triggers a response.²⁶ IgE-mediated release of histamine and other mediators from mast cells and basophils triggers reactions that typically involve one or more organ systems (Table 2).²⁵

Cutaneous symptoms are the most common manifestations of food allergy, occurring in 70% to 80% of childhood reactions. Gastrointestinal and oral or respiratory symptoms occur in, respectively, 40% to 50% and 25% of allergic reactions to food. Cardiovascular symptoms develop in fewer than 10% of allergic reactions.²⁶

Continue to: Anaphylaxis

Anaphylaxis is a serious allergic reaction that develops rapidly and can cause death; diagnosis is based on specific criteria (Table 3).²⁷ Data for rates of anaphylaxis due to food allergy are limited. The incidence of fatal reaction due to food allergy is estimated to be 1 in every 800,000 children annually.³

Clinical suspicion. Food allergy should be suspected in infants and children who present with anaphylaxis or other symptoms (Table 2²⁵) that occur within minutes to hours of ingesting food.⁴ Parental and self-reports alone are insufficient to diagnose food allergy. NIAID guidelines recommend that patient reports of food allergy be confirmed, because multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.⁴ Health care providers must obtain a detailed medical history and pertinent family history, plus perform a physical exam and allergy sensitivity testing. Methods to help diagnose food allergies include skin-prick tests, allergen-specific serum IgE tests, and oral food challenges.⁴

General principles and utility of testing

Before ordering tests, it’s important to distinguish between food sensitization and food allergy and to inform the families of children with suspected food allergy about the limitations of skin-prick tests and serum IgE tests. A child with IgE antibodies specific to a food or with a positive skin-prick test, but without symptoms upon ingestion of the food, is merely sensitized; food allergy indicates the appearance of symptoms following exposure to a specific food, in addition to the detection of specific IgE antibodies or a positive skin-prick test to that same food.²⁸

Skin-prick testing. Skin-prick tests can be performed at any age. The procedure involves pricking or scratching the surface of the skin, usually the volar aspect of the forearm or the back, with a commercial extract. Testing should be performed by a physician or other provider who is properly trained in the technique and in interpreting results. The extract contains specific allergenic proteins that activate mast cells, resulting in a characteristic wheal-and-flare response that is typically measured 15 to 20 minutes after application. Some medications, such as H₁- and H₂-receptor blockers and tricyclic antidepressants, can interfere with results and need to be held for 3 to 5 days before testing.

A positive skin-prick test result is defined as a wheal ≥ 3 mm larger in diameter than the negative control. The larger the size of the wheal, the higher the likelihood of a reaction to the tested food.²⁹ Patients who exhibit dermatographism might experience a wheal-and-flare response from the action of the skin-prick test, rather than from food-specific IgE antibodies. A negative skin-prick test has > 90% negative predictive value, so the test can rule out suspected food allergy.³⁰ However, the skin-prick test alone cannot be used to diagnose food allergy because it has a high false-positive rate.

Continue to: Allergen-specific serum IgE testing

Allergen-specific serum IgE ­testing. Measurement of food-specific serum IgE levels is routinely available and requires only a blood specimen. The test can be used in patients with skin disease, and results are not affected by concurrent medications. The presence of food-specific IgE indicates that the patient is sensitized to that allergen and might react upon exposure; children with a higher level of antibody are more likely to react.²⁹

Food-specific serum IgE tests are sensitive but nonspecific for food allergy.³¹ Broad food-allergy test panels often yield false-positive results that can lead to unnecessary dietary elimination, resulting in years of inconvenience, nutrition problems, and needless health care expense.³²

It is appropriate to order tests of specific serum IgE to foods ingested within the 2 to 3–hour window before onset of symptoms to avoid broad food allergy test panels. Like skin-prick testing, positive allergen-specific serum IgE tests alone cannot diagnose food allergy.

Oral food challenge. The double-blind, placebo-controlled oral food challenge is the gold standard for the diagnosis of food allergy. Because this test is time-consuming and technically difficult, single-blind or open food challenges are more common. Oral food challenges should be performed only by a physician or other provider who can identify and treat anaphylaxis.

The presence of a dog in the home lessens the probability of egg allergy in infants.

The oral challenge starts with a very low dose of suspected food allergen, which is gradually increased every 15 to 30 minutes as vital signs are monitored carefully. Patients are observed for an allergic reaction for 1 hour after the final dose.

Continue to: A retrospective study...

A retrospective study showed that, whereas 19% of patients reacted during an open food challenge, only 2% required epinephrine.³³ Another study showed that 89% of children whose serum IgE testing was positive for specific foods were able to reintroduce those foods into the diet after a reassuring oral food challenge.³⁴

Other diagnostic tests. The basophil activation assay, measurement of total serum IgE, atopy patch tests, and intradermal tests have been used, but are not recommended, for making the diagnosis of food allergy.⁴

How can food allergy be managed?

Medical options are few. No approved treatment exists for food allergy. However, it’s important to appropriately manage acute reactions and reduce the risk of subsequent reactions.¹ Parents or other caregivers can give an H₁ antihistamine, such as diphenhydramine, to infants and children with acute non-life-threatening symptoms. More severe symptoms require rapid administration of epinephrine.¹ Auto-injectable epinephrine should be prescribed for parents and caregivers to use as needed for emergency treatment of anaphylaxis.

Team approach. A multidisciplinary approach to managing food allergy—involving physicians, school nurses, dietitians, and teachers, and using educational materials—is ideal. This strategy expands knowledge about food allergies, enhances correct administration of epinephrine, and reduces allergic reactions.¹

Avoidance of food allergens can be challenging. Parents and caregivers should be taught to interpret the list of ingredients on food packages. Self-recognition of allergic reactions reduces the likelihood of a subsequent severe allergic reaction.³⁵

Continue to: Importance of individualized care

Importance of individualized care. Health care providers should develop personalized management plans for their patients.¹ (A good place to start is with the “Food Allergy & Anaphylaxis Emergency Care Plan”^a developed by Food Allergy Research & Education [FARE]). Keep in mind that children with multiple food allergies consume less calcium and protein, and tend to be shorter⁴; therefore, it’s wise to closely monitor growth in these children and consider referral to a dietitian who is familiar with food allergy.

Potential of immunotherapy. Current research focuses on immunotherapy to induce tolerance to food allergens and protect against life-threatening allergic reactions. The goal of immunotherapy is to lessen adverse reactions to allergenic food proteins; the strategy is to have patients repeatedly ingest small but gradually increasing doses of the food allergen over many months.³⁶ Although immunotherapy has successfully allowed some patients to consume larger quantities of a food without having an allergic reaction, it is unknown whether immunotherapy provides permanent resolution of food allergy. In addition, immunotherapy often causes serious systemic and local reactions.^1,36,37

Is prevention possible?

Maternal diet during pregnancy and lactation does not affect development of food allergy in infants.^38,39 Breastfeeding might prevent development of atopic disease, but evidence is insufficient to determine whether breastfeeding reduces the likelihood of food allergy.³⁹ In nonbreastfed infants at high risk of food allergy, extensively or partially hydrolyzed formula might help protect against food allergy, compared to standard cow’s milk formula.^9,39 Feeding with soy formula rather than cow’s milk formula does not help prevent food allergy.^39,40 Pregnant and breastfeeding women should not restrict their diet as a means of preventing food allergy.³⁹

Diet in infancy. Over the years, physicians have debated the proper timing of the introduction of solid foods into the diet of infants. Traditional teaching advocated delaying introduction of potentially allergenic foods to reduce the risk of food allergy; however, this guideline was based on inconsistent evidence,⁴¹ and the strategy did not reduce the incidence of food allergy. The prevalence of food allergy is lower in developing countries where caregivers introduce foods to infants at an earlier age.²⁰

Multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.

A recent large clinical trial indicates that early introduction of peanut-containing foods can help prevent peanut allergy. The study randomized 4- to 11-month-old infants with severe eczema, egg allergy, or both, to eat or avoid peanut products until 5 years of age. Infants assigned to eat peanuts were 81% less likely to develop peanut allergy than infants in the avoidance group. Absolute risk reduction was 14% (number need to treat = 7).⁴² Another study showed a nonsignificant (20%) lower relative risk of food allergy in breastfed infants who were fed potentially allergenic foods starting at 3 months of age, compared to being exclusively breastfed.⁴³

Continue to: Based on these data...

Based on these data,^42,43 NIAID instituted recommendations in 2017 aimed at preventing peanut allergy⁴⁴:

• In healthy infants without known food allergy and those with mild or moderate eczema, caregivers can introduce peanut-containing foods at home with other solid foods.Parents who are anxious about a possible allergic reaction can introduce peanut products in a physician’s office.
• Infants at high risk of peanut allergy (those with severe eczema or egg allergy, or both) should undergo peanut-specific IgE or skin-prick testing:
  • Negative test: indicates low risk of a reaction to peanuts; the infant should start consuming peanut-containing foods at 4 to 6 months of age, at home or in a physician’s office, depending on the parents’ preference
  • Positive test: Referral to an allergist is recommended.

Do children outgrow food allergy?

Approximately 85% of children who have an allergy to milk, egg, soy, or wheat outgrow their allergy; however, only 15% to 20% who have an allergy to peanuts, tree nuts, fish, or shellfish eventually tolerate these foods. The time to resolution of food allergy varies with the food, and might not occur until adolescence.⁴ No test reliably predicts which children develop tolerance to any given food. A decrease in the food-specific serum IgE level or a decrease in the size of the wheal on skin-prick testing might portend the onset of tolerance to the food.⁴

CORRESPONDENCE
Catherine M. Bettcher, MD, FAAFP, Briarwood Family Medicine, 1801 Briarwood Circle, Building #10, Ann Arbor, MI 48108; cbettche@umich.edu.

Food allergy is a complex condition that has become a growing concern for parents and an increasing public health problem in the United States. Food allergy affects social interactions, school attendance, and quality of life, especially when associated with comorbid atopic conditions such as asthma, atopic dermatitis, and allergic rhinitis.^1,2 It is the major cause of anaphylaxis in children, accounting for as many as 81% of cases.³ Societal costs of food allergy are great and are spread broadly across the health care system and the family. (See “What is the cost of food allergy?”².)

What a food allergy is—and isn’t

The National Institute of Allergy and Infectious Diseases ­(NIAID) defines food allergy as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food.”⁴ An adverse reaction to food or a food component that lacks an identified immunologic pathophysiology is not considered food allergy but is classified as food intolerance.⁴

The CDC estimates that 4% to 6% of children in the United States have a food allergy. Almost 40% of food-allergic children have a history of severe food-induced reactions.

Food allergy is caused by either immunoglobulin E (IgE)-mediated or non-IgE-mediated immunologic dysfunction. IgE antibodies can trigger an intense inflammatory response to certain allergens. Non-IgE-mediated food allergies are less common and not well understood.

© Joe Gorman

This article focuses only on the diagnosis and management of IgE-mediated food allergy.

The culprits

More than 170 foods have been reported to cause an IgE-­mediated reaction. Table 1^5-8 lists the 8 foods that most commonly cause allergic reactions in the United States and that account for > 50% of allergies to food.⁹ Studies vary in their methodology for estimating the prevalence of allergy to individual foods, but cow’s milk and peanuts appear to be the most common, each affecting as many as 2% to 2.5% of children.^7,8 In general, allergies to cow’s milk and to eggs are more prevalent in very young and preschool children, whereas allergies to peanuts, tree nuts, fish, and shellfish are more prevalent in older children.¹⁰ Labels on all packaged foods regulated by the US Food and Drug Administration must declare if the product contains even a trace of these 8 allergens.

How common is food allergy?

The Centers for Disease Control and Prevention (CDC) estimates that 4% to 6% of children in the United States have a food allergy.^11,12 Almost 40% of food-allergic children have a history of severe food-induced reactions.¹³ Other developed countries cite similar estimates of overall prevalence.^14,15

However, many estimates of the prevalence of food allergy are derived from self-reports, without objective data.⁹ Accurate evaluation of the prevalence of food allergy is challenging because of many factors, including differences in study methodology and the definition of allergy, geographic variation, racial and ethnic variations, and dietary exposure. Parents and children often confuse nonallergic food reactions, such as food intolerance, with food allergy. Precise determination of the prevalence and natural history of food allergy at the population level requires confirmatory oral food challenges of a representative sample of infants and young children with presumed food allergy.¹⁶

Continue to: The CDC concludes that the prevalence...

The CDC concludes that the prevalence of food allergy in children younger than 18 years increased by 18% from 1997 through 2007.^17,18 The cause of this increase is unclear but likely multifactorial; hypotheses include an increase in associated atopic conditions, delayed introduction of allergenic foods, and living in an overly sterile environment with reduced exposure to microbes.¹⁹ A recent population-based study of food allergy among children in Olmsted County, Minnesota, found that the incidence of food allergy increased between 2002 and 2007, stabilized subsequently, and appears to be declining among children 1 to 4 years of age, following a peak in 2006-2007.¹⁹

What are the risk factors?

Proposed risk factors for food allergy include demographics, genetics, a history of atopic disease, and environmental factors. Food allergy might be more common in boys than in girls, and in African Americans and Asians than in Whites.^12,16 A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.²⁰ Infants and children with eczema or asthma are more likely to develop food allergy; the severity of eczema correlates with risk.^12,20 Improvements in hygiene in Western societies have decreased the spread of infection, but this has been accompanied by a rise in atopic disease. In countries where health standards are poor and exposure to pathogens is greater, the prevalence of allergy is low.²¹

A child is 7 times more likely to be allergic to peanuts if a parent or sibling has peanut allergy.

Conversely, increased microbial exposure might help protect against atopy via a pathway in which T-helper cells prevent pro-allergic immune development and keep harmless environmental exposures from becoming allergens.²² Attendance at daycare and exposure to farm animals early in life reduces the likelihood of atopic disease.^16,21 The presence of a dog in the home lessens the probability of egg allergy in infants.²³ Food allergy is less common in younger siblings than in first-born children, possibly due to ­younger siblings’ increased exposure to infection and alterations in the gut microbiome.^23,24

Diagnosis: Established by presentation, positive testing

Onset of symptoms after exposure to a suspected food allergen almost always occurs within 2 hours and, typically, resolves within several hours. Symptoms should occur consistently after ingestion of the food allergen. Subsequent exposures can trigger more severe symptoms, depending on the amount, route, and duration of exposure to the allergen.²⁵ Reactions typically follow ingestion or cutaneous exposures; inhalation rarely triggers a response.²⁶ IgE-mediated release of histamine and other mediators from mast cells and basophils triggers reactions that typically involve one or more organ systems (Table 2).²⁵

Cutaneous symptoms are the most common manifestations of food allergy, occurring in 70% to 80% of childhood reactions. Gastrointestinal and oral or respiratory symptoms occur in, respectively, 40% to 50% and 25% of allergic reactions to food. Cardiovascular symptoms develop in fewer than 10% of allergic reactions.²⁶

Continue to: Anaphylaxis

Anaphylaxis is a serious allergic reaction that develops rapidly and can cause death; diagnosis is based on specific criteria (Table 3).²⁷ Data for rates of anaphylaxis due to food allergy are limited. The incidence of fatal reaction due to food allergy is estimated to be 1 in every 800,000 children annually.³

Clinical suspicion. Food allergy should be suspected in infants and children who present with anaphylaxis or other symptoms (Table 2²⁵) that occur within minutes to hours of ingesting food.⁴ Parental and self-reports alone are insufficient to diagnose food allergy. NIAID guidelines recommend that patient reports of food allergy be confirmed, because multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.⁴ Health care providers must obtain a detailed medical history and pertinent family history, plus perform a physical exam and allergy sensitivity testing. Methods to help diagnose food allergies include skin-prick tests, allergen-specific serum IgE tests, and oral food challenges.⁴

General principles and utility of testing

Before ordering tests, it’s important to distinguish between food sensitization and food allergy and to inform the families of children with suspected food allergy about the limitations of skin-prick tests and serum IgE tests. A child with IgE antibodies specific to a food or with a positive skin-prick test, but without symptoms upon ingestion of the food, is merely sensitized; food allergy indicates the appearance of symptoms following exposure to a specific food, in addition to the detection of specific IgE antibodies or a positive skin-prick test to that same food.²⁸

Skin-prick testing. Skin-prick tests can be performed at any age. The procedure involves pricking or scratching the surface of the skin, usually the volar aspect of the forearm or the back, with a commercial extract. Testing should be performed by a physician or other provider who is properly trained in the technique and in interpreting results. The extract contains specific allergenic proteins that activate mast cells, resulting in a characteristic wheal-and-flare response that is typically measured 15 to 20 minutes after application. Some medications, such as H₁- and H₂-receptor blockers and tricyclic antidepressants, can interfere with results and need to be held for 3 to 5 days before testing.

A positive skin-prick test result is defined as a wheal ≥ 3 mm larger in diameter than the negative control. The larger the size of the wheal, the higher the likelihood of a reaction to the tested food.²⁹ Patients who exhibit dermatographism might experience a wheal-and-flare response from the action of the skin-prick test, rather than from food-specific IgE antibodies. A negative skin-prick test has > 90% negative predictive value, so the test can rule out suspected food allergy.³⁰ However, the skin-prick test alone cannot be used to diagnose food allergy because it has a high false-positive rate.

Continue to: Allergen-specific serum IgE testing

Allergen-specific serum IgE ­testing. Measurement of food-specific serum IgE levels is routinely available and requires only a blood specimen. The test can be used in patients with skin disease, and results are not affected by concurrent medications. The presence of food-specific IgE indicates that the patient is sensitized to that allergen and might react upon exposure; children with a higher level of antibody are more likely to react.²⁹

Food-specific serum IgE tests are sensitive but nonspecific for food allergy.³¹ Broad food-allergy test panels often yield false-positive results that can lead to unnecessary dietary elimination, resulting in years of inconvenience, nutrition problems, and needless health care expense.³²

It is appropriate to order tests of specific serum IgE to foods ingested within the 2 to 3–hour window before onset of symptoms to avoid broad food allergy test panels. Like skin-prick testing, positive allergen-specific serum IgE tests alone cannot diagnose food allergy.

Oral food challenge. The double-blind, placebo-controlled oral food challenge is the gold standard for the diagnosis of food allergy. Because this test is time-consuming and technically difficult, single-blind or open food challenges are more common. Oral food challenges should be performed only by a physician or other provider who can identify and treat anaphylaxis.

The presence of a dog in the home lessens the probability of egg allergy in infants.

The oral challenge starts with a very low dose of suspected food allergen, which is gradually increased every 15 to 30 minutes as vital signs are monitored carefully. Patients are observed for an allergic reaction for 1 hour after the final dose.

Continue to: A retrospective study...

A retrospective study showed that, whereas 19% of patients reacted during an open food challenge, only 2% required epinephrine.³³ Another study showed that 89% of children whose serum IgE testing was positive for specific foods were able to reintroduce those foods into the diet after a reassuring oral food challenge.³⁴

Other diagnostic tests. The basophil activation assay, measurement of total serum IgE, atopy patch tests, and intradermal tests have been used, but are not recommended, for making the diagnosis of food allergy.⁴

How can food allergy be managed?

Medical options are few. No approved treatment exists for food allergy. However, it’s important to appropriately manage acute reactions and reduce the risk of subsequent reactions.¹ Parents or other caregivers can give an H₁ antihistamine, such as diphenhydramine, to infants and children with acute non-life-threatening symptoms. More severe symptoms require rapid administration of epinephrine.¹ Auto-injectable epinephrine should be prescribed for parents and caregivers to use as needed for emergency treatment of anaphylaxis.

Team approach. A multidisciplinary approach to managing food allergy—involving physicians, school nurses, dietitians, and teachers, and using educational materials—is ideal. This strategy expands knowledge about food allergies, enhances correct administration of epinephrine, and reduces allergic reactions.¹

Avoidance of food allergens can be challenging. Parents and caregivers should be taught to interpret the list of ingredients on food packages. Self-recognition of allergic reactions reduces the likelihood of a subsequent severe allergic reaction.³⁵

Continue to: Importance of individualized care

Importance of individualized care. Health care providers should develop personalized management plans for their patients.¹ (A good place to start is with the “Food Allergy & Anaphylaxis Emergency Care Plan”^a developed by Food Allergy Research & Education [FARE]). Keep in mind that children with multiple food allergies consume less calcium and protein, and tend to be shorter⁴; therefore, it’s wise to closely monitor growth in these children and consider referral to a dietitian who is familiar with food allergy.

Potential of immunotherapy. Current research focuses on immunotherapy to induce tolerance to food allergens and protect against life-threatening allergic reactions. The goal of immunotherapy is to lessen adverse reactions to allergenic food proteins; the strategy is to have patients repeatedly ingest small but gradually increasing doses of the food allergen over many months.³⁶ Although immunotherapy has successfully allowed some patients to consume larger quantities of a food without having an allergic reaction, it is unknown whether immunotherapy provides permanent resolution of food allergy. In addition, immunotherapy often causes serious systemic and local reactions.^1,36,37

Is prevention possible?

Maternal diet during pregnancy and lactation does not affect development of food allergy in infants.^38,39 Breastfeeding might prevent development of atopic disease, but evidence is insufficient to determine whether breastfeeding reduces the likelihood of food allergy.³⁹ In nonbreastfed infants at high risk of food allergy, extensively or partially hydrolyzed formula might help protect against food allergy, compared to standard cow’s milk formula.^9,39 Feeding with soy formula rather than cow’s milk formula does not help prevent food allergy.^39,40 Pregnant and breastfeeding women should not restrict their diet as a means of preventing food allergy.³⁹

Diet in infancy. Over the years, physicians have debated the proper timing of the introduction of solid foods into the diet of infants. Traditional teaching advocated delaying introduction of potentially allergenic foods to reduce the risk of food allergy; however, this guideline was based on inconsistent evidence,⁴¹ and the strategy did not reduce the incidence of food allergy. The prevalence of food allergy is lower in developing countries where caregivers introduce foods to infants at an earlier age.²⁰

Multiple studies demonstrate that 50% to 90% of presumed food allergies are not true allergy.

A recent large clinical trial indicates that early introduction of peanut-containing foods can help prevent peanut allergy. The study randomized 4- to 11-month-old infants with severe eczema, egg allergy, or both, to eat or avoid peanut products until 5 years of age. Infants assigned to eat peanuts were 81% less likely to develop peanut allergy than infants in the avoidance group. Absolute risk reduction was 14% (number need to treat = 7).⁴² Another study showed a nonsignificant (20%) lower relative risk of food allergy in breastfed infants who were fed potentially allergenic foods starting at 3 months of age, compared to being exclusively breastfed.⁴³

Continue to: Based on these data...

Based on these data,^42,43 NIAID instituted recommendations in 2017 aimed at preventing peanut allergy⁴⁴:

• In healthy infants without known food allergy and those with mild or moderate eczema, caregivers can introduce peanut-containing foods at home with other solid foods.Parents who are anxious about a possible allergic reaction can introduce peanut products in a physician’s office.
• Infants at high risk of peanut allergy (those with severe eczema or egg allergy, or both) should undergo peanut-specific IgE or skin-prick testing:
  • Negative test: indicates low risk of a reaction to peanuts; the infant should start consuming peanut-containing foods at 4 to 6 months of age, at home or in a physician’s office, depending on the parents’ preference
  • Positive test: Referral to an allergist is recommended.

Do children outgrow food allergy?

Approximately 85% of children who have an allergy to milk, egg, soy, or wheat outgrow their allergy; however, only 15% to 20% who have an allergy to peanuts, tree nuts, fish, or shellfish eventually tolerate these foods. The time to resolution of food allergy varies with the food, and might not occur until adolescence.⁴ No test reliably predicts which children develop tolerance to any given food. A decrease in the food-specific serum IgE level or a decrease in the size of the wheal on skin-prick testing might portend the onset of tolerance to the food.⁴

CORRESPONDENCE
Catherine M. Bettcher, MD, FAAFP, Briarwood Family Medicine, 1801 Briarwood Circle, Building #10, Ann Arbor, MI 48108; cbettche@umich.edu.

About 22% of children with COVID-19 infections were asymptomatic, and 66% of the symptomatic children had unrecognized symptoms at the time of diagnosis, based on data from a case series of 91 confirmed cases.

South_agency/Getty Images

Although recent reports suggest that COVID-19 infections in children are generally mild, data on the full spectrum of illness and duration of viral RNA in children are limited, wrote Mi Seon Han, MD, PhD, of Seoul (South Korea) Metropolitan Government–Seoul National University Boramae Medical Center, and colleagues.

To examine the full clinical course and duration of COVID-19 RNA detectability in children with confirmed infections, the researchers reviewed data from 91 individuals with confirmed infections. The children ranged in age from 27 days to 18 years, and 58% were male. The children were monitored at 20 hospitals and 2 isolation facilities for a mean 21.9 days. The findings were published in JAMA Pediatrics.

Overall, COVID-19 viral RNA was present in the study population for a mean 17.6 days, with testing done at a median interval of 3 days. A total of 20 children (22%) were asymptomatic throughout the study period. In these children, viral RNA was detected for a mean 14 days.

“The major hurdle implicated in this study in diagnosing and treating children with COVID-19 is that a considerable number of children are asymptomatic, and even if symptoms are present, they are unrecognized and overlooked before COVID-19 is diagnosed,” the researchers noted.

Of the 71 symptomatic children, 47 (66%) had unrecognized symptoms prior to diagnosis, 18 (25%) developed symptoms after diagnosis, and 6 (9%) were diagnosed at the time of symptom onset. The symptomatic children were symptomatic for a median of 11 days; 43 (61%) remained symptomatic at 7 days’ follow-up after the study period, 27 (38%) were symptomatic at 14 days, and 7 (10%) were symptomatic at 21 days.

A total of 41 children had upper respiratory infections (58%) and 22 children (24%) had lower respiratory tract infections. No difference in the duration of virus RNA was detected between children with upper respiratory tract infections and lower respiratory tract infections (average, 18.7 days vs. 19.9 days).

Among the symptomatic children, 46 (65%) had mild cases and 20 (28%) had moderate cases.

For treatment, 14 children (15%) received lopinavir-ritonavir and/or hydroxychloroquine. Two patients had severe illness and received oxygen via nasal prong, without the need for mechanical ventilation. All the children in the case series recovered from their infections with no fatalities.

The study’s main limitation was the inability to analyze the transmission potential of the children because of the quarantine and isolation policies in Korea, the researchers noted. In addition, the researchers did not perform follow-up testing at consistent intervals, so the duration of COVID-19 RNA detection may be inexact.

However, the results suggest “that suspecting and diagnosing COVID-19 in children based on their symptoms without epidemiologic information and virus testing is very challenging,” the researchers emphasized.

“Most of the children with COVID-19 have silent disease, but SARS-CoV-2 RNA can still be detected in the respiratory tract for a prolonged period,” they wrote. More research is needed to explore the potential for disease transmission by children in the community, and increased surveillance with laboratory screening can help identify children with unrecognized infections.

The study is the first known to focus on the frequency of asymptomatic infection in children and the duration of symptoms in both asymptomatic and symptomatic children, Roberta L. DeBiasi, MD, and Meghan Delaney, DO, both affiliated with Children’s National Hospital and Research Institute, Washington, and George Washington University, Washington, wrote in an accompanying editorial. The structure of the Korean public health system “allowed for the sequential observation, testing (median testing interval of every 3 days), and comparison of 91 asymptomatic, presymptomatic, and symptomatic children with mild to moderate upper and lower respiratory tract infection, identified primarily by contact tracing from laboratory-proven cases.”

Two take-home points from the study are that not all infected children are symptomatic, and the duration of symptoms in those who are varies widely, they noted. “Interestingly, this study aligns with adult data in which up to 40% of adults may remain asymptomatic in the face of infection.”

However, “The third and most important take-home point from this study relates to the duration of viral shedding in infected pediatric patients,” Dr. DeBiasi and Dr. Delaney said (JAMA Pediatr. 2020 Aug 28. doi: 10.1001/jamapediatrics.2020.3996).

“Fully half of symptomatic children with both upper and lower tract disease were still shedding virus at 21 days. These are striking data, particularly since 86 of 88 diagnosed children (98%) either had no symptoms or mild or moderate disease,” they explained. The results highlight the need for improvements in qualitative molecular testing and formal studies to identify differences in results from different testing scenarios, such as hospital entry, preprocedure screening, and symptomatic testing. In addition, “these findings are highly relevant to the development of public health strategies to mitigate and contain spread within communities, particularly as affected communities begin their recovery phases.”

The study is important because “schools are opening, and we don’t know what is going to happen,” Michael E. Pichichero, MD, of Rochester General Hospital, N.Y., said in an interview.

“Clinicians, parents, students, school administrators and politicians are worried,” he said. “This study adds to others recently published, bringing into focus the challenges to several suppositions that existed when the COVID-19 pandemic began and over the summer.”

“This study of 91 Korean children tells us that taking a child’s temperature as a screening tool to decide if they may enter school will not be a highly successful strategy,” he said. “Many children are without fever and asymptomatic when infected and contagious. The notion that children shed less virus or shed it for shorter lengths of time we keep learning from this type of research is not true. In another recent study the authors found that children shed as much of the SARS-CoV-2 virus as an adult in the ICU on a ventilator.”

Dr. Pichichero said he was not surprised by the study findings. “A similar paper was published last week in the Journal of Pediatrics from Massachusetts General Hospital, so the findings in the JAMA paper are similar to what has been reported in the United States.”

“Availability of testing will continue to be a challenge in some communities,” said Dr. Pichichero. “Here in the Rochester, New York, area we will use a screening questionnaire based on the CDC [Centers for Disease Control and Prevention] symptom criteria of SARS-CoV-2 infections to decide whom to test.”

As for additional research, “We have so much more to learn about SARS-CoV-2 in children,” he emphasized. “The focus has been on adults because the morbidity and mortality has been greatest in adults, especially the elderly and those with compromised health.”

“The National Institutes of Health has issued a call for more research in children to characterize the spectrum of SARS-CoV-2 illness, including the multisystem inflammatory syndrome in children [MIS-C] and try to identify biomarkers and/or biosignatures for a prognostic algorithm to predict the longitudinal risk of disease severity after a child is exposed to and may be infected with SARS-CoV-2,” said Dr. Pichichero. “NIH has asked researchers to answer the following questions.”

• Why do children have milder illness?
• Are there differences in childhood biology (e.g., gender, puberty, etc.) that contribute to illness severity?
• Are there genetic host differences associated with different disease severity phenotypes, including MIS-C?
• Are there innate mucosal, humoral, cellular and other adaptive immune profiles that are associated with reduced or increased risk of progressive disease, including previous coronavirus infections?
• Will SARS-CoV-2 reinfection cause worse disease as seen with antibody-dependent enhancement (ADE) in other viral infections (e.g., dengue)? Will future vaccines carry a risk of the ADE phenomenon?
• Does substance use (e.g., nicotine, marijuana) exacerbate or trigger MIS-C through immune activation?

“We have no knowledge yet about SARS-CoV-2 vaccination of children, especially young children,” Dr. Pichichero emphasized. “There are different types of vaccines – messenger RNA, adenovirus vector and purified spike proteins of the virus – among others, but questions remain: Will the vaccines work in children? What about side effects? Will the antibodies and cellular immunity protect partially or completely?”

The researchers and editorialists had no financial conflicts to disclose. Dr. Pichichero had no financial conflicts to disclose.

SOURCE: Han MS et al. JAMA Pediatr. 2020 Aug 28. doi:10.1001/jamapediatrics.2020.3988.

About 22% of children with COVID-19 infections were asymptomatic, and 66% of the symptomatic children had unrecognized symptoms at the time of diagnosis, based on data from a case series of 91 confirmed cases.

South_agency/Getty Images

Although recent reports suggest that COVID-19 infections in children are generally mild, data on the full spectrum of illness and duration of viral RNA in children are limited, wrote Mi Seon Han, MD, PhD, of Seoul (South Korea) Metropolitan Government–Seoul National University Boramae Medical Center, and colleagues.

To examine the full clinical course and duration of COVID-19 RNA detectability in children with confirmed infections, the researchers reviewed data from 91 individuals with confirmed infections. The children ranged in age from 27 days to 18 years, and 58% were male. The children were monitored at 20 hospitals and 2 isolation facilities for a mean 21.9 days. The findings were published in JAMA Pediatrics.

Overall, COVID-19 viral RNA was present in the study population for a mean 17.6 days, with testing done at a median interval of 3 days. A total of 20 children (22%) were asymptomatic throughout the study period. In these children, viral RNA was detected for a mean 14 days.

“The major hurdle implicated in this study in diagnosing and treating children with COVID-19 is that a considerable number of children are asymptomatic, and even if symptoms are present, they are unrecognized and overlooked before COVID-19 is diagnosed,” the researchers noted.

Of the 71 symptomatic children, 47 (66%) had unrecognized symptoms prior to diagnosis, 18 (25%) developed symptoms after diagnosis, and 6 (9%) were diagnosed at the time of symptom onset. The symptomatic children were symptomatic for a median of 11 days; 43 (61%) remained symptomatic at 7 days’ follow-up after the study period, 27 (38%) were symptomatic at 14 days, and 7 (10%) were symptomatic at 21 days.

A total of 41 children had upper respiratory infections (58%) and 22 children (24%) had lower respiratory tract infections. No difference in the duration of virus RNA was detected between children with upper respiratory tract infections and lower respiratory tract infections (average, 18.7 days vs. 19.9 days).

Among the symptomatic children, 46 (65%) had mild cases and 20 (28%) had moderate cases.

For treatment, 14 children (15%) received lopinavir-ritonavir and/or hydroxychloroquine. Two patients had severe illness and received oxygen via nasal prong, without the need for mechanical ventilation. All the children in the case series recovered from their infections with no fatalities.

The study’s main limitation was the inability to analyze the transmission potential of the children because of the quarantine and isolation policies in Korea, the researchers noted. In addition, the researchers did not perform follow-up testing at consistent intervals, so the duration of COVID-19 RNA detection may be inexact.

However, the results suggest “that suspecting and diagnosing COVID-19 in children based on their symptoms without epidemiologic information and virus testing is very challenging,” the researchers emphasized.

“Most of the children with COVID-19 have silent disease, but SARS-CoV-2 RNA can still be detected in the respiratory tract for a prolonged period,” they wrote. More research is needed to explore the potential for disease transmission by children in the community, and increased surveillance with laboratory screening can help identify children with unrecognized infections.

The study is the first known to focus on the frequency of asymptomatic infection in children and the duration of symptoms in both asymptomatic and symptomatic children, Roberta L. DeBiasi, MD, and Meghan Delaney, DO, both affiliated with Children’s National Hospital and Research Institute, Washington, and George Washington University, Washington, wrote in an accompanying editorial. The structure of the Korean public health system “allowed for the sequential observation, testing (median testing interval of every 3 days), and comparison of 91 asymptomatic, presymptomatic, and symptomatic children with mild to moderate upper and lower respiratory tract infection, identified primarily by contact tracing from laboratory-proven cases.”

Two take-home points from the study are that not all infected children are symptomatic, and the duration of symptoms in those who are varies widely, they noted. “Interestingly, this study aligns with adult data in which up to 40% of adults may remain asymptomatic in the face of infection.”

However, “The third and most important take-home point from this study relates to the duration of viral shedding in infected pediatric patients,” Dr. DeBiasi and Dr. Delaney said (JAMA Pediatr. 2020 Aug 28. doi: 10.1001/jamapediatrics.2020.3996).

“Fully half of symptomatic children with both upper and lower tract disease were still shedding virus at 21 days. These are striking data, particularly since 86 of 88 diagnosed children (98%) either had no symptoms or mild or moderate disease,” they explained. The results highlight the need for improvements in qualitative molecular testing and formal studies to identify differences in results from different testing scenarios, such as hospital entry, preprocedure screening, and symptomatic testing. In addition, “these findings are highly relevant to the development of public health strategies to mitigate and contain spread within communities, particularly as affected communities begin their recovery phases.”

The study is important because “schools are opening, and we don’t know what is going to happen,” Michael E. Pichichero, MD, of Rochester General Hospital, N.Y., said in an interview.

“Clinicians, parents, students, school administrators and politicians are worried,” he said. “This study adds to others recently published, bringing into focus the challenges to several suppositions that existed when the COVID-19 pandemic began and over the summer.”

“This study of 91 Korean children tells us that taking a child’s temperature as a screening tool to decide if they may enter school will not be a highly successful strategy,” he said. “Many children are without fever and asymptomatic when infected and contagious. The notion that children shed less virus or shed it for shorter lengths of time we keep learning from this type of research is not true. In another recent study the authors found that children shed as much of the SARS-CoV-2 virus as an adult in the ICU on a ventilator.”

Dr. Pichichero said he was not surprised by the study findings. “A similar paper was published last week in the Journal of Pediatrics from Massachusetts General Hospital, so the findings in the JAMA paper are similar to what has been reported in the United States.”

“Availability of testing will continue to be a challenge in some communities,” said Dr. Pichichero. “Here in the Rochester, New York, area we will use a screening questionnaire based on the CDC [Centers for Disease Control and Prevention] symptom criteria of SARS-CoV-2 infections to decide whom to test.”

As for additional research, “We have so much more to learn about SARS-CoV-2 in children,” he emphasized. “The focus has been on adults because the morbidity and mortality has been greatest in adults, especially the elderly and those with compromised health.”

“The National Institutes of Health has issued a call for more research in children to characterize the spectrum of SARS-CoV-2 illness, including the multisystem inflammatory syndrome in children [MIS-C] and try to identify biomarkers and/or biosignatures for a prognostic algorithm to predict the longitudinal risk of disease severity after a child is exposed to and may be infected with SARS-CoV-2,” said Dr. Pichichero. “NIH has asked researchers to answer the following questions.”

• Why do children have milder illness?
• Are there differences in childhood biology (e.g., gender, puberty, etc.) that contribute to illness severity?
• Are there genetic host differences associated with different disease severity phenotypes, including MIS-C?
• Are there innate mucosal, humoral, cellular and other adaptive immune profiles that are associated with reduced or increased risk of progressive disease, including previous coronavirus infections?
• Will SARS-CoV-2 reinfection cause worse disease as seen with antibody-dependent enhancement (ADE) in other viral infections (e.g., dengue)? Will future vaccines carry a risk of the ADE phenomenon?
• Does substance use (e.g., nicotine, marijuana) exacerbate or trigger MIS-C through immune activation?

“We have no knowledge yet about SARS-CoV-2 vaccination of children, especially young children,” Dr. Pichichero emphasized. “There are different types of vaccines – messenger RNA, adenovirus vector and purified spike proteins of the virus – among others, but questions remain: Will the vaccines work in children? What about side effects? Will the antibodies and cellular immunity protect partially or completely?”

The researchers and editorialists had no financial conflicts to disclose. Dr. Pichichero had no financial conflicts to disclose.

SOURCE: Han MS et al. JAMA Pediatr. 2020 Aug 28. doi:10.1001/jamapediatrics.2020.3988.

About 22% of children with COVID-19 infections were asymptomatic, and 66% of the symptomatic children had unrecognized symptoms at the time of diagnosis, based on data from a case series of 91 confirmed cases.

South_agency/Getty Images

Although recent reports suggest that COVID-19 infections in children are generally mild, data on the full spectrum of illness and duration of viral RNA in children are limited, wrote Mi Seon Han, MD, PhD, of Seoul (South Korea) Metropolitan Government–Seoul National University Boramae Medical Center, and colleagues.

To examine the full clinical course and duration of COVID-19 RNA detectability in children with confirmed infections, the researchers reviewed data from 91 individuals with confirmed infections. The children ranged in age from 27 days to 18 years, and 58% were male. The children were monitored at 20 hospitals and 2 isolation facilities for a mean 21.9 days. The findings were published in JAMA Pediatrics.

Overall, COVID-19 viral RNA was present in the study population for a mean 17.6 days, with testing done at a median interval of 3 days. A total of 20 children (22%) were asymptomatic throughout the study period. In these children, viral RNA was detected for a mean 14 days.

“The major hurdle implicated in this study in diagnosing and treating children with COVID-19 is that a considerable number of children are asymptomatic, and even if symptoms are present, they are unrecognized and overlooked before COVID-19 is diagnosed,” the researchers noted.

Of the 71 symptomatic children, 47 (66%) had unrecognized symptoms prior to diagnosis, 18 (25%) developed symptoms after diagnosis, and 6 (9%) were diagnosed at the time of symptom onset. The symptomatic children were symptomatic for a median of 11 days; 43 (61%) remained symptomatic at 7 days’ follow-up after the study period, 27 (38%) were symptomatic at 14 days, and 7 (10%) were symptomatic at 21 days.

A total of 41 children had upper respiratory infections (58%) and 22 children (24%) had lower respiratory tract infections. No difference in the duration of virus RNA was detected between children with upper respiratory tract infections and lower respiratory tract infections (average, 18.7 days vs. 19.9 days).

Among the symptomatic children, 46 (65%) had mild cases and 20 (28%) had moderate cases.

For treatment, 14 children (15%) received lopinavir-ritonavir and/or hydroxychloroquine. Two patients had severe illness and received oxygen via nasal prong, without the need for mechanical ventilation. All the children in the case series recovered from their infections with no fatalities.

The study’s main limitation was the inability to analyze the transmission potential of the children because of the quarantine and isolation policies in Korea, the researchers noted. In addition, the researchers did not perform follow-up testing at consistent intervals, so the duration of COVID-19 RNA detection may be inexact.

However, the results suggest “that suspecting and diagnosing COVID-19 in children based on their symptoms without epidemiologic information and virus testing is very challenging,” the researchers emphasized.

“Most of the children with COVID-19 have silent disease, but SARS-CoV-2 RNA can still be detected in the respiratory tract for a prolonged period,” they wrote. More research is needed to explore the potential for disease transmission by children in the community, and increased surveillance with laboratory screening can help identify children with unrecognized infections.

The study is the first known to focus on the frequency of asymptomatic infection in children and the duration of symptoms in both asymptomatic and symptomatic children, Roberta L. DeBiasi, MD, and Meghan Delaney, DO, both affiliated with Children’s National Hospital and Research Institute, Washington, and George Washington University, Washington, wrote in an accompanying editorial. The structure of the Korean public health system “allowed for the sequential observation, testing (median testing interval of every 3 days), and comparison of 91 asymptomatic, presymptomatic, and symptomatic children with mild to moderate upper and lower respiratory tract infection, identified primarily by contact tracing from laboratory-proven cases.”

Two take-home points from the study are that not all infected children are symptomatic, and the duration of symptoms in those who are varies widely, they noted. “Interestingly, this study aligns with adult data in which up to 40% of adults may remain asymptomatic in the face of infection.”

However, “The third and most important take-home point from this study relates to the duration of viral shedding in infected pediatric patients,” Dr. DeBiasi and Dr. Delaney said (JAMA Pediatr. 2020 Aug 28. doi: 10.1001/jamapediatrics.2020.3996).

“Fully half of symptomatic children with both upper and lower tract disease were still shedding virus at 21 days. These are striking data, particularly since 86 of 88 diagnosed children (98%) either had no symptoms or mild or moderate disease,” they explained. The results highlight the need for improvements in qualitative molecular testing and formal studies to identify differences in results from different testing scenarios, such as hospital entry, preprocedure screening, and symptomatic testing. In addition, “these findings are highly relevant to the development of public health strategies to mitigate and contain spread within communities, particularly as affected communities begin their recovery phases.”

The study is important because “schools are opening, and we don’t know what is going to happen,” Michael E. Pichichero, MD, of Rochester General Hospital, N.Y., said in an interview.

“Clinicians, parents, students, school administrators and politicians are worried,” he said. “This study adds to others recently published, bringing into focus the challenges to several suppositions that existed when the COVID-19 pandemic began and over the summer.”

“This study of 91 Korean children tells us that taking a child’s temperature as a screening tool to decide if they may enter school will not be a highly successful strategy,” he said. “Many children are without fever and asymptomatic when infected and contagious. The notion that children shed less virus or shed it for shorter lengths of time we keep learning from this type of research is not true. In another recent study the authors found that children shed as much of the SARS-CoV-2 virus as an adult in the ICU on a ventilator.”

Dr. Pichichero said he was not surprised by the study findings. “A similar paper was published last week in the Journal of Pediatrics from Massachusetts General Hospital, so the findings in the JAMA paper are similar to what has been reported in the United States.”

“Availability of testing will continue to be a challenge in some communities,” said Dr. Pichichero. “Here in the Rochester, New York, area we will use a screening questionnaire based on the CDC [Centers for Disease Control and Prevention] symptom criteria of SARS-CoV-2 infections to decide whom to test.”

As for additional research, “We have so much more to learn about SARS-CoV-2 in children,” he emphasized. “The focus has been on adults because the morbidity and mortality has been greatest in adults, especially the elderly and those with compromised health.”

“The National Institutes of Health has issued a call for more research in children to characterize the spectrum of SARS-CoV-2 illness, including the multisystem inflammatory syndrome in children [MIS-C] and try to identify biomarkers and/or biosignatures for a prognostic algorithm to predict the longitudinal risk of disease severity after a child is exposed to and may be infected with SARS-CoV-2,” said Dr. Pichichero. “NIH has asked researchers to answer the following questions.”

• Why do children have milder illness?
• Are there differences in childhood biology (e.g., gender, puberty, etc.) that contribute to illness severity?
• Are there genetic host differences associated with different disease severity phenotypes, including MIS-C?
• Are there innate mucosal, humoral, cellular and other adaptive immune profiles that are associated with reduced or increased risk of progressive disease, including previous coronavirus infections?
• Will SARS-CoV-2 reinfection cause worse disease as seen with antibody-dependent enhancement (ADE) in other viral infections (e.g., dengue)? Will future vaccines carry a risk of the ADE phenomenon?
• Does substance use (e.g., nicotine, marijuana) exacerbate or trigger MIS-C through immune activation?

“We have no knowledge yet about SARS-CoV-2 vaccination of children, especially young children,” Dr. Pichichero emphasized. “There are different types of vaccines – messenger RNA, adenovirus vector and purified spike proteins of the virus – among others, but questions remain: Will the vaccines work in children? What about side effects? Will the antibodies and cellular immunity protect partially or completely?”

The researchers and editorialists had no financial conflicts to disclose. Dr. Pichichero had no financial conflicts to disclose.

SOURCE: Han MS et al. JAMA Pediatr. 2020 Aug 28. doi:10.1001/jamapediatrics.2020.3988.

Nasal papules that resemble angiofibromas are rarely described in the literature as a sequela of acne, but researchers believe the condition could be an underrecognized problem, affecting patients with skin of color in particular, according to the authors of a case series published in Pediatric Dermatology.

Courtesy Dr. Jorge Roman

Jorge Roman, MD, and coauthors in the department of dermatology at New York (N.Y.) University identified 20 patients with a history of acne who had nasal papules, in a retrospective review of electronic medical records at NYU over 1 year (April 2018 to April 2019). The presentation ranged from “a few, small skin-colored papules to large, dome-shaped papulonodules, to more extensive rhinophymatous-like” changes with some patients having papular lesions on the chin in addition to the nose, they wrote in the report.

These papules greatly resembled angiofibromas, but appear to be a sequela of acne, according to the authors. In five patients who had biopsies, the results showed “a dome-shaped proliferation of spindle and stellate-shaped cells with thickened collagen bundles and dilated thin-walled blood vessels,” the authors wrote. “The histopathological findings of these nasal papules were indistinguishable from those of a conventional angiofibroma.”

In addition, the patients did not have evidence of underlying genetic conditions that could explain the angiofibroma-like lesions. “Although acne has not previously been implicated in the development of angiofibromas, based on the data available for our patients, it seems extremely unlikely that the lesions would be related to anything else,” Dr. Roman, a dermatology resident at New York University, said in an interview.

He said he first recognized the nasal papules in clinic as a first-year resident, but was surprised to find a lack of information on the condition. “Dermatology has a name for just about every skin disease imaginable, so I found it very odd when I couldn’t find much describing this condition,” he said. “There was a large disparity between what we were seeing in clinic and what was reported in the literature.”

Nearly all the patients were Hispanic (17 of 20) and adolescent males (17 patients), with a median age of 16 years at the time of presentation. There were two Black patients and one Asian patient. Race and ethnicity were not mentioned in two previous reports describing papular acne scarring, but Dr. Roman and colleagues noted that in their clinic, the condition appeared to affect adolescent patients with skin of color predominantly.

Reasons why nasal papules may be underreported are unclear, Dr. Roman noted. One possible explanation is lower use of dermatologic care among patients with skin of color. “Interestingly, previous research has shown that racial minorities are lower utilizers of dermatologic care. It is possible that the patient demographic most afflicted by this condition face significant barriers when seeking care,” he said.

Due to a low level of awareness of acne-related nasal papules, “clinicians may not recognize it as an acne-related scarring process. This is significant, as early recognition and treatment can prevent the development or progression of these potentially disfiguring sequelae,” Dr. Roman said.

Although the results are from a small case series at a single center, Dr. Roman said this condition may be more prevalent than realized. “Having been raised in a predominately Latino community in Texas, I can easily recall seeing people with these papules growing up. I don’t think it would be surprising for dermatologists reading our paper to say, ‘I’ve seen this in clinic before,’ ” he said.

Regarding treatment, there is an ongoing investigation into what treatments are effective for the acne-related nasal papules. “Physical treatment modalities such as ablative laser or surgical removal seem to be the most efficacious,” Dr. Roman said. “In the future, a prospective clinical study will help to better define the prevalence and risk factors for the condition,” he said.

He and coauthors reported no conflicts of interest. No funding source was listed.

SOURCE: Roman J et al. Pediatr Dermatol. 2020 Aug 7. doi: 10.1111/pde.14319.

Nasal papules that resemble angiofibromas are rarely described in the literature as a sequela of acne, but researchers believe the condition could be an underrecognized problem, affecting patients with skin of color in particular, according to the authors of a case series published in Pediatric Dermatology.

Courtesy Dr. Jorge Roman

Jorge Roman, MD, and coauthors in the department of dermatology at New York (N.Y.) University identified 20 patients with a history of acne who had nasal papules, in a retrospective review of electronic medical records at NYU over 1 year (April 2018 to April 2019). The presentation ranged from “a few, small skin-colored papules to large, dome-shaped papulonodules, to more extensive rhinophymatous-like” changes with some patients having papular lesions on the chin in addition to the nose, they wrote in the report.

These papules greatly resembled angiofibromas, but appear to be a sequela of acne, according to the authors. In five patients who had biopsies, the results showed “a dome-shaped proliferation of spindle and stellate-shaped cells with thickened collagen bundles and dilated thin-walled blood vessels,” the authors wrote. “The histopathological findings of these nasal papules were indistinguishable from those of a conventional angiofibroma.”

In addition, the patients did not have evidence of underlying genetic conditions that could explain the angiofibroma-like lesions. “Although acne has not previously been implicated in the development of angiofibromas, based on the data available for our patients, it seems extremely unlikely that the lesions would be related to anything else,” Dr. Roman, a dermatology resident at New York University, said in an interview.

He said he first recognized the nasal papules in clinic as a first-year resident, but was surprised to find a lack of information on the condition. “Dermatology has a name for just about every skin disease imaginable, so I found it very odd when I couldn’t find much describing this condition,” he said. “There was a large disparity between what we were seeing in clinic and what was reported in the literature.”

Nearly all the patients were Hispanic (17 of 20) and adolescent males (17 patients), with a median age of 16 years at the time of presentation. There were two Black patients and one Asian patient. Race and ethnicity were not mentioned in two previous reports describing papular acne scarring, but Dr. Roman and colleagues noted that in their clinic, the condition appeared to affect adolescent patients with skin of color predominantly.

Reasons why nasal papules may be underreported are unclear, Dr. Roman noted. One possible explanation is lower use of dermatologic care among patients with skin of color. “Interestingly, previous research has shown that racial minorities are lower utilizers of dermatologic care. It is possible that the patient demographic most afflicted by this condition face significant barriers when seeking care,” he said.

Due to a low level of awareness of acne-related nasal papules, “clinicians may not recognize it as an acne-related scarring process. This is significant, as early recognition and treatment can prevent the development or progression of these potentially disfiguring sequelae,” Dr. Roman said.

Although the results are from a small case series at a single center, Dr. Roman said this condition may be more prevalent than realized. “Having been raised in a predominately Latino community in Texas, I can easily recall seeing people with these papules growing up. I don’t think it would be surprising for dermatologists reading our paper to say, ‘I’ve seen this in clinic before,’ ” he said.

Regarding treatment, there is an ongoing investigation into what treatments are effective for the acne-related nasal papules. “Physical treatment modalities such as ablative laser or surgical removal seem to be the most efficacious,” Dr. Roman said. “In the future, a prospective clinical study will help to better define the prevalence and risk factors for the condition,” he said.

He and coauthors reported no conflicts of interest. No funding source was listed.

SOURCE: Roman J et al. Pediatr Dermatol. 2020 Aug 7. doi: 10.1111/pde.14319.

Nasal papules that resemble angiofibromas are rarely described in the literature as a sequela of acne, but researchers believe the condition could be an underrecognized problem, affecting patients with skin of color in particular, according to the authors of a case series published in Pediatric Dermatology.

Courtesy Dr. Jorge Roman

Jorge Roman, MD, and coauthors in the department of dermatology at New York (N.Y.) University identified 20 patients with a history of acne who had nasal papules, in a retrospective review of electronic medical records at NYU over 1 year (April 2018 to April 2019). The presentation ranged from “a few, small skin-colored papules to large, dome-shaped papulonodules, to more extensive rhinophymatous-like” changes with some patients having papular lesions on the chin in addition to the nose, they wrote in the report.

These papules greatly resembled angiofibromas, but appear to be a sequela of acne, according to the authors. In five patients who had biopsies, the results showed “a dome-shaped proliferation of spindle and stellate-shaped cells with thickened collagen bundles and dilated thin-walled blood vessels,” the authors wrote. “The histopathological findings of these nasal papules were indistinguishable from those of a conventional angiofibroma.”

In addition, the patients did not have evidence of underlying genetic conditions that could explain the angiofibroma-like lesions. “Although acne has not previously been implicated in the development of angiofibromas, based on the data available for our patients, it seems extremely unlikely that the lesions would be related to anything else,” Dr. Roman, a dermatology resident at New York University, said in an interview.

He said he first recognized the nasal papules in clinic as a first-year resident, but was surprised to find a lack of information on the condition. “Dermatology has a name for just about every skin disease imaginable, so I found it very odd when I couldn’t find much describing this condition,” he said. “There was a large disparity between what we were seeing in clinic and what was reported in the literature.”

Nearly all the patients were Hispanic (17 of 20) and adolescent males (17 patients), with a median age of 16 years at the time of presentation. There were two Black patients and one Asian patient. Race and ethnicity were not mentioned in two previous reports describing papular acne scarring, but Dr. Roman and colleagues noted that in their clinic, the condition appeared to affect adolescent patients with skin of color predominantly.

Reasons why nasal papules may be underreported are unclear, Dr. Roman noted. One possible explanation is lower use of dermatologic care among patients with skin of color. “Interestingly, previous research has shown that racial minorities are lower utilizers of dermatologic care. It is possible that the patient demographic most afflicted by this condition face significant barriers when seeking care,” he said.

Due to a low level of awareness of acne-related nasal papules, “clinicians may not recognize it as an acne-related scarring process. This is significant, as early recognition and treatment can prevent the development or progression of these potentially disfiguring sequelae,” Dr. Roman said.

Although the results are from a small case series at a single center, Dr. Roman said this condition may be more prevalent than realized. “Having been raised in a predominately Latino community in Texas, I can easily recall seeing people with these papules growing up. I don’t think it would be surprising for dermatologists reading our paper to say, ‘I’ve seen this in clinic before,’ ” he said.

Regarding treatment, there is an ongoing investigation into what treatments are effective for the acne-related nasal papules. “Physical treatment modalities such as ablative laser or surgical removal seem to be the most efficacious,” Dr. Roman said. “In the future, a prospective clinical study will help to better define the prevalence and risk factors for the condition,” he said.

He and coauthors reported no conflicts of interest. No funding source was listed.

SOURCE: Roman J et al. Pediatr Dermatol. 2020 Aug 7. doi: 10.1111/pde.14319.

In 2019, more than five times as many high school students were using tobacco electronically than smoking actual cigarettes, according to the Centers for Disease Control and Prevention.

From 2015 to 2019, current use of electronic vapor products among students in grades 9-12 rose from 24.1% to 32.7%, while the same level of cigarette use – on 1 or more days in the previous 30 – dropped from 10.8% to 6.0%, based on data from the Youth Risk Behavior Survey.

Among the survey respondents, 50.1% had at least tried an electronic vapor product by 2019, up from 44.9% in 2015. Cigarettes again showed a decline, as ever use fell from 32.3% to 24.1%, or less than half of the e-product prevalence. Everyday use of vaping products was 7.2% in 2019 (up from 2.0% in 2015), compared with 1.1% for cigarettes (down from 2.3%), the YRBS data show.

“The dramatic increase in electronic vapor product use among high school students has led to increases in overall tobacco product use among U.S. youths, erasing gains made in previous years and leading the U.S. Surgeon General to declare youth e-cigarette use an epidemic in the United States,” MeLisa R. Creamer, PhD, and associates at the CDC wrote in the MMWR.

Electronic vapor products, as defined by the survey, “include e-cigarettes, vapes, vape pens, e-cigars, e-hookahs, hookah pens, and mods.”

Current use of cigarettes among high school students, as measured by the YRBS, has been declining since reaching a high of 36.4% in 1997; the prevalence of everyday use peaked at 12.8% in 1999. Current use of cigars declined as well, falling from 17.7% in 1999 to 5.7% in 2019, according to YRBS data.

“In 2019, a total of 36.5% of high school students currently used any tobacco product, with electronic vapor products being the most commonly used product,” Dr. Creamer and associates wrote in their recent analysis of the YRBS data (MMWR Supp. 2020 Aug 21;69[1]:56-63).

For the first time since the use of electronic vapor products was included in the every-other-year survey in 2015, females were more likely than males to be current users of vaping products last year, 33.5% to 32.0%. Males were heavier users of cigarettes by a margin of 6.9% to 4.9%, the CDC reported.

Geographically speaking, use of both electronic vapor products and cigarettes varied considerably among the 43 states with available data. Current use of electronic products ranged from a low of 9.7% in Utah to a high of 35.7% in West Virginia, with the two states in the same positions regarding current cigarette use: Utah (2.2%) lowest and West Virginia (13.5%) highest, based on the 2019 YRBS data.

“Tobacco product usage has evolved, and the increasing prevalence of electronic vapor product use among youths during recent years is concerning,” Dr. Creamer and associates wrote.

rfranki@mdedge.com

In 2019, more than five times as many high school students were using tobacco electronically than smoking actual cigarettes, according to the Centers for Disease Control and Prevention.

From 2015 to 2019, current use of electronic vapor products among students in grades 9-12 rose from 24.1% to 32.7%, while the same level of cigarette use – on 1 or more days in the previous 30 – dropped from 10.8% to 6.0%, based on data from the Youth Risk Behavior Survey.

Among the survey respondents, 50.1% had at least tried an electronic vapor product by 2019, up from 44.9% in 2015. Cigarettes again showed a decline, as ever use fell from 32.3% to 24.1%, or less than half of the e-product prevalence. Everyday use of vaping products was 7.2% in 2019 (up from 2.0% in 2015), compared with 1.1% for cigarettes (down from 2.3%), the YRBS data show.

“The dramatic increase in electronic vapor product use among high school students has led to increases in overall tobacco product use among U.S. youths, erasing gains made in previous years and leading the U.S. Surgeon General to declare youth e-cigarette use an epidemic in the United States,” MeLisa R. Creamer, PhD, and associates at the CDC wrote in the MMWR.

Electronic vapor products, as defined by the survey, “include e-cigarettes, vapes, vape pens, e-cigars, e-hookahs, hookah pens, and mods.”

Current use of cigarettes among high school students, as measured by the YRBS, has been declining since reaching a high of 36.4% in 1997; the prevalence of everyday use peaked at 12.8% in 1999. Current use of cigars declined as well, falling from 17.7% in 1999 to 5.7% in 2019, according to YRBS data.

“In 2019, a total of 36.5% of high school students currently used any tobacco product, with electronic vapor products being the most commonly used product,” Dr. Creamer and associates wrote in their recent analysis of the YRBS data (MMWR Supp. 2020 Aug 21;69[1]:56-63).

For the first time since the use of electronic vapor products was included in the every-other-year survey in 2015, females were more likely than males to be current users of vaping products last year, 33.5% to 32.0%. Males were heavier users of cigarettes by a margin of 6.9% to 4.9%, the CDC reported.

Geographically speaking, use of both electronic vapor products and cigarettes varied considerably among the 43 states with available data. Current use of electronic products ranged from a low of 9.7% in Utah to a high of 35.7% in West Virginia, with the two states in the same positions regarding current cigarette use: Utah (2.2%) lowest and West Virginia (13.5%) highest, based on the 2019 YRBS data.

“Tobacco product usage has evolved, and the increasing prevalence of electronic vapor product use among youths during recent years is concerning,” Dr. Creamer and associates wrote.

rfranki@mdedge.com

In 2019, more than five times as many high school students were using tobacco electronically than smoking actual cigarettes, according to the Centers for Disease Control and Prevention.

From 2015 to 2019, current use of electronic vapor products among students in grades 9-12 rose from 24.1% to 32.7%, while the same level of cigarette use – on 1 or more days in the previous 30 – dropped from 10.8% to 6.0%, based on data from the Youth Risk Behavior Survey.

Among the survey respondents, 50.1% had at least tried an electronic vapor product by 2019, up from 44.9% in 2015. Cigarettes again showed a decline, as ever use fell from 32.3% to 24.1%, or less than half of the e-product prevalence. Everyday use of vaping products was 7.2% in 2019 (up from 2.0% in 2015), compared with 1.1% for cigarettes (down from 2.3%), the YRBS data show.

“The dramatic increase in electronic vapor product use among high school students has led to increases in overall tobacco product use among U.S. youths, erasing gains made in previous years and leading the U.S. Surgeon General to declare youth e-cigarette use an epidemic in the United States,” MeLisa R. Creamer, PhD, and associates at the CDC wrote in the MMWR.

Electronic vapor products, as defined by the survey, “include e-cigarettes, vapes, vape pens, e-cigars, e-hookahs, hookah pens, and mods.”

Current use of cigarettes among high school students, as measured by the YRBS, has been declining since reaching a high of 36.4% in 1997; the prevalence of everyday use peaked at 12.8% in 1999. Current use of cigars declined as well, falling from 17.7% in 1999 to 5.7% in 2019, according to YRBS data.

“In 2019, a total of 36.5% of high school students currently used any tobacco product, with electronic vapor products being the most commonly used product,” Dr. Creamer and associates wrote in their recent analysis of the YRBS data (MMWR Supp. 2020 Aug 21;69[1]:56-63).

For the first time since the use of electronic vapor products was included in the every-other-year survey in 2015, females were more likely than males to be current users of vaping products last year, 33.5% to 32.0%. Males were heavier users of cigarettes by a margin of 6.9% to 4.9%, the CDC reported.

Geographically speaking, use of both electronic vapor products and cigarettes varied considerably among the 43 states with available data. Current use of electronic products ranged from a low of 9.7% in Utah to a high of 35.7% in West Virginia, with the two states in the same positions regarding current cigarette use: Utah (2.2%) lowest and West Virginia (13.5%) highest, based on the 2019 YRBS data.

“Tobacco product usage has evolved, and the increasing prevalence of electronic vapor product use among youths during recent years is concerning,” Dr. Creamer and associates wrote.

rfranki@mdedge.com

Malignant melanomas in children and adolescents are thankfully rare, but they can be challenging to diagnose, and fatal disease can manifest itself in any of several different ways, results of a retrospective multicenter study showed.

“The most striking thing that we learned from this study is that pediatric melanoma can present in so many different ways, and it’s distinct from the adult population in that we see more presentations associated with congenital nevi, or spitz melanoma, which is a special class of pigmented lesions that looks a little different under the microscope,” Elena B. Hawryluk, MD, PhD, of the department of dermatology at Massachusetts General Hospital (MGH) and Harvard University, Boston, said in an interview. Dr. Hawryluk is lead author of the study, which was published online ahead of print in the Journal of the American Academy of Dermatology.

Dr. Hawryluk and colleagues at MGH and 11 other centers conducted a retrospective review of all cases of fatal pediatric melanoma among patients younger than 20 years diagnosed from late 1994 through early 2017.

They identified a total of 38 fatal cases over more than 2 decades. The cases were distinguished primarily by their heterogeneous clinical presentation and by the diversity of the patients, their precursor lesions, and the tumor histopathology, she said in an interview.

“We were surprised to find that patients with each of these presentations could end up with a fatal course, it wasn’t just all the adolescents, or all the patients with giant congenital nevi; it really presented quite diversely.”
 

Rare malignancy

Melanoma is far less common in the pediatric population than in adults, with an annual incidence of 18 per 1 million among adolescents aged 15-18 years, and 1 per 1 million in children under 10 years, the authors noted.

“Melanoma in children and adolescents often has distinct clinical presentations such as association with a congenital melanocytic nevus (CMN), spitzoid melanoma, or amelanotic melanoma, which are more rarely observed in adult melanoma patients. Unique pediatric-specific clinical detection criteria have been proposed to highlight these differences, such as a tendency to present amelanotically,” they wrote.

Factors associated with worse prognosis, such as higher Breslow thickness and mitotic index, are more frequently present at the time of diagnosis in children compared with adults, particularly those diagnosed before age 11 years.

“It is unclear if this difference is secondary to diagnostic delays due to low clinical suspicion, atypical clinical presentations, or more rapid tumor growth rate, as many childhood melanomas are of nodular or spitzoid subtypes,” Dr. Hawryluk and her coauthors wrote.
 

Study details

The investigators sought to characterize the clinical and histopathologic features of fatal pediatric melanomas.

They found that 21 of the 38 patients (57%) were of White heritage, 7 (19%) were of Hispanic or Latino background, 1 (3%) was of Asian lineage, and 1 each were of Black African American or Black Hispanic background. The remaining children were classified as “other” or did not have their ethnic backgrounds recorded.

The “striking prevalence” of Hispanic patients observed in the study is consistent with surveillance reports of an increasing incidence of melanoma among children of Hispanic background, they noted.

The mean age at diagnosis was 12.7 years, and the mean age at death was 15.6 years.

Of the 16 cases with known identifiable disease subtypes, 8 (50%) were nodular, 5 (31%) were superficial spreading, and 3 (19%) were spitzoid melanomas. Of the 38 fatal melanomas, 10 were thought to have originated from congenital melanocytic nevi.
 

Outlook improving

Recent therapeutic breakthroughs such as targeted agents and immunotherapy with checkpoint inhibitors augur well for children diagnosed with melanoma, Dr. Hawryluk said.

“Fortunately, it’s not superaggressive in children at high frequency, so we generally use adult algorithms to inform treatment decisions,” she said. “It’s just important to note that melanomas that arise in congenital nevi tend to have different driver mutations than those that arise in older patients who may have lots of sun exposure.”

“Nowadays, we’re lucky to have a lot of extra tests and workups so that, if a patient does have metastatic or advance disease, they can have a better genetic profile that would guide our choice of medications,” she added.

The study was supported by a Pediatric Dermatology Research Alliance Study Support grant and Society for Pediatric Dermatology, Pediatric Dermatology Research Alliance Pilot award. Dr. Hawryluk is supported by the Dermatology Foundation and the Harvard Medical School Eleanor and Miles Shore Fellowship award. The authors reported no conflicts of interest.

SOURCE: Hawryluk EB et al. J Am Acad Dermatol. 2020 Jul 1. doi: 10.1016/j.jaad.2020.06.1010.

Malignant melanomas in children and adolescents are thankfully rare, but they can be challenging to diagnose, and fatal disease can manifest itself in any of several different ways, results of a retrospective multicenter study showed.

“The most striking thing that we learned from this study is that pediatric melanoma can present in so many different ways, and it’s distinct from the adult population in that we see more presentations associated with congenital nevi, or spitz melanoma, which is a special class of pigmented lesions that looks a little different under the microscope,” Elena B. Hawryluk, MD, PhD, of the department of dermatology at Massachusetts General Hospital (MGH) and Harvard University, Boston, said in an interview. Dr. Hawryluk is lead author of the study, which was published online ahead of print in the Journal of the American Academy of Dermatology.

Dr. Hawryluk and colleagues at MGH and 11 other centers conducted a retrospective review of all cases of fatal pediatric melanoma among patients younger than 20 years diagnosed from late 1994 through early 2017.

They identified a total of 38 fatal cases over more than 2 decades. The cases were distinguished primarily by their heterogeneous clinical presentation and by the diversity of the patients, their precursor lesions, and the tumor histopathology, she said in an interview.

“We were surprised to find that patients with each of these presentations could end up with a fatal course, it wasn’t just all the adolescents, or all the patients with giant congenital nevi; it really presented quite diversely.”
 

Rare malignancy

Melanoma is far less common in the pediatric population than in adults, with an annual incidence of 18 per 1 million among adolescents aged 15-18 years, and 1 per 1 million in children under 10 years, the authors noted.

“Melanoma in children and adolescents often has distinct clinical presentations such as association with a congenital melanocytic nevus (CMN), spitzoid melanoma, or amelanotic melanoma, which are more rarely observed in adult melanoma patients. Unique pediatric-specific clinical detection criteria have been proposed to highlight these differences, such as a tendency to present amelanotically,” they wrote.

Factors associated with worse prognosis, such as higher Breslow thickness and mitotic index, are more frequently present at the time of diagnosis in children compared with adults, particularly those diagnosed before age 11 years.

“It is unclear if this difference is secondary to diagnostic delays due to low clinical suspicion, atypical clinical presentations, or more rapid tumor growth rate, as many childhood melanomas are of nodular or spitzoid subtypes,” Dr. Hawryluk and her coauthors wrote.
 

Study details

The investigators sought to characterize the clinical and histopathologic features of fatal pediatric melanomas.

They found that 21 of the 38 patients (57%) were of White heritage, 7 (19%) were of Hispanic or Latino background, 1 (3%) was of Asian lineage, and 1 each were of Black African American or Black Hispanic background. The remaining children were classified as “other” or did not have their ethnic backgrounds recorded.

The “striking prevalence” of Hispanic patients observed in the study is consistent with surveillance reports of an increasing incidence of melanoma among children of Hispanic background, they noted.

The mean age at diagnosis was 12.7 years, and the mean age at death was 15.6 years.

Of the 16 cases with known identifiable disease subtypes, 8 (50%) were nodular, 5 (31%) were superficial spreading, and 3 (19%) were spitzoid melanomas. Of the 38 fatal melanomas, 10 were thought to have originated from congenital melanocytic nevi.
 

Outlook improving

Recent therapeutic breakthroughs such as targeted agents and immunotherapy with checkpoint inhibitors augur well for children diagnosed with melanoma, Dr. Hawryluk said.

“Fortunately, it’s not superaggressive in children at high frequency, so we generally use adult algorithms to inform treatment decisions,” she said. “It’s just important to note that melanomas that arise in congenital nevi tend to have different driver mutations than those that arise in older patients who may have lots of sun exposure.”

“Nowadays, we’re lucky to have a lot of extra tests and workups so that, if a patient does have metastatic or advance disease, they can have a better genetic profile that would guide our choice of medications,” she added.

The study was supported by a Pediatric Dermatology Research Alliance Study Support grant and Society for Pediatric Dermatology, Pediatric Dermatology Research Alliance Pilot award. Dr. Hawryluk is supported by the Dermatology Foundation and the Harvard Medical School Eleanor and Miles Shore Fellowship award. The authors reported no conflicts of interest.

SOURCE: Hawryluk EB et al. J Am Acad Dermatol. 2020 Jul 1. doi: 10.1016/j.jaad.2020.06.1010.

Malignant melanomas in children and adolescents are thankfully rare, but they can be challenging to diagnose, and fatal disease can manifest itself in any of several different ways, results of a retrospective multicenter study showed.

“The most striking thing that we learned from this study is that pediatric melanoma can present in so many different ways, and it’s distinct from the adult population in that we see more presentations associated with congenital nevi, or spitz melanoma, which is a special class of pigmented lesions that looks a little different under the microscope,” Elena B. Hawryluk, MD, PhD, of the department of dermatology at Massachusetts General Hospital (MGH) and Harvard University, Boston, said in an interview. Dr. Hawryluk is lead author of the study, which was published online ahead of print in the Journal of the American Academy of Dermatology.

Dr. Hawryluk and colleagues at MGH and 11 other centers conducted a retrospective review of all cases of fatal pediatric melanoma among patients younger than 20 years diagnosed from late 1994 through early 2017.

They identified a total of 38 fatal cases over more than 2 decades. The cases were distinguished primarily by their heterogeneous clinical presentation and by the diversity of the patients, their precursor lesions, and the tumor histopathology, she said in an interview.

“We were surprised to find that patients with each of these presentations could end up with a fatal course, it wasn’t just all the adolescents, or all the patients with giant congenital nevi; it really presented quite diversely.”
 

Rare malignancy

Melanoma is far less common in the pediatric population than in adults, with an annual incidence of 18 per 1 million among adolescents aged 15-18 years, and 1 per 1 million in children under 10 years, the authors noted.

“Melanoma in children and adolescents often has distinct clinical presentations such as association with a congenital melanocytic nevus (CMN), spitzoid melanoma, or amelanotic melanoma, which are more rarely observed in adult melanoma patients. Unique pediatric-specific clinical detection criteria have been proposed to highlight these differences, such as a tendency to present amelanotically,” they wrote.

Factors associated with worse prognosis, such as higher Breslow thickness and mitotic index, are more frequently present at the time of diagnosis in children compared with adults, particularly those diagnosed before age 11 years.

“It is unclear if this difference is secondary to diagnostic delays due to low clinical suspicion, atypical clinical presentations, or more rapid tumor growth rate, as many childhood melanomas are of nodular or spitzoid subtypes,” Dr. Hawryluk and her coauthors wrote.
 

Study details

The investigators sought to characterize the clinical and histopathologic features of fatal pediatric melanomas.

They found that 21 of the 38 patients (57%) were of White heritage, 7 (19%) were of Hispanic or Latino background, 1 (3%) was of Asian lineage, and 1 each were of Black African American or Black Hispanic background. The remaining children were classified as “other” or did not have their ethnic backgrounds recorded.

The “striking prevalence” of Hispanic patients observed in the study is consistent with surveillance reports of an increasing incidence of melanoma among children of Hispanic background, they noted.

The mean age at diagnosis was 12.7 years, and the mean age at death was 15.6 years.

Of the 16 cases with known identifiable disease subtypes, 8 (50%) were nodular, 5 (31%) were superficial spreading, and 3 (19%) were spitzoid melanomas. Of the 38 fatal melanomas, 10 were thought to have originated from congenital melanocytic nevi.
 

Outlook improving

Recent therapeutic breakthroughs such as targeted agents and immunotherapy with checkpoint inhibitors augur well for children diagnosed with melanoma, Dr. Hawryluk said.

“Fortunately, it’s not superaggressive in children at high frequency, so we generally use adult algorithms to inform treatment decisions,” she said. “It’s just important to note that melanomas that arise in congenital nevi tend to have different driver mutations than those that arise in older patients who may have lots of sun exposure.”

“Nowadays, we’re lucky to have a lot of extra tests and workups so that, if a patient does have metastatic or advance disease, they can have a better genetic profile that would guide our choice of medications,” she added.

The study was supported by a Pediatric Dermatology Research Alliance Study Support grant and Society for Pediatric Dermatology, Pediatric Dermatology Research Alliance Pilot award. Dr. Hawryluk is supported by the Dermatology Foundation and the Harvard Medical School Eleanor and Miles Shore Fellowship award. The authors reported no conflicts of interest.

SOURCE: Hawryluk EB et al. J Am Acad Dermatol. 2020 Jul 1. doi: 10.1016/j.jaad.2020.06.1010.

The color hue of a person’s skin is the most obvious criteria for society to judge a person and has always been deeply rooted in racism. Discrimination based on skin color is called colorism and is usually meted out by members of the same race and in the same family. The general belief is that someone with a lighter complexion is more beautiful, intelligent, or valuable than someone with a darker complexion. The term colorism can be widely applied in our assessment of conflict within families and society. The following case example gives guidance for psychiatrists faced with a family where colorism fuels family conflict.

Meeting the family

The Jaspers, a Black family, arrive at the psychiatrist’s office. They come in and look around before they choose their seats. Dr. Sally watches who sits next to whom and how they organize themselves in the office. After brief introductions, Mr. Jaspers begins, explaining why they are there.

“We are always fighting. We need this to stop. She, my wife, contradicts me all the time. Our kids are getting frustrated, and Bruce is acting out in school. He got in a fight again last week.”

Everyone looks at Bruce. He is darker skinned than the other siblings and carries all the African features in a family that favors the lighter end of the color spectrum. He sits next to his mother who leans into him. Mrs. Jaspers speaks next.

“Bruce gets picked on in school.”

Mr. Jaspers responds, “Well, if you didn’t run in there all the time and take him out, maybe he would learn how to deal with it better!”

“But they are mistreating him,” Mrs. Jaspers says.

The other children look away and play with their phones. Dr. Sally wonders whether this is a pattern: The parents fighting about how to deal with Bruce and his difficulties in the world – and the other siblings getting ignored and not included.

Dr. Sally asks Mrs. Jaspers for more details. She tells a narrative that is a strong thread in this family’s story.

“As you can see, Bruce is darker than the rest of our children. When we see the rest of our family, they all comment on what good skin and light coloring and good hair the other children have. Bruce just sits there. He is always being left out. He doesn’t speak up for himself. Maybe they think he can’t hear them, but I know he does and it affects him. They say the others are more intelligent, but I don’t think that is true. Bruce just gets picked on in school and he doesn’t feel like he matters. He doesn’t say anything, so maybe people think he doesn’t care, but I know he does.”

Dr. Sally turns to Bruce, who is still sitting silently next to his mother, his head down.

“Bruce, what do you have to say?”

Bruce shrugs his shoulders. His siblings still do not want to be drawn in and are otherwise occupied.

At this point, Dr. Sally might be thinking that she could see Bruce alone to assess his depression/self-esteem and maybe find ways to try to build him up. She does not want this to be an opportunity wasted. The goal is to work with the family to get Bruce where he needs to be faster and help the whole family.

Dr. Sally presses on. “Mr. Jaspers, what is your opinion?”

“She babies him. She treats him differently from the other kids. She is driving a wedge between him and his siblings. We fight about it all the time. She is driving a wedge between us, too.”

Mrs. Jaspers jumps in: “But you don’t know what it is like! When I was the only Black person in math class, I got picked on all the time! It made me self-conscious, and I couldn’t do my work. “

The other siblings look up briefly then back down at their devices. Dr. Sally asks them as a group:

“Can I ask you a question as a family? Can I ask the children a question?” They look up again. “Is this what goes on at home?” They all nod but offer no details.

Dr. Sally asks the oldest: “How does this affect your relationship with Bruce?”

They all look back and forth at each other. There is another long silence.

“See!” says Mr. Jaspers! “You can't protect him forever, and you are just ostracizing him from the rest of us! “

“But, but, he, he needs to learn different things. He is different. He faces different struggles. The police will stop him more. I am afraid for him.” Mrs. Jaspers starts to cry.

“You can’t protect him forever,” says her husband, gently reaching over to her.

Bruce has psychologically disappeared from the room, hiding behind his mother, who is now the largest and neediest presence in the room. Mr. Jaspers looks at Dr. Sally helplessly.

Dr. Sally asks the important question to the whole family.

“How do you all think this should work? If you don’t think Mrs. Jaspers is right, what do you think should be the way forward?”

This question is the turning point and indicates that Dr. Sally sees that the solution lies in how the family wants to manage things.

“I believe that your whole family has the answers, that you all have thought through this situation much more deeply and for much longer than I have. I am just hearing about it, and I am White and don’t have this experience. I have faith in your family, that with an opportunity to openly discuss this issue, that this knot can be unraveled. It does not mean that there are not more knots to unravel. For today, how to help you all help Bruce, is the work."

Dr. Sally talks to everyone but finishes up by looking at Mr. Jaspers, who has indicated that Bruce is part of the family and should not be treated differently from the other children.

Sean, the oldest sibling, now pipes up: “Bruce gets everything he wants. Mum spoils him; she always takes his side if there are arguments. Bruce knows this, and he steals our stuff because he knows he will get away with it.”

Bruce is quiet and leans in more to his mother. Dr. Sally motions to the mother not to speak.

“Is this true, Bruce?” Silence speaks that the answer is yes. The disparities in the family are aired for a while longer.

“Mrs. Jaspers, it is now your turn to respond.”

“Bruce is darker and faces more challenges than the others; he needs more protection and to know that he is loved.”

“Your family seems to think otherwise. They seem to think that your protection, while admirable, needs to be tempered to allow him to grow into a man who can stand on his own feet.”

Dr. Sally guides the family as a whole to a place where they can agree on the problem. The problem is now framed as a mother who cares too much and is too protective of Bruce but now her love and care need to be tempered. As a mother, she feels that it is her duty to protect her most vulnerable son. The family knows that Bruce will face more social scrutiny than the others, that he will have more internal struggles with self-worth than the others. How can the family help?

This conceptualization causes the family to look searchingly at one another. It is nothing they haven’t thought about privately, but this is the first time they are together thinking about it.

Dr. Sally says that she can help by providing time and space for them to wok through this together. They all agree to come back the following week with some thoughts about moving forward.
 

Offering perspective on colorism

In her book “Facing the Black Shadow,” couples and family therapist Marlene F. Watson, PhD, discusses colorism.

“African Americans still have a tough time talking about slavery – the origin of colorism. Seriously, what can we really expect to change without acknowledging and challenging the psychological residuals of slavery in our families and communities? What doesn’t get resolved in one generation is passed on to the next so our issues from slavery go from one generation to the next.”

Dr. Watson continues: “Confronting the secret about skin color in our families and communities is necessary for all Black girls to feel lovable, worthy, and deserving of care and for all Black boys to feel their value lies within them, not a dark, light, bright, near-white or White woman. African Americans need to get that preferring light over dark or dark over light is problematic for all of us. Skin color preferences in the African American community follow society’s racial hierarchy. African Americans as a group are at the bottom in the larger society and dark-skinned African Americans are at the bottom in the Black community.”

Dr. Watson suggests a way that we can help our patients. She encourages families to draw a family tree that tracks the family’s beliefs and patterns about skin color. Her advice is to ask each family member, from oldest to youngest, to identify the spoken and unspoken skin color beliefs he or she experiences in the family. Ask about skin color beliefs from outside that affect family members, and what each person thinks the family could do to stop promoting the “less than/better than” mentality that is often present with skin color assignment.



Thank you to Lynette Ramsingh Barros, who collaborated on creating the case.
 

Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest.

The color hue of a person’s skin is the most obvious criteria for society to judge a person and has always been deeply rooted in racism. Discrimination based on skin color is called colorism and is usually meted out by members of the same race and in the same family. The general belief is that someone with a lighter complexion is more beautiful, intelligent, or valuable than someone with a darker complexion. The term colorism can be widely applied in our assessment of conflict within families and society. The following case example gives guidance for psychiatrists faced with a family where colorism fuels family conflict.

Meeting the family

The Jaspers, a Black family, arrive at the psychiatrist’s office. They come in and look around before they choose their seats. Dr. Sally watches who sits next to whom and how they organize themselves in the office. After brief introductions, Mr. Jaspers begins, explaining why they are there.

“We are always fighting. We need this to stop. She, my wife, contradicts me all the time. Our kids are getting frustrated, and Bruce is acting out in school. He got in a fight again last week.”

Everyone looks at Bruce. He is darker skinned than the other siblings and carries all the African features in a family that favors the lighter end of the color spectrum. He sits next to his mother who leans into him. Mrs. Jaspers speaks next.

“Bruce gets picked on in school.”

Mr. Jaspers responds, “Well, if you didn’t run in there all the time and take him out, maybe he would learn how to deal with it better!”

“But they are mistreating him,” Mrs. Jaspers says.

The other children look away and play with their phones. Dr. Sally wonders whether this is a pattern: The parents fighting about how to deal with Bruce and his difficulties in the world – and the other siblings getting ignored and not included.

Dr. Sally asks Mrs. Jaspers for more details. She tells a narrative that is a strong thread in this family’s story.

“As you can see, Bruce is darker than the rest of our children. When we see the rest of our family, they all comment on what good skin and light coloring and good hair the other children have. Bruce just sits there. He is always being left out. He doesn’t speak up for himself. Maybe they think he can’t hear them, but I know he does and it affects him. They say the others are more intelligent, but I don’t think that is true. Bruce just gets picked on in school and he doesn’t feel like he matters. He doesn’t say anything, so maybe people think he doesn’t care, but I know he does.”

Dr. Sally turns to Bruce, who is still sitting silently next to his mother, his head down.

“Bruce, what do you have to say?”

Bruce shrugs his shoulders. His siblings still do not want to be drawn in and are otherwise occupied.

At this point, Dr. Sally might be thinking that she could see Bruce alone to assess his depression/self-esteem and maybe find ways to try to build him up. She does not want this to be an opportunity wasted. The goal is to work with the family to get Bruce where he needs to be faster and help the whole family.

Dr. Sally presses on. “Mr. Jaspers, what is your opinion?”

“She babies him. She treats him differently from the other kids. She is driving a wedge between him and his siblings. We fight about it all the time. She is driving a wedge between us, too.”

Mrs. Jaspers jumps in: “But you don’t know what it is like! When I was the only Black person in math class, I got picked on all the time! It made me self-conscious, and I couldn’t do my work. “

The other siblings look up briefly then back down at their devices. Dr. Sally asks them as a group:

“Can I ask you a question as a family? Can I ask the children a question?” They look up again. “Is this what goes on at home?” They all nod but offer no details.

Dr. Sally asks the oldest: “How does this affect your relationship with Bruce?”

They all look back and forth at each other. There is another long silence.

“See!” says Mr. Jaspers! “You can't protect him forever, and you are just ostracizing him from the rest of us! “

“But, but, he, he needs to learn different things. He is different. He faces different struggles. The police will stop him more. I am afraid for him.” Mrs. Jaspers starts to cry.

“You can’t protect him forever,” says her husband, gently reaching over to her.

Bruce has psychologically disappeared from the room, hiding behind his mother, who is now the largest and neediest presence in the room. Mr. Jaspers looks at Dr. Sally helplessly.

Dr. Sally asks the important question to the whole family.

“How do you all think this should work? If you don’t think Mrs. Jaspers is right, what do you think should be the way forward?”

This question is the turning point and indicates that Dr. Sally sees that the solution lies in how the family wants to manage things.

“I believe that your whole family has the answers, that you all have thought through this situation much more deeply and for much longer than I have. I am just hearing about it, and I am White and don’t have this experience. I have faith in your family, that with an opportunity to openly discuss this issue, that this knot can be unraveled. It does not mean that there are not more knots to unravel. For today, how to help you all help Bruce, is the work."

Dr. Sally talks to everyone but finishes up by looking at Mr. Jaspers, who has indicated that Bruce is part of the family and should not be treated differently from the other children.

Sean, the oldest sibling, now pipes up: “Bruce gets everything he wants. Mum spoils him; she always takes his side if there are arguments. Bruce knows this, and he steals our stuff because he knows he will get away with it.”

Bruce is quiet and leans in more to his mother. Dr. Sally motions to the mother not to speak.

“Is this true, Bruce?” Silence speaks that the answer is yes. The disparities in the family are aired for a while longer.

“Mrs. Jaspers, it is now your turn to respond.”

“Bruce is darker and faces more challenges than the others; he needs more protection and to know that he is loved.”

“Your family seems to think otherwise. They seem to think that your protection, while admirable, needs to be tempered to allow him to grow into a man who can stand on his own feet.”

Dr. Sally guides the family as a whole to a place where they can agree on the problem. The problem is now framed as a mother who cares too much and is too protective of Bruce but now her love and care need to be tempered. As a mother, she feels that it is her duty to protect her most vulnerable son. The family knows that Bruce will face more social scrutiny than the others, that he will have more internal struggles with self-worth than the others. How can the family help?

This conceptualization causes the family to look searchingly at one another. It is nothing they haven’t thought about privately, but this is the first time they are together thinking about it.

Dr. Sally says that she can help by providing time and space for them to wok through this together. They all agree to come back the following week with some thoughts about moving forward.
 

Offering perspective on colorism

In her book “Facing the Black Shadow,” couples and family therapist Marlene F. Watson, PhD, discusses colorism.

“African Americans still have a tough time talking about slavery – the origin of colorism. Seriously, what can we really expect to change without acknowledging and challenging the psychological residuals of slavery in our families and communities? What doesn’t get resolved in one generation is passed on to the next so our issues from slavery go from one generation to the next.”

Dr. Watson continues: “Confronting the secret about skin color in our families and communities is necessary for all Black girls to feel lovable, worthy, and deserving of care and for all Black boys to feel their value lies within them, not a dark, light, bright, near-white or White woman. African Americans need to get that preferring light over dark or dark over light is problematic for all of us. Skin color preferences in the African American community follow society’s racial hierarchy. African Americans as a group are at the bottom in the larger society and dark-skinned African Americans are at the bottom in the Black community.”

Dr. Watson suggests a way that we can help our patients. She encourages families to draw a family tree that tracks the family’s beliefs and patterns about skin color. Her advice is to ask each family member, from oldest to youngest, to identify the spoken and unspoken skin color beliefs he or she experiences in the family. Ask about skin color beliefs from outside that affect family members, and what each person thinks the family could do to stop promoting the “less than/better than” mentality that is often present with skin color assignment.



Thank you to Lynette Ramsingh Barros, who collaborated on creating the case.
 

Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest.

The color hue of a person’s skin is the most obvious criteria for society to judge a person and has always been deeply rooted in racism. Discrimination based on skin color is called colorism and is usually meted out by members of the same race and in the same family. The general belief is that someone with a lighter complexion is more beautiful, intelligent, or valuable than someone with a darker complexion. The term colorism can be widely applied in our assessment of conflict within families and society. The following case example gives guidance for psychiatrists faced with a family where colorism fuels family conflict.

Meeting the family

The Jaspers, a Black family, arrive at the psychiatrist’s office. They come in and look around before they choose their seats. Dr. Sally watches who sits next to whom and how they organize themselves in the office. After brief introductions, Mr. Jaspers begins, explaining why they are there.

“We are always fighting. We need this to stop. She, my wife, contradicts me all the time. Our kids are getting frustrated, and Bruce is acting out in school. He got in a fight again last week.”

Everyone looks at Bruce. He is darker skinned than the other siblings and carries all the African features in a family that favors the lighter end of the color spectrum. He sits next to his mother who leans into him. Mrs. Jaspers speaks next.

“Bruce gets picked on in school.”

Mr. Jaspers responds, “Well, if you didn’t run in there all the time and take him out, maybe he would learn how to deal with it better!”

“But they are mistreating him,” Mrs. Jaspers says.

The other children look away and play with their phones. Dr. Sally wonders whether this is a pattern: The parents fighting about how to deal with Bruce and his difficulties in the world – and the other siblings getting ignored and not included.

Dr. Sally asks Mrs. Jaspers for more details. She tells a narrative that is a strong thread in this family’s story.

“As you can see, Bruce is darker than the rest of our children. When we see the rest of our family, they all comment on what good skin and light coloring and good hair the other children have. Bruce just sits there. He is always being left out. He doesn’t speak up for himself. Maybe they think he can’t hear them, but I know he does and it affects him. They say the others are more intelligent, but I don’t think that is true. Bruce just gets picked on in school and he doesn’t feel like he matters. He doesn’t say anything, so maybe people think he doesn’t care, but I know he does.”

Dr. Sally turns to Bruce, who is still sitting silently next to his mother, his head down.

“Bruce, what do you have to say?”

Bruce shrugs his shoulders. His siblings still do not want to be drawn in and are otherwise occupied.

At this point, Dr. Sally might be thinking that she could see Bruce alone to assess his depression/self-esteem and maybe find ways to try to build him up. She does not want this to be an opportunity wasted. The goal is to work with the family to get Bruce where he needs to be faster and help the whole family.

Dr. Sally presses on. “Mr. Jaspers, what is your opinion?”

“She babies him. She treats him differently from the other kids. She is driving a wedge between him and his siblings. We fight about it all the time. She is driving a wedge between us, too.”

Mrs. Jaspers jumps in: “But you don’t know what it is like! When I was the only Black person in math class, I got picked on all the time! It made me self-conscious, and I couldn’t do my work. “

The other siblings look up briefly then back down at their devices. Dr. Sally asks them as a group:

“Can I ask you a question as a family? Can I ask the children a question?” They look up again. “Is this what goes on at home?” They all nod but offer no details.

Dr. Sally asks the oldest: “How does this affect your relationship with Bruce?”

They all look back and forth at each other. There is another long silence.

“See!” says Mr. Jaspers! “You can't protect him forever, and you are just ostracizing him from the rest of us! “

“But, but, he, he needs to learn different things. He is different. He faces different struggles. The police will stop him more. I am afraid for him.” Mrs. Jaspers starts to cry.

“You can’t protect him forever,” says her husband, gently reaching over to her.

Bruce has psychologically disappeared from the room, hiding behind his mother, who is now the largest and neediest presence in the room. Mr. Jaspers looks at Dr. Sally helplessly.

Dr. Sally asks the important question to the whole family.

“How do you all think this should work? If you don’t think Mrs. Jaspers is right, what do you think should be the way forward?”

This question is the turning point and indicates that Dr. Sally sees that the solution lies in how the family wants to manage things.

“I believe that your whole family has the answers, that you all have thought through this situation much more deeply and for much longer than I have. I am just hearing about it, and I am White and don’t have this experience. I have faith in your family, that with an opportunity to openly discuss this issue, that this knot can be unraveled. It does not mean that there are not more knots to unravel. For today, how to help you all help Bruce, is the work."

Dr. Sally talks to everyone but finishes up by looking at Mr. Jaspers, who has indicated that Bruce is part of the family and should not be treated differently from the other children.

Sean, the oldest sibling, now pipes up: “Bruce gets everything he wants. Mum spoils him; she always takes his side if there are arguments. Bruce knows this, and he steals our stuff because he knows he will get away with it.”

Bruce is quiet and leans in more to his mother. Dr. Sally motions to the mother not to speak.

“Is this true, Bruce?” Silence speaks that the answer is yes. The disparities in the family are aired for a while longer.

“Mrs. Jaspers, it is now your turn to respond.”

“Bruce is darker and faces more challenges than the others; he needs more protection and to know that he is loved.”

“Your family seems to think otherwise. They seem to think that your protection, while admirable, needs to be tempered to allow him to grow into a man who can stand on his own feet.”

Dr. Sally guides the family as a whole to a place where they can agree on the problem. The problem is now framed as a mother who cares too much and is too protective of Bruce but now her love and care need to be tempered. As a mother, she feels that it is her duty to protect her most vulnerable son. The family knows that Bruce will face more social scrutiny than the others, that he will have more internal struggles with self-worth than the others. How can the family help?

This conceptualization causes the family to look searchingly at one another. It is nothing they haven’t thought about privately, but this is the first time they are together thinking about it.

Dr. Sally says that she can help by providing time and space for them to wok through this together. They all agree to come back the following week with some thoughts about moving forward.
 

Offering perspective on colorism

In her book “Facing the Black Shadow,” couples and family therapist Marlene F. Watson, PhD, discusses colorism.

“African Americans still have a tough time talking about slavery – the origin of colorism. Seriously, what can we really expect to change without acknowledging and challenging the psychological residuals of slavery in our families and communities? What doesn’t get resolved in one generation is passed on to the next so our issues from slavery go from one generation to the next.”

Dr. Watson continues: “Confronting the secret about skin color in our families and communities is necessary for all Black girls to feel lovable, worthy, and deserving of care and for all Black boys to feel their value lies within them, not a dark, light, bright, near-white or White woman. African Americans need to get that preferring light over dark or dark over light is problematic for all of us. Skin color preferences in the African American community follow society’s racial hierarchy. African Americans as a group are at the bottom in the larger society and dark-skinned African Americans are at the bottom in the Black community.”

Dr. Watson suggests a way that we can help our patients. She encourages families to draw a family tree that tracks the family’s beliefs and patterns about skin color. Her advice is to ask each family member, from oldest to youngest, to identify the spoken and unspoken skin color beliefs he or she experiences in the family. Ask about skin color beliefs from outside that affect family members, and what each person thinks the family could do to stop promoting the “less than/better than” mentality that is often present with skin color assignment.



Thank you to Lynette Ramsingh Barros, who collaborated on creating the case.
 

Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest.

Child cases moved up to 9.5% of the cumulative COVID-19 population as the United States added almost 44,000 pediatric cases for the week ending Aug. 27, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

The new cases bring the cumulative number of infected children to over 476,000, and that figure represents 9.5% of the over 5 million COVID-19 cases reported among all ages, the AAP and the CHA said in their weekly report. The cumulative number of children covers 49 states (New York is not reporting age distribution), the District of Columbia, New York City, Puerto Rico, and Guam.

From lowest to highest, the states occupying opposite ends of the cumulative proportion spectrum are New Jersey at 3.4% – New York City was lower with a 3.2% figure but is not a state – and Wyoming at 18.3%, the report showed.

Children represent more than 15% of all reported COVID-19 cases in five other states: Tennessee (17.1%), North Dakota (16.0%), Alaska (15.9%), New Mexico (15.7%), and Minnesota (15.1%). The states just above New Jersey are Florida (5.8%), Connecticut (5.9%), and Massachusetts (6.7%). Texas has a rate of 5.6% but has reported age for only 8% of confirmed cases, the AAP and CHA noted.

Children make up a much lower share of COVID-19 hospitalizations – 1.7% of the cumulative number for all ages – although that figure has been slowly rising over the course of the pandemic: it was 1.2% on July 9 and 0.9% on May 8. Arizona (4.1%) is the highest of the 22 states reporting age for hospitalizations and Hawaii (0.6%) is the lowest, based on the AAP/CHA data.

Mortality figures for children continue to be even lower. Nationwide, 0.07% of all COVID-19 deaths occurred in children, and 19 of the 43 states reporting age distributions have had no deaths yet. Pediatric deaths totaled 101 as of Aug. 27, the two groups reported.

rfranki@mdedge.com

Child cases moved up to 9.5% of the cumulative COVID-19 population as the United States added almost 44,000 pediatric cases for the week ending Aug. 27, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

The new cases bring the cumulative number of infected children to over 476,000, and that figure represents 9.5% of the over 5 million COVID-19 cases reported among all ages, the AAP and the CHA said in their weekly report. The cumulative number of children covers 49 states (New York is not reporting age distribution), the District of Columbia, New York City, Puerto Rico, and Guam.

From lowest to highest, the states occupying opposite ends of the cumulative proportion spectrum are New Jersey at 3.4% – New York City was lower with a 3.2% figure but is not a state – and Wyoming at 18.3%, the report showed.

Children represent more than 15% of all reported COVID-19 cases in five other states: Tennessee (17.1%), North Dakota (16.0%), Alaska (15.9%), New Mexico (15.7%), and Minnesota (15.1%). The states just above New Jersey are Florida (5.8%), Connecticut (5.9%), and Massachusetts (6.7%). Texas has a rate of 5.6% but has reported age for only 8% of confirmed cases, the AAP and CHA noted.

Children make up a much lower share of COVID-19 hospitalizations – 1.7% of the cumulative number for all ages – although that figure has been slowly rising over the course of the pandemic: it was 1.2% on July 9 and 0.9% on May 8. Arizona (4.1%) is the highest of the 22 states reporting age for hospitalizations and Hawaii (0.6%) is the lowest, based on the AAP/CHA data.

Mortality figures for children continue to be even lower. Nationwide, 0.07% of all COVID-19 deaths occurred in children, and 19 of the 43 states reporting age distributions have had no deaths yet. Pediatric deaths totaled 101 as of Aug. 27, the two groups reported.

rfranki@mdedge.com

Child cases moved up to 9.5% of the cumulative COVID-19 population as the United States added almost 44,000 pediatric cases for the week ending Aug. 27, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

The new cases bring the cumulative number of infected children to over 476,000, and that figure represents 9.5% of the over 5 million COVID-19 cases reported among all ages, the AAP and the CHA said in their weekly report. The cumulative number of children covers 49 states (New York is not reporting age distribution), the District of Columbia, New York City, Puerto Rico, and Guam.

From lowest to highest, the states occupying opposite ends of the cumulative proportion spectrum are New Jersey at 3.4% – New York City was lower with a 3.2% figure but is not a state – and Wyoming at 18.3%, the report showed.

Children represent more than 15% of all reported COVID-19 cases in five other states: Tennessee (17.1%), North Dakota (16.0%), Alaska (15.9%), New Mexico (15.7%), and Minnesota (15.1%). The states just above New Jersey are Florida (5.8%), Connecticut (5.9%), and Massachusetts (6.7%). Texas has a rate of 5.6% but has reported age for only 8% of confirmed cases, the AAP and CHA noted.

Children make up a much lower share of COVID-19 hospitalizations – 1.7% of the cumulative number for all ages – although that figure has been slowly rising over the course of the pandemic: it was 1.2% on July 9 and 0.9% on May 8. Arizona (4.1%) is the highest of the 22 states reporting age for hospitalizations and Hawaii (0.6%) is the lowest, based on the AAP/CHA data.

Mortality figures for children continue to be even lower. Nationwide, 0.07% of all COVID-19 deaths occurred in children, and 19 of the 43 states reporting age distributions have had no deaths yet. Pediatric deaths totaled 101 as of Aug. 27, the two groups reported.

rfranki@mdedge.com