Atopic Dermatitis

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

Severe atopic eczema could significantly increase the risk of cardiovascular disease, including stroke and heart failure, according to a case-control study published online May 23 in BMJ.

In a population-based cohort study, researchers compared the electronic health records of 387,439 adults with eczema and 1,528,477 patients without eczema in the United Kingddom, matched according to age, sex, general practice, and calendar time, during 1998-2015. Patients were followed up for a median of 5.1 years

With the exception of cardiovascular death, atopic eczema was associated with all cardiovascular outcomes (MI, unstable angina, heart failure, atrial fibrillation, and stroke). The associations were stronger for severe atopic eczema, with significantly higher risks of MI, unstable angina, atrial fibrillation, stroke, cardiovascular death, and coronary revascularization among individuals with severe atopic eczema, compared with controls.

After adjustment for potential mediators such as body mass index, smoking, hyperlipidemia, diabetes, and severe alcohol use, individuals with severe eczema had a significant 37% increased risk of MI, 67% greater risk of heart failure, 35% greater risk of atrial fibrillation, 30% greater risk of cardiovascular death, and 36% greater risk of coronary revascularization, compared with controls with no eczema.

Increased cardiovascular risks also were seen in individuals whose atopic eczema was active more than half the time at follow-up. This group had a 37% greater risk of heart failure, 36% greater risk of unstable angina, and 19% greater risk of stroke, as well as significantly elevated risks of MI, atrial fibrillation, cardiovascular death, and coronary revascularization, compared with those without eczema.

Overall, atopic eczema contributed around 2.4% of the population-attributable risk for unstable angina, and 1.9% for heart failure (the highest population attributable risks). Ethnicity or high-dose corticosteroid use did not significantly impact outcomes.

Richard J. Silverwood, PhD, from the London School of Hygiene and Tropical Medicine, and his coauthors wrote that previous work examining the relationship between atopic eczema and cardiovascular disease had shown inconsistent outcomes, with some studies even pointing to a possible protective effect of mild atopic eczema.

SOURCE: Silverwood R et al. BMJ 2018 May 23;361:k1786. doi: 10.1136/bmj.k1786.

Severe atopic eczema could significantly increase the risk of cardiovascular disease, including stroke and heart failure, according to a case-control study published online May 23 in BMJ.

In a population-based cohort study, researchers compared the electronic health records of 387,439 adults with eczema and 1,528,477 patients without eczema in the United Kingddom, matched according to age, sex, general practice, and calendar time, during 1998-2015. Patients were followed up for a median of 5.1 years

With the exception of cardiovascular death, atopic eczema was associated with all cardiovascular outcomes (MI, unstable angina, heart failure, atrial fibrillation, and stroke). The associations were stronger for severe atopic eczema, with significantly higher risks of MI, unstable angina, atrial fibrillation, stroke, cardiovascular death, and coronary revascularization among individuals with severe atopic eczema, compared with controls.

After adjustment for potential mediators such as body mass index, smoking, hyperlipidemia, diabetes, and severe alcohol use, individuals with severe eczema had a significant 37% increased risk of MI, 67% greater risk of heart failure, 35% greater risk of atrial fibrillation, 30% greater risk of cardiovascular death, and 36% greater risk of coronary revascularization, compared with controls with no eczema.

Increased cardiovascular risks also were seen in individuals whose atopic eczema was active more than half the time at follow-up. This group had a 37% greater risk of heart failure, 36% greater risk of unstable angina, and 19% greater risk of stroke, as well as significantly elevated risks of MI, atrial fibrillation, cardiovascular death, and coronary revascularization, compared with those without eczema.

Overall, atopic eczema contributed around 2.4% of the population-attributable risk for unstable angina, and 1.9% for heart failure (the highest population attributable risks). Ethnicity or high-dose corticosteroid use did not significantly impact outcomes.

Richard J. Silverwood, PhD, from the London School of Hygiene and Tropical Medicine, and his coauthors wrote that previous work examining the relationship between atopic eczema and cardiovascular disease had shown inconsistent outcomes, with some studies even pointing to a possible protective effect of mild atopic eczema.

SOURCE: Silverwood R et al. BMJ 2018 May 23;361:k1786. doi: 10.1136/bmj.k1786.

Severe atopic eczema could significantly increase the risk of cardiovascular disease, including stroke and heart failure, according to a case-control study published online May 23 in BMJ.

In a population-based cohort study, researchers compared the electronic health records of 387,439 adults with eczema and 1,528,477 patients without eczema in the United Kingddom, matched according to age, sex, general practice, and calendar time, during 1998-2015. Patients were followed up for a median of 5.1 years

With the exception of cardiovascular death, atopic eczema was associated with all cardiovascular outcomes (MI, unstable angina, heart failure, atrial fibrillation, and stroke). The associations were stronger for severe atopic eczema, with significantly higher risks of MI, unstable angina, atrial fibrillation, stroke, cardiovascular death, and coronary revascularization among individuals with severe atopic eczema, compared with controls.

After adjustment for potential mediators such as body mass index, smoking, hyperlipidemia, diabetes, and severe alcohol use, individuals with severe eczema had a significant 37% increased risk of MI, 67% greater risk of heart failure, 35% greater risk of atrial fibrillation, 30% greater risk of cardiovascular death, and 36% greater risk of coronary revascularization, compared with controls with no eczema.

Increased cardiovascular risks also were seen in individuals whose atopic eczema was active more than half the time at follow-up. This group had a 37% greater risk of heart failure, 36% greater risk of unstable angina, and 19% greater risk of stroke, as well as significantly elevated risks of MI, atrial fibrillation, cardiovascular death, and coronary revascularization, compared with those without eczema.

Overall, atopic eczema contributed around 2.4% of the population-attributable risk for unstable angina, and 1.9% for heart failure (the highest population attributable risks). Ethnicity or high-dose corticosteroid use did not significantly impact outcomes.

Richard J. Silverwood, PhD, from the London School of Hygiene and Tropical Medicine, and his coauthors wrote that previous work examining the relationship between atopic eczema and cardiovascular disease had shown inconsistent outcomes, with some studies even pointing to a possible protective effect of mild atopic eczema.

SOURCE: Silverwood R et al. BMJ 2018 May 23;361:k1786. doi: 10.1136/bmj.k1786.

Roseomonas mucosa bacteria obtained from healthy volunteers without atopic dermatitis reduced the severity of the disorder in a small, early-phase study of 10 adults and 5 children with atopic dermatitis.

The Beginning Assessment of Cutaneous Treatment Efficacy of Roseomonas in Atopic Dermatitis trial; BACTERiAD I/II study, an open-label phase I/II trial, first looked at the therapeutic use of R. mucosa in 10 adults aged 18 years or older. Three sucrose mixtures with increasing doses of live R. mucosa bacteria were topically applied to two body areas – the antecubital fossae and a body surface of their choice – twice per week for 2 weeks per dose. At 6 weeks, the patients stopped using the mixtures and followed a 4-week washout phase.

Treatment was found to reduce mean antecubital SCORAD (SCORing Atopic Dermatitis) scores by 59.8%. Reduction in pruritus was even more pronounced, with a mean decrease of 78.5%. Treating the hands did not improve disease severity, even in patients whose symptoms improved in other body areas. One explanation may be the increased exposure of the hands to topical antimicrobials and environmental exposures, the researchers noted.

With the success in the adult cohort, the researchers enrolled five children aged 7-17 years in the study. These patients were treated twice weekly for 16 weeks. The pediatric patients experienced a mean decrease of 70.3% in their SCORAD scores. The mean decrease in pruritis was 78.8%.

All adults who responded continued to report improved symptoms after the washout period. The pediatric patients are now being evaluated in a washout period.

Four patients did not respond; three of them had a family history of AD persisting into adulthood. “The association between these complex medical histories and the lack of clinical response suggests that differences in heritable host and/or microbial factors may impact treatment responses,” wrote Ian A. Myles, MD, and his colleagues.

“Overall, our findings suggest the safety of topical R. mucosa therapy and justify continuation of our ongoing trial to assess safety and activity in a pediatric cohort of patients with AD. These studies will additionally assess changes in host serum markers, skin metabolomics, and the skin microbiota by culture and genomic methods.”

The researchers noted that expanding to the pediatric population will deepen understanding of topical microbiome transplantation and lay the foundation for placebo-controlled trials to assess efficacy.

This work was supported by the Intramural Research Program of the National Institutes of Allergy and Infectious Diseases and the National Institutes of Health. The researchers had no disclosures.

ilacy@mdedge.com

SOURCE: Myles IA et al. JCI Insight. 2018 May 3. doi: 10.1172/jci.insight.120608.

Roseomonas mucosa bacteria obtained from healthy volunteers without atopic dermatitis reduced the severity of the disorder in a small, early-phase study of 10 adults and 5 children with atopic dermatitis.

The Beginning Assessment of Cutaneous Treatment Efficacy of Roseomonas in Atopic Dermatitis trial; BACTERiAD I/II study, an open-label phase I/II trial, first looked at the therapeutic use of R. mucosa in 10 adults aged 18 years or older. Three sucrose mixtures with increasing doses of live R. mucosa bacteria were topically applied to two body areas – the antecubital fossae and a body surface of their choice – twice per week for 2 weeks per dose. At 6 weeks, the patients stopped using the mixtures and followed a 4-week washout phase.

Treatment was found to reduce mean antecubital SCORAD (SCORing Atopic Dermatitis) scores by 59.8%. Reduction in pruritus was even more pronounced, with a mean decrease of 78.5%. Treating the hands did not improve disease severity, even in patients whose symptoms improved in other body areas. One explanation may be the increased exposure of the hands to topical antimicrobials and environmental exposures, the researchers noted.

With the success in the adult cohort, the researchers enrolled five children aged 7-17 years in the study. These patients were treated twice weekly for 16 weeks. The pediatric patients experienced a mean decrease of 70.3% in their SCORAD scores. The mean decrease in pruritis was 78.8%.

All adults who responded continued to report improved symptoms after the washout period. The pediatric patients are now being evaluated in a washout period.

Four patients did not respond; three of them had a family history of AD persisting into adulthood. “The association between these complex medical histories and the lack of clinical response suggests that differences in heritable host and/or microbial factors may impact treatment responses,” wrote Ian A. Myles, MD, and his colleagues.

“Overall, our findings suggest the safety of topical R. mucosa therapy and justify continuation of our ongoing trial to assess safety and activity in a pediatric cohort of patients with AD. These studies will additionally assess changes in host serum markers, skin metabolomics, and the skin microbiota by culture and genomic methods.”

The researchers noted that expanding to the pediatric population will deepen understanding of topical microbiome transplantation and lay the foundation for placebo-controlled trials to assess efficacy.

This work was supported by the Intramural Research Program of the National Institutes of Allergy and Infectious Diseases and the National Institutes of Health. The researchers had no disclosures.

ilacy@mdedge.com

SOURCE: Myles IA et al. JCI Insight. 2018 May 3. doi: 10.1172/jci.insight.120608.

Roseomonas mucosa bacteria obtained from healthy volunteers without atopic dermatitis reduced the severity of the disorder in a small, early-phase study of 10 adults and 5 children with atopic dermatitis.

The Beginning Assessment of Cutaneous Treatment Efficacy of Roseomonas in Atopic Dermatitis trial; BACTERiAD I/II study, an open-label phase I/II trial, first looked at the therapeutic use of R. mucosa in 10 adults aged 18 years or older. Three sucrose mixtures with increasing doses of live R. mucosa bacteria were topically applied to two body areas – the antecubital fossae and a body surface of their choice – twice per week for 2 weeks per dose. At 6 weeks, the patients stopped using the mixtures and followed a 4-week washout phase.

Treatment was found to reduce mean antecubital SCORAD (SCORing Atopic Dermatitis) scores by 59.8%. Reduction in pruritus was even more pronounced, with a mean decrease of 78.5%. Treating the hands did not improve disease severity, even in patients whose symptoms improved in other body areas. One explanation may be the increased exposure of the hands to topical antimicrobials and environmental exposures, the researchers noted.

With the success in the adult cohort, the researchers enrolled five children aged 7-17 years in the study. These patients were treated twice weekly for 16 weeks. The pediatric patients experienced a mean decrease of 70.3% in their SCORAD scores. The mean decrease in pruritis was 78.8%.

All adults who responded continued to report improved symptoms after the washout period. The pediatric patients are now being evaluated in a washout period.

Four patients did not respond; three of them had a family history of AD persisting into adulthood. “The association between these complex medical histories and the lack of clinical response suggests that differences in heritable host and/or microbial factors may impact treatment responses,” wrote Ian A. Myles, MD, and his colleagues.

“Overall, our findings suggest the safety of topical R. mucosa therapy and justify continuation of our ongoing trial to assess safety and activity in a pediatric cohort of patients with AD. These studies will additionally assess changes in host serum markers, skin metabolomics, and the skin microbiota by culture and genomic methods.”

The researchers noted that expanding to the pediatric population will deepen understanding of topical microbiome transplantation and lay the foundation for placebo-controlled trials to assess efficacy.

This work was supported by the Intramural Research Program of the National Institutes of Allergy and Infectious Diseases and the National Institutes of Health. The researchers had no disclosures.

ilacy@mdedge.com

SOURCE: Myles IA et al. JCI Insight. 2018 May 3. doi: 10.1172/jci.insight.120608.

How to handle opioid constipation. Bath emollients are a washout for childhood eczema. Does warfarin cause acute kidney injury? And there may be a new option for postpartum depression.

Listen to the MDedge Daily News podcast for all the details on today’s top news.


 

How to handle opioid constipation. Bath emollients are a washout for childhood eczema. Does warfarin cause acute kidney injury? And there may be a new option for postpartum depression.

Listen to the MDedge Daily News podcast for all the details on today’s top news.


 

How to handle opioid constipation. Bath emollients are a washout for childhood eczema. Does warfarin cause acute kidney injury? And there may be a new option for postpartum depression.

Listen to the MDedge Daily News podcast for all the details on today’s top news.


 

Emollient bath additives do not appear to offer any clinical benefit for childhood eczema, according to an open-label randomized trial.

In a trial of 482 children with atopic dermatitis who were randomized to either use of prescribed emollient bath additives regularly for 12 months or no additives, in addition to usual care, there was no significant difference between the two groups in the patient-oriented eczema measure (POEM) – a score of symptoms in the previous week – for the first 16 weeks of treatment, reported Miriam Santer, MD, of the University of Southampton, England, and her coauthors. The mean POEM score was 7.5 in the bath additives group and 8.4 in the no bath additives group.

LucaLorenzelli/Thinkstock

SOURCE: Santer M et al. BMJ 2018 May 2. doi: 10.1136/bmj.k1332
 

Emollient bath additives do not appear to offer any clinical benefit for childhood eczema, according to an open-label randomized trial.

In a trial of 482 children with atopic dermatitis who were randomized to either use of prescribed emollient bath additives regularly for 12 months or no additives, in addition to usual care, there was no significant difference between the two groups in the patient-oriented eczema measure (POEM) – a score of symptoms in the previous week – for the first 16 weeks of treatment, reported Miriam Santer, MD, of the University of Southampton, England, and her coauthors. The mean POEM score was 7.5 in the bath additives group and 8.4 in the no bath additives group.

LucaLorenzelli/Thinkstock

SOURCE: Santer M et al. BMJ 2018 May 2. doi: 10.1136/bmj.k1332
 

Emollient bath additives do not appear to offer any clinical benefit for childhood eczema, according to an open-label randomized trial.

In a trial of 482 children with atopic dermatitis who were randomized to either use of prescribed emollient bath additives regularly for 12 months or no additives, in addition to usual care, there was no significant difference between the two groups in the patient-oriented eczema measure (POEM) – a score of symptoms in the previous week – for the first 16 weeks of treatment, reported Miriam Santer, MD, of the University of Southampton, England, and her coauthors. The mean POEM score was 7.5 in the bath additives group and 8.4 in the no bath additives group.

LucaLorenzelli/Thinkstock

SOURCE: Santer M et al. BMJ 2018 May 2. doi: 10.1136/bmj.k1332
 

A total of 34% of children who underwent solid organ transplantation subsequently developed eczema, food allergy, rhinitis, eosinophilic gastrointestinal disease, or asthma, according to the results of a single-center retrospective cohort study.

Another 6.6% of patients developed autoimmunity, usually autoimmune cytopenia, inflammatory bowel disease, or vasculitis, wrote Nufar Marcus, MD, of the University of Toronto, and her associates.

Posttransplant allergy, autoimmunity, and immune-mediated disorders (PTAA) likely share a common pathogenesis “and may represent a unique state of post-transplant immune-dysregulation,” they wrote. The report was published in the Journal of Pediatrics.

The study included 273 children who underwent solid organ transplantation and were followed for a median 3.6 years (range, 1.7-6.3 years). None had immune-mediated conditions or allergies diagnosed at baseline. Posttransplantation allergies most commonly included eczema (51%), asthma (32%), food allergy (25%, including 5% with associated anaphylaxis), rhinitis (17%), and eosinophilic esophagitis, gastritis, or enteritis (13%).

aniaostudio/Thinkstock.com

SOURCE: Marcus N et al. J Pediatr. 2018;196:154-60.

A total of 34% of children who underwent solid organ transplantation subsequently developed eczema, food allergy, rhinitis, eosinophilic gastrointestinal disease, or asthma, according to the results of a single-center retrospective cohort study.

Another 6.6% of patients developed autoimmunity, usually autoimmune cytopenia, inflammatory bowel disease, or vasculitis, wrote Nufar Marcus, MD, of the University of Toronto, and her associates.

Posttransplant allergy, autoimmunity, and immune-mediated disorders (PTAA) likely share a common pathogenesis “and may represent a unique state of post-transplant immune-dysregulation,” they wrote. The report was published in the Journal of Pediatrics.

The study included 273 children who underwent solid organ transplantation and were followed for a median 3.6 years (range, 1.7-6.3 years). None had immune-mediated conditions or allergies diagnosed at baseline. Posttransplantation allergies most commonly included eczema (51%), asthma (32%), food allergy (25%, including 5% with associated anaphylaxis), rhinitis (17%), and eosinophilic esophagitis, gastritis, or enteritis (13%).

aniaostudio/Thinkstock.com

SOURCE: Marcus N et al. J Pediatr. 2018;196:154-60.

A total of 34% of children who underwent solid organ transplantation subsequently developed eczema, food allergy, rhinitis, eosinophilic gastrointestinal disease, or asthma, according to the results of a single-center retrospective cohort study.

Another 6.6% of patients developed autoimmunity, usually autoimmune cytopenia, inflammatory bowel disease, or vasculitis, wrote Nufar Marcus, MD, of the University of Toronto, and her associates.

Posttransplant allergy, autoimmunity, and immune-mediated disorders (PTAA) likely share a common pathogenesis “and may represent a unique state of post-transplant immune-dysregulation,” they wrote. The report was published in the Journal of Pediatrics.

The study included 273 children who underwent solid organ transplantation and were followed for a median 3.6 years (range, 1.7-6.3 years). None had immune-mediated conditions or allergies diagnosed at baseline. Posttransplantation allergies most commonly included eczema (51%), asthma (32%), food allergy (25%, including 5% with associated anaphylaxis), rhinitis (17%), and eosinophilic esophagitis, gastritis, or enteritis (13%).

aniaostudio/Thinkstock.com

SOURCE: Marcus N et al. J Pediatr. 2018;196:154-60.

Absurdity is everywhere you look. Or don’t look.

As the old comedian Henny Youngman might have said:

Take my prior authorizations. Please!
 

Prior authorizations

1. Marissa had been taking isotretinoin for 2 months. She learned that three 20-mg capsules would cost her less than the two 30-mg capsules she’d been on.

cglade/E+/Getty Images

I got on the phone.

“Forgive me,” I said, gently, “but Marissa has been taking isotretinoin for 2 months, 60-mg per day. She was taking two 30’s. I want her to have three 20’s. They both add up to 60 mg. It’s the same dose. Why do you need to authorize it again?”

“Let me input that,” she replied. “Oh, now it’s accepting it. Your patient can have up to four pills a day.”

I was going to say she only needs three, but kept my mouth shut. Maybe Jensen only authorizes even numbers. 2. Danny has the worst atopic dermatitis I’ve ever seen. It’s all over him and never lets up. Topical steroids don’t touch it. Even prednisone – he’s had plenty over the years – barely makes a dent. I put in a Prior Authorization request for dupilumab.

“Your request for dupilumab has been denied,” read the insurer’s reply. “You have not shown failure with tacrolimus ointment or crisaborole.”

Say what? Prednisone didn’t help, and they expect tacrolimus or crisaborole to do the job?

I prescribed tacrolimus (which doesn’t come in a big enough tube to cover Daniel’s affected area anyway). It failed. Amazing.

“Your request for dupilumab has been denied,” said the insurer. “You have not also shown failure with crisaborole.”

Really? OK, I prescribed crisaborole. They denied coverage for it.

Now I was really getting into this. I wrote them. “I prescribed crisaborole.” I observed, “because you asked me to.”

They approved crisaborole. It failed. I reapplied for dupilumab. No response.

I called the insurer’s medical director, on a mobile with a Missouri exchange. After some telephone tag, he called back. “I cannot discuss this case with you,” he said, “because I have already made my determination.” Then he hung up without telling me what his determination was.

Further phone calls went unanswered. I thought Missouri was the Show-Me state.

The patient remained miserable. I decided to try one last time and wrote a long, sarcastic letter, detailing the whole episode. My secretary sent it off.

They approved dupilumab within the hour.

Malice? Nah, that’s giving them too much credit.

Now all Daniel has to do is improve.

Patient privacy!

Some news from abroad: what we know as HIPAA is called the “Data Protection Act” in the United Kingdom.

“We are obliged to conform to the demands of the Data Protection Act, and this specifically applies to the rabbi publicly mentioning the names of individuals who are unwell. The rabbi can only mention specific individuals with their permission or that of a relative designated by the sick person to do so. Anyone wishing for the rabbi to say a public prayer on their behalf must contact him directly by phone, text, or e-mail. To do anything else is breaking the law.”

If someone breaks this law, perhaps the rabbi can assist with atonement.

In any event, henceforth all entreaties to the Almighty must be encrypted. At least in the U.K.

What???!!!

Marina showed me her sunscreen. The label read, “Protects against UVA and UVB rays.”

“What’s the problem?” I asked.

She showed me our American Academy of Dermatology-produced sunscreen handout, which recommends “a broad-spectrum sunscreen that protects against both UVA and UVB rays, both of which cause cancer.”

“Does this mean my sunscreen causes cancer?” asked Marina.

“Not to worry,” I assured her.

I sighed and wafted a small prayer heavenward. Encrypted, of course.

Lo, the answer from above may tarry, but He will never forget His password.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

Absurdity is everywhere you look. Or don’t look.

As the old comedian Henny Youngman might have said:

Take my prior authorizations. Please!
 

Prior authorizations

1. Marissa had been taking isotretinoin for 2 months. She learned that three 20-mg capsules would cost her less than the two 30-mg capsules she’d been on.

cglade/E+/Getty Images

I got on the phone.

“Forgive me,” I said, gently, “but Marissa has been taking isotretinoin for 2 months, 60-mg per day. She was taking two 30’s. I want her to have three 20’s. They both add up to 60 mg. It’s the same dose. Why do you need to authorize it again?”

“Let me input that,” she replied. “Oh, now it’s accepting it. Your patient can have up to four pills a day.”

I was going to say she only needs three, but kept my mouth shut. Maybe Jensen only authorizes even numbers. 2. Danny has the worst atopic dermatitis I’ve ever seen. It’s all over him and never lets up. Topical steroids don’t touch it. Even prednisone – he’s had plenty over the years – barely makes a dent. I put in a Prior Authorization request for dupilumab.

“Your request for dupilumab has been denied,” read the insurer’s reply. “You have not shown failure with tacrolimus ointment or crisaborole.”

Say what? Prednisone didn’t help, and they expect tacrolimus or crisaborole to do the job?

I prescribed tacrolimus (which doesn’t come in a big enough tube to cover Daniel’s affected area anyway). It failed. Amazing.

“Your request for dupilumab has been denied,” said the insurer. “You have not also shown failure with crisaborole.”

Really? OK, I prescribed crisaborole. They denied coverage for it.

Now I was really getting into this. I wrote them. “I prescribed crisaborole.” I observed, “because you asked me to.”

They approved crisaborole. It failed. I reapplied for dupilumab. No response.

I called the insurer’s medical director, on a mobile with a Missouri exchange. After some telephone tag, he called back. “I cannot discuss this case with you,” he said, “because I have already made my determination.” Then he hung up without telling me what his determination was.

Further phone calls went unanswered. I thought Missouri was the Show-Me state.

The patient remained miserable. I decided to try one last time and wrote a long, sarcastic letter, detailing the whole episode. My secretary sent it off.

They approved dupilumab within the hour.

Malice? Nah, that’s giving them too much credit.

Now all Daniel has to do is improve.

Patient privacy!

Some news from abroad: what we know as HIPAA is called the “Data Protection Act” in the United Kingdom.

“We are obliged to conform to the demands of the Data Protection Act, and this specifically applies to the rabbi publicly mentioning the names of individuals who are unwell. The rabbi can only mention specific individuals with their permission or that of a relative designated by the sick person to do so. Anyone wishing for the rabbi to say a public prayer on their behalf must contact him directly by phone, text, or e-mail. To do anything else is breaking the law.”

If someone breaks this law, perhaps the rabbi can assist with atonement.

In any event, henceforth all entreaties to the Almighty must be encrypted. At least in the U.K.

What???!!!

Marina showed me her sunscreen. The label read, “Protects against UVA and UVB rays.”

“What’s the problem?” I asked.

She showed me our American Academy of Dermatology-produced sunscreen handout, which recommends “a broad-spectrum sunscreen that protects against both UVA and UVB rays, both of which cause cancer.”

“Does this mean my sunscreen causes cancer?” asked Marina.

“Not to worry,” I assured her.

I sighed and wafted a small prayer heavenward. Encrypted, of course.

Lo, the answer from above may tarry, but He will never forget His password.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

Absurdity is everywhere you look. Or don’t look.

As the old comedian Henny Youngman might have said:

Take my prior authorizations. Please!
 

Prior authorizations

1. Marissa had been taking isotretinoin for 2 months. She learned that three 20-mg capsules would cost her less than the two 30-mg capsules she’d been on.

cglade/E+/Getty Images

I got on the phone.

“Forgive me,” I said, gently, “but Marissa has been taking isotretinoin for 2 months, 60-mg per day. She was taking two 30’s. I want her to have three 20’s. They both add up to 60 mg. It’s the same dose. Why do you need to authorize it again?”

“Let me input that,” she replied. “Oh, now it’s accepting it. Your patient can have up to four pills a day.”

I was going to say she only needs three, but kept my mouth shut. Maybe Jensen only authorizes even numbers. 2. Danny has the worst atopic dermatitis I’ve ever seen. It’s all over him and never lets up. Topical steroids don’t touch it. Even prednisone – he’s had plenty over the years – barely makes a dent. I put in a Prior Authorization request for dupilumab.

“Your request for dupilumab has been denied,” read the insurer’s reply. “You have not shown failure with tacrolimus ointment or crisaborole.”

Say what? Prednisone didn’t help, and they expect tacrolimus or crisaborole to do the job?

I prescribed tacrolimus (which doesn’t come in a big enough tube to cover Daniel’s affected area anyway). It failed. Amazing.

“Your request for dupilumab has been denied,” said the insurer. “You have not also shown failure with crisaborole.”

Really? OK, I prescribed crisaborole. They denied coverage for it.

Now I was really getting into this. I wrote them. “I prescribed crisaborole.” I observed, “because you asked me to.”

They approved crisaborole. It failed. I reapplied for dupilumab. No response.

I called the insurer’s medical director, on a mobile with a Missouri exchange. After some telephone tag, he called back. “I cannot discuss this case with you,” he said, “because I have already made my determination.” Then he hung up without telling me what his determination was.

Further phone calls went unanswered. I thought Missouri was the Show-Me state.

The patient remained miserable. I decided to try one last time and wrote a long, sarcastic letter, detailing the whole episode. My secretary sent it off.

They approved dupilumab within the hour.

Malice? Nah, that’s giving them too much credit.

Now all Daniel has to do is improve.

Patient privacy!

Some news from abroad: what we know as HIPAA is called the “Data Protection Act” in the United Kingdom.

“We are obliged to conform to the demands of the Data Protection Act, and this specifically applies to the rabbi publicly mentioning the names of individuals who are unwell. The rabbi can only mention specific individuals with their permission or that of a relative designated by the sick person to do so. Anyone wishing for the rabbi to say a public prayer on their behalf must contact him directly by phone, text, or e-mail. To do anything else is breaking the law.”

If someone breaks this law, perhaps the rabbi can assist with atonement.

In any event, henceforth all entreaties to the Almighty must be encrypted. At least in the U.K.

What???!!!

Marina showed me her sunscreen. The label read, “Protects against UVA and UVB rays.”

“What’s the problem?” I asked.

She showed me our American Academy of Dermatology-produced sunscreen handout, which recommends “a broad-spectrum sunscreen that protects against both UVA and UVB rays, both of which cause cancer.”

“Does this mean my sunscreen causes cancer?” asked Marina.

“Not to worry,” I assured her.

I sighed and wafted a small prayer heavenward. Encrypted, of course.

Lo, the answer from above may tarry, but He will never forget His password.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@mdedge.com.

Fezakinumab, an interleukin-22 monoclonal antibody, “resulted in consistent improvements in clinical and molecular disease scores as compared with placebo” in a phase 2a study of adults with moderate to severe atopic dermatitis (AD), according to Emma Guttman-Yassky, MD, of Icahn School of Medicine at Mount Sinai, New York, and her associates.

In the double-blind, placebo-controlled trial, 60 patients were randomized to intravenous fezakinumab every 2 weeks for 10 weeks (40 patients) or placebo (20). Beginning at week 4, those who received fezakinumab “showed a consistently stronger and more significant mean SCORAD decline from baseline” compared with those on placebo. This became statistically significant at weeks 6-10 (P less than .05). “Differences between drug and placebo extended beyond the last dose” at week 10, they noted.*

The primary endpoint, the change in the SCORAD score from baseline at 12 weeks, was not statistically significant, however. 

In addition, progressive reductions were seen during weeks 14-20, with a significant difference between the drug and placebo arms (P = .049) observed at week 20.

llaubach@mdedge.com

SOURCE: Guttman-Yassky et al. J Am Acad Dermatol. 78(5);872-81.

Correction, 4/27/17: An earlier version of this article misstated the statistical significance of the primary endpoint.

Fezakinumab, an interleukin-22 monoclonal antibody, “resulted in consistent improvements in clinical and molecular disease scores as compared with placebo” in a phase 2a study of adults with moderate to severe atopic dermatitis (AD), according to Emma Guttman-Yassky, MD, of Icahn School of Medicine at Mount Sinai, New York, and her associates.

In the double-blind, placebo-controlled trial, 60 patients were randomized to intravenous fezakinumab every 2 weeks for 10 weeks (40 patients) or placebo (20). Beginning at week 4, those who received fezakinumab “showed a consistently stronger and more significant mean SCORAD decline from baseline” compared with those on placebo. This became statistically significant at weeks 6-10 (P less than .05). “Differences between drug and placebo extended beyond the last dose” at week 10, they noted.*

The primary endpoint, the change in the SCORAD score from baseline at 12 weeks, was not statistically significant, however. 

In addition, progressive reductions were seen during weeks 14-20, with a significant difference between the drug and placebo arms (P = .049) observed at week 20.

llaubach@mdedge.com

SOURCE: Guttman-Yassky et al. J Am Acad Dermatol. 78(5);872-81.

Correction, 4/27/17: An earlier version of this article misstated the statistical significance of the primary endpoint.

Fezakinumab, an interleukin-22 monoclonal antibody, “resulted in consistent improvements in clinical and molecular disease scores as compared with placebo” in a phase 2a study of adults with moderate to severe atopic dermatitis (AD), according to Emma Guttman-Yassky, MD, of Icahn School of Medicine at Mount Sinai, New York, and her associates.

In the double-blind, placebo-controlled trial, 60 patients were randomized to intravenous fezakinumab every 2 weeks for 10 weeks (40 patients) or placebo (20). Beginning at week 4, those who received fezakinumab “showed a consistently stronger and more significant mean SCORAD decline from baseline” compared with those on placebo. This became statistically significant at weeks 6-10 (P less than .05). “Differences between drug and placebo extended beyond the last dose” at week 10, they noted.*

The primary endpoint, the change in the SCORAD score from baseline at 12 weeks, was not statistically significant, however. 

In addition, progressive reductions were seen during weeks 14-20, with a significant difference between the drug and placebo arms (P = .049) observed at week 20.

llaubach@mdedge.com

SOURCE: Guttman-Yassky et al. J Am Acad Dermatol. 78(5);872-81.

Correction, 4/27/17: An earlier version of this article misstated the statistical significance of the primary endpoint.

Early consumption of peanuts in infants at high risk of peanut allergy, shown to reduce the risk of peanut allergy, does not prevent the development of other allergic disease and does not hasten the resolution of eczema, according to George du Toit, MB, and his associates.

In a study published in The Journal of Allergy and Clinical Immunology, they reported on the results of a 12-month extension of the Learning Early About Peanut Allergy (LEAP) study, which found that early introduction of peanuts into the diets of infants at high risk of peanut allergy markedly reduced their risk of developing peanut allergy at age 5, compared with those who did not consume peanuts. As infants, the majority had severe eczema, which, with egg allergy, was used to identify those at high risk.

In the extension study, the rates of eczema decreased across study time points to 72 months of age in both groups, to 39% in the peanut avoidance group and 37% in the peanut consumption group. Eczema severity decreased across study time points, and there were no significant differences in severity between the two groups at any time point.

There were also no differences between the two groups in the rates of asthma, seasonal rhinoconjunctivitis, and perennial rhinoconjunctivitis at 30, 60, and 72 months of age.

“The underlying immune mechanisms associated with tolerance to peanut do not alter the natural history of allergic disease,” the researchers concluded. “Different prevention strategies or strategies that include multiple dietary interventions need to be tested to assess whether the reduction in peanut allergy observed in the LEAP consumption group can be extended to other common food allergens and allergic diseases.”

llaubach@mdedge.com

SOURCE: Du Toit G et al. J Allergy Clin Immunol. 2018 Apr;141[4]1343-53.

Early consumption of peanuts in infants at high risk of peanut allergy, shown to reduce the risk of peanut allergy, does not prevent the development of other allergic disease and does not hasten the resolution of eczema, according to George du Toit, MB, and his associates.

In a study published in The Journal of Allergy and Clinical Immunology, they reported on the results of a 12-month extension of the Learning Early About Peanut Allergy (LEAP) study, which found that early introduction of peanuts into the diets of infants at high risk of peanut allergy markedly reduced their risk of developing peanut allergy at age 5, compared with those who did not consume peanuts. As infants, the majority had severe eczema, which, with egg allergy, was used to identify those at high risk.

In the extension study, the rates of eczema decreased across study time points to 72 months of age in both groups, to 39% in the peanut avoidance group and 37% in the peanut consumption group. Eczema severity decreased across study time points, and there were no significant differences in severity between the two groups at any time point.

There were also no differences between the two groups in the rates of asthma, seasonal rhinoconjunctivitis, and perennial rhinoconjunctivitis at 30, 60, and 72 months of age.

“The underlying immune mechanisms associated with tolerance to peanut do not alter the natural history of allergic disease,” the researchers concluded. “Different prevention strategies or strategies that include multiple dietary interventions need to be tested to assess whether the reduction in peanut allergy observed in the LEAP consumption group can be extended to other common food allergens and allergic diseases.”

llaubach@mdedge.com

SOURCE: Du Toit G et al. J Allergy Clin Immunol. 2018 Apr;141[4]1343-53.

Early consumption of peanuts in infants at high risk of peanut allergy, shown to reduce the risk of peanut allergy, does not prevent the development of other allergic disease and does not hasten the resolution of eczema, according to George du Toit, MB, and his associates.

In a study published in The Journal of Allergy and Clinical Immunology, they reported on the results of a 12-month extension of the Learning Early About Peanut Allergy (LEAP) study, which found that early introduction of peanuts into the diets of infants at high risk of peanut allergy markedly reduced their risk of developing peanut allergy at age 5, compared with those who did not consume peanuts. As infants, the majority had severe eczema, which, with egg allergy, was used to identify those at high risk.

In the extension study, the rates of eczema decreased across study time points to 72 months of age in both groups, to 39% in the peanut avoidance group and 37% in the peanut consumption group. Eczema severity decreased across study time points, and there were no significant differences in severity between the two groups at any time point.

There were also no differences between the two groups in the rates of asthma, seasonal rhinoconjunctivitis, and perennial rhinoconjunctivitis at 30, 60, and 72 months of age.

“The underlying immune mechanisms associated with tolerance to peanut do not alter the natural history of allergic disease,” the researchers concluded. “Different prevention strategies or strategies that include multiple dietary interventions need to be tested to assess whether the reduction in peanut allergy observed in the LEAP consumption group can be extended to other common food allergens and allergic diseases.”

llaubach@mdedge.com

SOURCE: Du Toit G et al. J Allergy Clin Immunol. 2018 Apr;141[4]1343-53.

Myth: Children eventually outgrow atopic dermatitis and therefore do not need treatment

The negative impact of atopic dermatitis (AD) on quality of life in the pediatric population often prompts parents/guardians to inquire about whether a child with AD will ever outgrow their disease. If remission is expected as the child gets older, many may question if it is necessary to pursue treatment or just let the disease run its course. Although AD often is reported to resolve soon after the first decade of life, symptoms can persist well into the second decade and beyond, suggesting that AD may be a lifelong disease with periods of waxing and waning symptoms that require persistent treatment throughout the patient’s life.

A 2014 study included 7157 children with AD (mean age of disease onset, 1.7 years) who were enrolled in the Pediatric Eczema Elective Registry (PEER) program between the ages of 2 and 17 years with measurement of disease activity at regular 6-month intervals for up to 5 years. The study results indicated that more than 80% of patients at every age (age range, 2–26 years) had symptoms of AD and/or were using medication to treat their disease, and the majority (64%) of patients had never reported a 6-month period during which they achieved clearance of symptoms without medication. At the age of 20 years, 50% of patients reported at least 1 lifetime 6-month period during which they were both symptom and treatment free. In another study of adolescents with AD who also had AD in childhood (N=82), 48% of patients remained in the same AD severity grades and 13% deteriorated from childhood to adolescence; only 39% of patients showed improvement in disease severity from childhood to adolescence. The findings of these reports are contradictory to conventional clinical teaching, which indicates that AD generally resolves by age 12 in 50% to 70% of children.

Even though some children with AD may experience periods of disease clearance, these findings often do not persist and should not be confused with a permanent remission. Most patients require continued treatment with medications to achieve relief of symptoms. Therefore, physicians should not assure parents/guardians that a child can outgrow AD; rather, they should educate pediatric patients and their caregivers about the potentially lifelong disease course and encourage early intervention to mitigate symptoms and manage comorbidities as the patient ages.

Myth: Children eventually outgrow atopic dermatitis and therefore do not need treatment

The negative impact of atopic dermatitis (AD) on quality of life in the pediatric population often prompts parents/guardians to inquire about whether a child with AD will ever outgrow their disease. If remission is expected as the child gets older, many may question if it is necessary to pursue treatment or just let the disease run its course. Although AD often is reported to resolve soon after the first decade of life, symptoms can persist well into the second decade and beyond, suggesting that AD may be a lifelong disease with periods of waxing and waning symptoms that require persistent treatment throughout the patient’s life.

A 2014 study included 7157 children with AD (mean age of disease onset, 1.7 years) who were enrolled in the Pediatric Eczema Elective Registry (PEER) program between the ages of 2 and 17 years with measurement of disease activity at regular 6-month intervals for up to 5 years. The study results indicated that more than 80% of patients at every age (age range, 2–26 years) had symptoms of AD and/or were using medication to treat their disease, and the majority (64%) of patients had never reported a 6-month period during which they achieved clearance of symptoms without medication. At the age of 20 years, 50% of patients reported at least 1 lifetime 6-month period during which they were both symptom and treatment free. In another study of adolescents with AD who also had AD in childhood (N=82), 48% of patients remained in the same AD severity grades and 13% deteriorated from childhood to adolescence; only 39% of patients showed improvement in disease severity from childhood to adolescence. The findings of these reports are contradictory to conventional clinical teaching, which indicates that AD generally resolves by age 12 in 50% to 70% of children.

Even though some children with AD may experience periods of disease clearance, these findings often do not persist and should not be confused with a permanent remission. Most patients require continued treatment with medications to achieve relief of symptoms. Therefore, physicians should not assure parents/guardians that a child can outgrow AD; rather, they should educate pediatric patients and their caregivers about the potentially lifelong disease course and encourage early intervention to mitigate symptoms and manage comorbidities as the patient ages.

Myth: Children eventually outgrow atopic dermatitis and therefore do not need treatment

The negative impact of atopic dermatitis (AD) on quality of life in the pediatric population often prompts parents/guardians to inquire about whether a child with AD will ever outgrow their disease. If remission is expected as the child gets older, many may question if it is necessary to pursue treatment or just let the disease run its course. Although AD often is reported to resolve soon after the first decade of life, symptoms can persist well into the second decade and beyond, suggesting that AD may be a lifelong disease with periods of waxing and waning symptoms that require persistent treatment throughout the patient’s life.

A 2014 study included 7157 children with AD (mean age of disease onset, 1.7 years) who were enrolled in the Pediatric Eczema Elective Registry (PEER) program between the ages of 2 and 17 years with measurement of disease activity at regular 6-month intervals for up to 5 years. The study results indicated that more than 80% of patients at every age (age range, 2–26 years) had symptoms of AD and/or were using medication to treat their disease, and the majority (64%) of patients had never reported a 6-month period during which they achieved clearance of symptoms without medication. At the age of 20 years, 50% of patients reported at least 1 lifetime 6-month period during which they were both symptom and treatment free. In another study of adolescents with AD who also had AD in childhood (N=82), 48% of patients remained in the same AD severity grades and 13% deteriorated from childhood to adolescence; only 39% of patients showed improvement in disease severity from childhood to adolescence. The findings of these reports are contradictory to conventional clinical teaching, which indicates that AD generally resolves by age 12 in 50% to 70% of children.

Even though some children with AD may experience periods of disease clearance, these findings often do not persist and should not be confused with a permanent remission. Most patients require continued treatment with medications to achieve relief of symptoms. Therefore, physicians should not assure parents/guardians that a child can outgrow AD; rather, they should educate pediatric patients and their caregivers about the potentially lifelong disease course and encourage early intervention to mitigate symptoms and manage comorbidities as the patient ages.