Pediatrics

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Researchers in Japan report that infants with atopic dermatitis who are treated early and aggressively with corticosteroids develop fewer food allergies by age 2 years.

For their research published in the Journal of Allergy and Clinical Immunology: In Practice, Yumiko Miyaji, MD, PhD, of Japan’s National Center for Child Health and Development in Tokyo and colleagues looked at 3 years’ worth of records for 177 infants younger than 1 year of age seen at a hospital allergy center for eczema. Of these infants, 89 were treated with betamethasone valerate within 4 months of disease onset, and 88 were treated after 4 months of onset. Most (142) were followed-up at 22-24 months, when all were in complete remission or near remission from eczema.

At follow-up, clinicians collected information about anaphylactic reactions to food, administered specific food challenges, and tested serum immunoglobin E levels for food allergens. Dr. Miyaji and colleagues found a significant difference in the prevalence of allergies between the early-treated and late-treated groups to chicken egg, cow’s milk, wheat, peanuts, soy, or fish (25% vs. 46%, respectively; P equal to .013). For individual food allergies, only chicken egg was associated with a statistically significant difference in prevalence (15% vs 36%, P equal to .006).

“Our present study may be the first to demonstrate that early aggressive topical corticosteroid treatment to shorten the duration of eczema in infants was significantly associated with a decrease in later development of [food allergies],” Dr. Miyaji and colleagues wrote in their analysis.

The investigators acknowledged as limitations of their study some between-group differences at baseline, with characteristics such as Staphylococcus aureus infections and some inflammatory biomarkers higher in the early treatment group.

The Japan Agency for Medical Research and Development supported the study, and the investigators disclosed no conflicts of interest related to their findings.

SOURCE: Miyaji Y et al. J Allergy Clin Immunol Pract. 2019. doi: 10.1016/j.jaip.2019.11.036

Children with atopic dermatitis and allergies to eggs and milk were at increased risk for anaphylactic reactions, compared with allergic patients without atopic dermatitis, based on retrospective data from 347 individuals.

Atopic dermatitis has been associated with increased risk of food allergies, but the association and predictive factors of skin reactions to certain foods remain unclear, wrote Bryce C. Hoffman, MD, of National Jewish Health, Denver, and colleagues.

In a letter published in the Annals of Allergy, Asthma & Immunology, the researchers identified children aged 0-18 years with peanut, cow’s milk, and/or egg allergies with or without atopic dermatitis (AD) using an institutional research database and conducted a retrospective study of medical records.

Overall, children with egg and milk allergies plus AD had significantly higher rates of anaphylaxis than allergic children without AD (47% vs. 11% for egg, 50% vs. 19% for milk). Anaphylaxis rates were similar in children with peanut allergies with or without AD (27% vs. 23%).

“This finding may suggest that skin barrier dysfunction plays a role in the severity of [food allergy]. However, this is not universal to all food antigens, and other mechanisms are likely important in the association of anaphylaxis with a particular food,” the researchers noted.

Rates of tolerance for both baked egg and baked milk were similar between AD and non-AD patients (83% vs. 61% for milk; 82% vs. 67% for egg). In addition, levels of total IgE were increased in children with egg and milk allergies plus AD, compared with children without AD. However, children with peanut allergies plus AD had decreased total IgE, compared with children with peanut allergies but no AD. This “may support a link between T_h2 polarization and [food allergy] severity, ” Dr. Hoffman and associates wrote.

The findings were limited by several factors, including the retrospective study design, exclusion of many patients, and lack of data on the amount of food that triggered anaphylactic reactions, the researchers noted.

Nonetheless, the results suggest that children with atopic dermatitis and allergies to eggs and milk are at increased risk and that clinicians should counsel these patients and families about the potential for more-severe reactions to oral food challenges, Dr. Hoffman and associates concluded.

The study was supported by National Jewish Health and the Edelstein Family Chair of Pediatric Allergy and Immunology. The researchers had no financial conflicts to disclose.

SOURCE: Hoffman BC et al. Ann Allergy Asthma Immunol. 2019 Sep 11. doi: 10.1016/j.anai.2019.09.008.

Children with atopic dermatitis and allergies to eggs and milk were at increased risk for anaphylactic reactions, compared with allergic patients without atopic dermatitis, based on retrospective data from 347 individuals.

Atopic dermatitis has been associated with increased risk of food allergies, but the association and predictive factors of skin reactions to certain foods remain unclear, wrote Bryce C. Hoffman, MD, of National Jewish Health, Denver, and colleagues.

In a letter published in the Annals of Allergy, Asthma & Immunology, the researchers identified children aged 0-18 years with peanut, cow’s milk, and/or egg allergies with or without atopic dermatitis (AD) using an institutional research database and conducted a retrospective study of medical records.

Overall, children with egg and milk allergies plus AD had significantly higher rates of anaphylaxis than allergic children without AD (47% vs. 11% for egg, 50% vs. 19% for milk). Anaphylaxis rates were similar in children with peanut allergies with or without AD (27% vs. 23%).

“This finding may suggest that skin barrier dysfunction plays a role in the severity of [food allergy]. However, this is not universal to all food antigens, and other mechanisms are likely important in the association of anaphylaxis with a particular food,” the researchers noted.

Rates of tolerance for both baked egg and baked milk were similar between AD and non-AD patients (83% vs. 61% for milk; 82% vs. 67% for egg). In addition, levels of total IgE were increased in children with egg and milk allergies plus AD, compared with children without AD. However, children with peanut allergies plus AD had decreased total IgE, compared with children with peanut allergies but no AD. This “may support a link between T_h2 polarization and [food allergy] severity, ” Dr. Hoffman and associates wrote.

The findings were limited by several factors, including the retrospective study design, exclusion of many patients, and lack of data on the amount of food that triggered anaphylactic reactions, the researchers noted.

Nonetheless, the results suggest that children with atopic dermatitis and allergies to eggs and milk are at increased risk and that clinicians should counsel these patients and families about the potential for more-severe reactions to oral food challenges, Dr. Hoffman and associates concluded.

The study was supported by National Jewish Health and the Edelstein Family Chair of Pediatric Allergy and Immunology. The researchers had no financial conflicts to disclose.

SOURCE: Hoffman BC et al. Ann Allergy Asthma Immunol. 2019 Sep 11. doi: 10.1016/j.anai.2019.09.008.

Children with atopic dermatitis and allergies to eggs and milk were at increased risk for anaphylactic reactions, compared with allergic patients without atopic dermatitis, based on retrospective data from 347 individuals.

Atopic dermatitis has been associated with increased risk of food allergies, but the association and predictive factors of skin reactions to certain foods remain unclear, wrote Bryce C. Hoffman, MD, of National Jewish Health, Denver, and colleagues.

In a letter published in the Annals of Allergy, Asthma & Immunology, the researchers identified children aged 0-18 years with peanut, cow’s milk, and/or egg allergies with or without atopic dermatitis (AD) using an institutional research database and conducted a retrospective study of medical records.

Overall, children with egg and milk allergies plus AD had significantly higher rates of anaphylaxis than allergic children without AD (47% vs. 11% for egg, 50% vs. 19% for milk). Anaphylaxis rates were similar in children with peanut allergies with or without AD (27% vs. 23%).

“This finding may suggest that skin barrier dysfunction plays a role in the severity of [food allergy]. However, this is not universal to all food antigens, and other mechanisms are likely important in the association of anaphylaxis with a particular food,” the researchers noted.

Rates of tolerance for both baked egg and baked milk were similar between AD and non-AD patients (83% vs. 61% for milk; 82% vs. 67% for egg). In addition, levels of total IgE were increased in children with egg and milk allergies plus AD, compared with children without AD. However, children with peanut allergies plus AD had decreased total IgE, compared with children with peanut allergies but no AD. This “may support a link between T_h2 polarization and [food allergy] severity, ” Dr. Hoffman and associates wrote.

The findings were limited by several factors, including the retrospective study design, exclusion of many patients, and lack of data on the amount of food that triggered anaphylactic reactions, the researchers noted.

Nonetheless, the results suggest that children with atopic dermatitis and allergies to eggs and milk are at increased risk and that clinicians should counsel these patients and families about the potential for more-severe reactions to oral food challenges, Dr. Hoffman and associates concluded.

The study was supported by National Jewish Health and the Edelstein Family Chair of Pediatric Allergy and Immunology. The researchers had no financial conflicts to disclose.

SOURCE: Hoffman BC et al. Ann Allergy Asthma Immunol. 2019 Sep 11. doi: 10.1016/j.anai.2019.09.008.

Medicine is a rewarding but demanding field. Part of being a professional is handling the stresses of the job. That ability is as important as tying strong horizontal mattress sutures, choosing correct antibiotics to treat staph, and gently breaking bad news.

doomu/Thinkstock

The divorce and suicide rate among physicians are evidence that many physicians handle stress poorly. Our rates of depression, burnout, alcoholism, and substance abuse are further evidence of the suffering caused by unmitigated stress. It is endemic and destructive, harming physicians, their loved ones, and their patients. While this situation has long been true, in the past decade its importance has become better recognized. Some scholars have added physician wellness or fulfillment as a fourth aim of medical care to complement the triple aims of patient outcomes, consumer experience, and financial stewardship.

The sources of stress can be either external or internal. Internally, many physicians feel torn between competing professional roles. Recently one fellow in pediatric intensive care wrote an insightful reflective essay about two conflicting roles (“Virtue and Suffering: Where the Personal and Professional Collide,” Lauren Rissman, MD. reflectivemeded.org). One side is the potential benefits of technology and modern medical interventions. The other side is compassion and knowing when to say enough. Finding that balance – or boundary – or mixture is difficult. Even more difficult is helping patients/parents who are struggling with those choices.

Some old models of the doctor-patient relationship insisted on an emotional detachment to promote objectivity. This often is paired with using nondirective counseling. The admonishment for a physician to be nondirective comes up in end-of-life care choices in the ICU. It comes up in genetic counseling, particularly in the prenatal time frame, and when I do ethics consults requiring values clarification and mediation. But I also have found times during shared decision making when the model of a fully informed consumer choice is not valid. There are situations in which a paradigm of emotional detachment impairs the ability to convey empathy, compassion, and presence. Being detached also may prevent the moments of personal connection between doctor and patient that are the intangible rewards of the vocation. A good physician knows how to choose among these idealized models. It requires being genuine when employing a diverse bag of bedside tools.

High technology and highly invasive care pose dilemmas in assessing outcomes, minimizing suffering, and ensuring financial stewardship. When one addresses those different types of dilemmas happening simultaneously, the initial approach can be to separate the different influences into separate vectors. But when one does this on a regular basis, it fractures one’s self-image. To survive and flourish, the physician juggling these competing, conflicting goals must shun the split personality and seek to live as an integrated moral agent. This integration is not achieved by working harder or longer or even smarter. It requires time and effort directed to self-reflection. When pediatric ethicists get together at conferences, I notice that about one-half of them are neonatal ICU docs and one-quarter are pediatric ICU docs. Many view their work in ethics as a survival mechanism. We all are looking for answers to questions we may not be able to fully articulate.

In this short column I will not endeavor to offer a neat package of advice on how to achieve being whole. Dr. Rissman in her essay is just starting her career while I’m nearing the end of mine. It is a lifelong process to integrate oneself rather than exist in turmoil. It truly is a journey, not a destination. After a career dedicated to considering technology, compassion, and costs, I know there are no simple solutions. I also know that it is important to keep seeking better answers.

To encourage group discussion of ethical problems, I have heard facilitators say that there are no right and wrong answers. I strongly disagree. In ethics, there often is more than one correct answer. Ethicists can write books on why one right answer is slightly better than another right answer for a particular individual or population. We live for debates over such minutiae. In the real world of medical ethics, there also are definitely wrong answers.

The difference between medical ethics and philosophy is that, when all the talking is done, in medical ethics something happens. That makes a difference. Professional athletes know the importance of recovery after an intense workout. Muscles have accumulated microscopic tears that must heal. Professional physicians must develop a personal regimen of caring for overexertion of their own emotional and moral/spiritual muscles in order to remain whole.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

Medicine is a rewarding but demanding field. Part of being a professional is handling the stresses of the job. That ability is as important as tying strong horizontal mattress sutures, choosing correct antibiotics to treat staph, and gently breaking bad news.

doomu/Thinkstock

The divorce and suicide rate among physicians are evidence that many physicians handle stress poorly. Our rates of depression, burnout, alcoholism, and substance abuse are further evidence of the suffering caused by unmitigated stress. It is endemic and destructive, harming physicians, their loved ones, and their patients. While this situation has long been true, in the past decade its importance has become better recognized. Some scholars have added physician wellness or fulfillment as a fourth aim of medical care to complement the triple aims of patient outcomes, consumer experience, and financial stewardship.

The sources of stress can be either external or internal. Internally, many physicians feel torn between competing professional roles. Recently one fellow in pediatric intensive care wrote an insightful reflective essay about two conflicting roles (“Virtue and Suffering: Where the Personal and Professional Collide,” Lauren Rissman, MD. reflectivemeded.org). One side is the potential benefits of technology and modern medical interventions. The other side is compassion and knowing when to say enough. Finding that balance – or boundary – or mixture is difficult. Even more difficult is helping patients/parents who are struggling with those choices.

Some old models of the doctor-patient relationship insisted on an emotional detachment to promote objectivity. This often is paired with using nondirective counseling. The admonishment for a physician to be nondirective comes up in end-of-life care choices in the ICU. It comes up in genetic counseling, particularly in the prenatal time frame, and when I do ethics consults requiring values clarification and mediation. But I also have found times during shared decision making when the model of a fully informed consumer choice is not valid. There are situations in which a paradigm of emotional detachment impairs the ability to convey empathy, compassion, and presence. Being detached also may prevent the moments of personal connection between doctor and patient that are the intangible rewards of the vocation. A good physician knows how to choose among these idealized models. It requires being genuine when employing a diverse bag of bedside tools.

High technology and highly invasive care pose dilemmas in assessing outcomes, minimizing suffering, and ensuring financial stewardship. When one addresses those different types of dilemmas happening simultaneously, the initial approach can be to separate the different influences into separate vectors. But when one does this on a regular basis, it fractures one’s self-image. To survive and flourish, the physician juggling these competing, conflicting goals must shun the split personality and seek to live as an integrated moral agent. This integration is not achieved by working harder or longer or even smarter. It requires time and effort directed to self-reflection. When pediatric ethicists get together at conferences, I notice that about one-half of them are neonatal ICU docs and one-quarter are pediatric ICU docs. Many view their work in ethics as a survival mechanism. We all are looking for answers to questions we may not be able to fully articulate.

In this short column I will not endeavor to offer a neat package of advice on how to achieve being whole. Dr. Rissman in her essay is just starting her career while I’m nearing the end of mine. It is a lifelong process to integrate oneself rather than exist in turmoil. It truly is a journey, not a destination. After a career dedicated to considering technology, compassion, and costs, I know there are no simple solutions. I also know that it is important to keep seeking better answers.

To encourage group discussion of ethical problems, I have heard facilitators say that there are no right and wrong answers. I strongly disagree. In ethics, there often is more than one correct answer. Ethicists can write books on why one right answer is slightly better than another right answer for a particular individual or population. We live for debates over such minutiae. In the real world of medical ethics, there also are definitely wrong answers.

The difference between medical ethics and philosophy is that, when all the talking is done, in medical ethics something happens. That makes a difference. Professional athletes know the importance of recovery after an intense workout. Muscles have accumulated microscopic tears that must heal. Professional physicians must develop a personal regimen of caring for overexertion of their own emotional and moral/spiritual muscles in order to remain whole.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

Medicine is a rewarding but demanding field. Part of being a professional is handling the stresses of the job. That ability is as important as tying strong horizontal mattress sutures, choosing correct antibiotics to treat staph, and gently breaking bad news.

doomu/Thinkstock

The divorce and suicide rate among physicians are evidence that many physicians handle stress poorly. Our rates of depression, burnout, alcoholism, and substance abuse are further evidence of the suffering caused by unmitigated stress. It is endemic and destructive, harming physicians, their loved ones, and their patients. While this situation has long been true, in the past decade its importance has become better recognized. Some scholars have added physician wellness or fulfillment as a fourth aim of medical care to complement the triple aims of patient outcomes, consumer experience, and financial stewardship.

The sources of stress can be either external or internal. Internally, many physicians feel torn between competing professional roles. Recently one fellow in pediatric intensive care wrote an insightful reflective essay about two conflicting roles (“Virtue and Suffering: Where the Personal and Professional Collide,” Lauren Rissman, MD. reflectivemeded.org). One side is the potential benefits of technology and modern medical interventions. The other side is compassion and knowing when to say enough. Finding that balance – or boundary – or mixture is difficult. Even more difficult is helping patients/parents who are struggling with those choices.

Some old models of the doctor-patient relationship insisted on an emotional detachment to promote objectivity. This often is paired with using nondirective counseling. The admonishment for a physician to be nondirective comes up in end-of-life care choices in the ICU. It comes up in genetic counseling, particularly in the prenatal time frame, and when I do ethics consults requiring values clarification and mediation. But I also have found times during shared decision making when the model of a fully informed consumer choice is not valid. There are situations in which a paradigm of emotional detachment impairs the ability to convey empathy, compassion, and presence. Being detached also may prevent the moments of personal connection between doctor and patient that are the intangible rewards of the vocation. A good physician knows how to choose among these idealized models. It requires being genuine when employing a diverse bag of bedside tools.

High technology and highly invasive care pose dilemmas in assessing outcomes, minimizing suffering, and ensuring financial stewardship. When one addresses those different types of dilemmas happening simultaneously, the initial approach can be to separate the different influences into separate vectors. But when one does this on a regular basis, it fractures one’s self-image. To survive and flourish, the physician juggling these competing, conflicting goals must shun the split personality and seek to live as an integrated moral agent. This integration is not achieved by working harder or longer or even smarter. It requires time and effort directed to self-reflection. When pediatric ethicists get together at conferences, I notice that about one-half of them are neonatal ICU docs and one-quarter are pediatric ICU docs. Many view their work in ethics as a survival mechanism. We all are looking for answers to questions we may not be able to fully articulate.

In this short column I will not endeavor to offer a neat package of advice on how to achieve being whole. Dr. Rissman in her essay is just starting her career while I’m nearing the end of mine. It is a lifelong process to integrate oneself rather than exist in turmoil. It truly is a journey, not a destination. After a career dedicated to considering technology, compassion, and costs, I know there are no simple solutions. I also know that it is important to keep seeking better answers.

To encourage group discussion of ethical problems, I have heard facilitators say that there are no right and wrong answers. I strongly disagree. In ethics, there often is more than one correct answer. Ethicists can write books on why one right answer is slightly better than another right answer for a particular individual or population. We live for debates over such minutiae. In the real world of medical ethics, there also are definitely wrong answers.

The difference between medical ethics and philosophy is that, when all the talking is done, in medical ethics something happens. That makes a difference. Professional athletes know the importance of recovery after an intense workout. Muscles have accumulated microscopic tears that must heal. Professional physicians must develop a personal regimen of caring for overexertion of their own emotional and moral/spiritual muscles in order to remain whole.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

A regimen of twice-daily baths followed by occlusive moisturizer improved atopic dermatitis in children with moderate to severe disease more effectively than did a twice-weekly protocol, based on data from 42 children.

Guidelines for bathing frequency for children with atopic dermatitis are inconsistent and often confusing for parents, according to Ivan D. Cardona, MD, of Maine Medical Research Institute, Portland, and colleagues.

In a study published in the Journal of Allergy and Clinical Immunology: In Practice, the researchers randomized 42 children aged 6 months to 11 years with moderate to severe atopic dermatitis to a routine of twice-weekly “soak and seal” (SS) procedures consisting of soaking baths for 10 minutes or less, followed by an occlusive emollient, or to twice-daily SS with baths of 15-20 minutes followed by emollient. The groups were treated for 2 weeks, then switched protocols. The study included a total of four clinic visits over 5 weeks. All patients also received standard of care low-potency topical corticosteroids and moisturizer.

Overall, the frequent bathing (“wet method”) led to a decrease of 21.2 on the SCORing Atopic Dermatitis Index (SCORAD) compared with the less frequent bathing (“dry method”). Improvements in SCORAD (the primary outcome) correlated with a secondary outcome of improved scores on the parent-rated Atopic Dermatitis Quickscore.

The findings were limited by several factors including the small sample size, large rate of attrition prior to randomization among initially screened children, lack of data on environmental factors such as water temperature and quality, and the lack of a washout period between the treatment protocols, the researchers noted. They acknowledged that “twice-daily SS bathing in the real world can be time consuming, making adherence difficult for families.”

However, the results suggest that the frequent bathing protocol was safe and effective at improving symptoms of atopic dermatitis, and may reduce steroid use, they concluded.

The researchers had no financial conflicts to disclose.

SOURCE: Cardona ID et al. J Allergy Clin Immunol Pract. 2019 Nov 13. doi: 10.1016/j.jaip.2019.10.042.

A regimen of twice-daily baths followed by occlusive moisturizer improved atopic dermatitis in children with moderate to severe disease more effectively than did a twice-weekly protocol, based on data from 42 children.

Guidelines for bathing frequency for children with atopic dermatitis are inconsistent and often confusing for parents, according to Ivan D. Cardona, MD, of Maine Medical Research Institute, Portland, and colleagues.

In a study published in the Journal of Allergy and Clinical Immunology: In Practice, the researchers randomized 42 children aged 6 months to 11 years with moderate to severe atopic dermatitis to a routine of twice-weekly “soak and seal” (SS) procedures consisting of soaking baths for 10 minutes or less, followed by an occlusive emollient, or to twice-daily SS with baths of 15-20 minutes followed by emollient. The groups were treated for 2 weeks, then switched protocols. The study included a total of four clinic visits over 5 weeks. All patients also received standard of care low-potency topical corticosteroids and moisturizer.

Overall, the frequent bathing (“wet method”) led to a decrease of 21.2 on the SCORing Atopic Dermatitis Index (SCORAD) compared with the less frequent bathing (“dry method”). Improvements in SCORAD (the primary outcome) correlated with a secondary outcome of improved scores on the parent-rated Atopic Dermatitis Quickscore.

The findings were limited by several factors including the small sample size, large rate of attrition prior to randomization among initially screened children, lack of data on environmental factors such as water temperature and quality, and the lack of a washout period between the treatment protocols, the researchers noted. They acknowledged that “twice-daily SS bathing in the real world can be time consuming, making adherence difficult for families.”

However, the results suggest that the frequent bathing protocol was safe and effective at improving symptoms of atopic dermatitis, and may reduce steroid use, they concluded.

The researchers had no financial conflicts to disclose.

SOURCE: Cardona ID et al. J Allergy Clin Immunol Pract. 2019 Nov 13. doi: 10.1016/j.jaip.2019.10.042.

A regimen of twice-daily baths followed by occlusive moisturizer improved atopic dermatitis in children with moderate to severe disease more effectively than did a twice-weekly protocol, based on data from 42 children.

Guidelines for bathing frequency for children with atopic dermatitis are inconsistent and often confusing for parents, according to Ivan D. Cardona, MD, of Maine Medical Research Institute, Portland, and colleagues.

In a study published in the Journal of Allergy and Clinical Immunology: In Practice, the researchers randomized 42 children aged 6 months to 11 years with moderate to severe atopic dermatitis to a routine of twice-weekly “soak and seal” (SS) procedures consisting of soaking baths for 10 minutes or less, followed by an occlusive emollient, or to twice-daily SS with baths of 15-20 minutes followed by emollient. The groups were treated for 2 weeks, then switched protocols. The study included a total of four clinic visits over 5 weeks. All patients also received standard of care low-potency topical corticosteroids and moisturizer.

Overall, the frequent bathing (“wet method”) led to a decrease of 21.2 on the SCORing Atopic Dermatitis Index (SCORAD) compared with the less frequent bathing (“dry method”). Improvements in SCORAD (the primary outcome) correlated with a secondary outcome of improved scores on the parent-rated Atopic Dermatitis Quickscore.

The findings were limited by several factors including the small sample size, large rate of attrition prior to randomization among initially screened children, lack of data on environmental factors such as water temperature and quality, and the lack of a washout period between the treatment protocols, the researchers noted. They acknowledged that “twice-daily SS bathing in the real world can be time consuming, making adherence difficult for families.”

However, the results suggest that the frequent bathing protocol was safe and effective at improving symptoms of atopic dermatitis, and may reduce steroid use, they concluded.

The researchers had no financial conflicts to disclose.

SOURCE: Cardona ID et al. J Allergy Clin Immunol Pract. 2019 Nov 13. doi: 10.1016/j.jaip.2019.10.042.

NEW ORLEANS – After Massachusetts passed antibullying legislation in 2009, Peter C. Raffalli, MD, saw an opportunity to improve care for the increasing numbers of children presenting to his neurology practice at Boston Children’s Hospital who were victims of bullying – especially those with developmental disabilities.

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“I had been thinking of a clinic to help kids with these issues, aside from just helping them deal with the fallout: the depression, anxiety, et cetera, that comes with being bullied,” Dr. Raffalli recalled at the annual meeting of the American Academy of Pediatrics. “I wanted to do something to help present to families the evidence-based strategies regarding bullying prevention, detection, and intervention that might help to stop the bullying.”

This led him to launch the Bullying and Cyberbullying Prevention and Advocacy Collaborative (BACPAC) at Boston Children’s Hospital, which began in 2009 as an educational resource for families, medical colleagues, and schools. Dr. Raffalli also formed an alliance with the Massachusetts Aggression Reduction Center at Bridgewater State University (Ann Neurol. 2016;79[2]:167-8).

Two years later in 2011, BACPAC became a formal clinic at Boston Children’s that serves as a subspecialty consult service for victims of bullying and their families. The clinic team consists of a child neurologist, a social worker, and an education resource specialist who meet with the bullying victim and his/her family in initial consultation for 90 minutes. The goal is to develop an evidence-based plan for bullying prevention, detection, and intervention that is individualized to the patient’s developmental and social needs.

“We tell families that bullying is recognized medically and legally as a form of abuse,” said Dr. Raffalli. “The medical and psychological consequences are similar to other forms of abuse. In the clinic, I explain to families that bullying is never the victim’s fault, and they should not blame themselves for the bullying. You’d be surprised how often patients do think the bullying is their fault.”
 

The extent of the problem

Researchers estimate that 25%-30% of children will experience some form of bullying between kindergarten and grade 12, and about 8% will engage in bullying themselves. When BACPAC began in 2009, Dr. Raffalli conducted an informal search of peer-reviewed literature on bullying in children with special needs; it yielded just four articles. “Since then, there’s been an exponential explosion of literature on various aspects of bullying,” he said. Now there is ample evidence in the peer-reviewed literature to show the increased risk for bullying/cyberbullying in children/teens, not just with neurodevelopmental disorders, but also for kids with other medical disorders such as obesity, asthma, and allergies.

“We’ve had a good number of kids over the years with peanut allergy who were literally threatened physically with peanut butter at school,” he said. “It’s incredible how callous some kids can be. Kids with oppositional defiant disorder, impulse control disorder, and callous/unemotional traits from a psychological standpoint are hardest to reach when it comes to getting them to stop bullying. You’d be surprised how frequently bullies use the phrase [to their victims], ‘You should kill yourself.’ They don’t realize the damage they’re doing to people. Bullying can lead to severe psychological but also long-term medical problems, including suicidal ideation.”

Published studies show that the highest incidences of bullying occur in children with neurodevelopmental conditions such as ADHD, autistic spectrum disorders, Tourette syndrome, and other learning disabilities (Eur J Spec Needs Ed. 2010;25[1]:77-91). This population of children is overrepresented in bullying “because the services they receive at school make their disabilities more visible,” explained Dr. Raffalli, who is also an assistant professor of neurology at Harvard Medical School, Boston. “They stand out, and they have social information–processing deficits or distortions that exacerbate bullying involvement. They also have difficulty interpreting social cues or attributing hostile characteristics to their peer’s behavior.”
 

The consequences of bullying

The psychological and educational consequences of bullying among children in general include being more likely to develop depression, loneliness, low self-esteem, alcohol and drug abuse, sleeping difficulties, self-harm, and suicidal ideation and attempts. “We’re social creatures, and when we don’t have those social connections, we get very depressed.”

Bullying victims also are more likely to develop school avoidance and absence, decreased school performance, poor concentration, high anxiety, and social withdrawal – all of which limit their opportunities to learn. “The No. 1 thing you can do to help these kids is to believe their story – to explain to them that it’s not their fault, and to explain that you are there for them and that you support them,” he said. “When a kid gets the feeling that someone is willing to listen to them and believe them, it does an enormous good for their emotional state.”

Doug Brunk/MDedge News

Dr. Raffalli added that a toxic stress response can occur when a child experiences strong, frequent, and/or prolonged adversity – such as physical or emotional abuse, chronic neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship – without adequate adult support. This kind of prolonged activation of the stress response systems can disrupt the development of brain architecture and other organ systems, and increase the risk for stress-related disease and cognitive impairment well into the adult years.

In the Harvard Review of Psychiatry, researchers set out to investigate what’s known about the long-term health effects of childhood bullying. They found that bullying can induce “aspects of the stress response, via epigenetic, inflammatory, and metabolic mediators [that] have the capacity to compromise mental and physical health, and to increase the risk of disease.” The researchers advised clinicians who care for children to assess the mental and physical health effects of bullying (Harv Rev Psychiatry. 2017;25[2]:89-95).

Additional vulnerabilities for bullying victims include parents and children whose primary language is not English, as well as parents with mental illness or substance abuse and families living in poverty. “We have to keep in mind how much additional stress they may be dealing with. This can make it harder for them to cope. Bullies also are shown to be at higher risk for psychological and legal trouble into adulthood, so we should be trying to help them too. We have to keep in mind that these are all developing kids.”
 

Cyberbullying

In Dr. Raffalli’s clinical experience, cyberbullying has become the bully’s weapon of choice. “I call it the stealth bomber of bullying,” he said. “Cyberbullying can start as early as the second or third grade. Most parents are not giving phones to second-graders. I’m worried that it’s going to get worse, though, with the excuse that ‘I feel safer if they have a cell phone so they can call me.’ I tell parents that they still make flip phones. You don’t have to get a smartphone for a second- or third-grader, or even for a sixth-grader.”

By the time kids reach fourth and fifth grade, he continued, they begin to form their opinion “about what they believe is cool and not cool, and they begin to get into cliques that have similar beliefs, and support each other, and may break off from old friends.” He added that, while adult predation “makes the news and is certainly something we should all be concerned about, the incidence of being harassed and bullied by someone in your own age group at school is actually much higher and still has serious outcomes, including the possibility of death.”

The Massachusetts antibullying law stipulates that all teachers and all school personnel have to participate in mandatory bullying training. Schools also are required to draft and follow a bullying investigative protocol.

“Apparently the schools have all done this, yet the number of times that schools use interventions that are not advisable, such as mediation, is incredible to me,” Dr. Raffalli said. “Bringing the bully and the victim together for a ‘cup of coffee and a handshake’ is not advisable. Mediation has been shown in a number of studies to be detrimental in bullying situations. Things can easily get worse.”

Often, family members who bring their child to the BACPAC “feel that their child’s school is not helping them,” he said. “We should try to figure out why those schools are having such a hard time and see if we can help them.”

Dr. Raffalli reported having no financial disclosures.

[email protected]

NEW ORLEANS – After Massachusetts passed antibullying legislation in 2009, Peter C. Raffalli, MD, saw an opportunity to improve care for the increasing numbers of children presenting to his neurology practice at Boston Children’s Hospital who were victims of bullying – especially those with developmental disabilities.

omgimages/thinkstockphotos.com

“I had been thinking of a clinic to help kids with these issues, aside from just helping them deal with the fallout: the depression, anxiety, et cetera, that comes with being bullied,” Dr. Raffalli recalled at the annual meeting of the American Academy of Pediatrics. “I wanted to do something to help present to families the evidence-based strategies regarding bullying prevention, detection, and intervention that might help to stop the bullying.”

This led him to launch the Bullying and Cyberbullying Prevention and Advocacy Collaborative (BACPAC) at Boston Children’s Hospital, which began in 2009 as an educational resource for families, medical colleagues, and schools. Dr. Raffalli also formed an alliance with the Massachusetts Aggression Reduction Center at Bridgewater State University (Ann Neurol. 2016;79[2]:167-8).

Two years later in 2011, BACPAC became a formal clinic at Boston Children’s that serves as a subspecialty consult service for victims of bullying and their families. The clinic team consists of a child neurologist, a social worker, and an education resource specialist who meet with the bullying victim and his/her family in initial consultation for 90 minutes. The goal is to develop an evidence-based plan for bullying prevention, detection, and intervention that is individualized to the patient’s developmental and social needs.

“We tell families that bullying is recognized medically and legally as a form of abuse,” said Dr. Raffalli. “The medical and psychological consequences are similar to other forms of abuse. In the clinic, I explain to families that bullying is never the victim’s fault, and they should not blame themselves for the bullying. You’d be surprised how often patients do think the bullying is their fault.”
 

The extent of the problem

Researchers estimate that 25%-30% of children will experience some form of bullying between kindergarten and grade 12, and about 8% will engage in bullying themselves. When BACPAC began in 2009, Dr. Raffalli conducted an informal search of peer-reviewed literature on bullying in children with special needs; it yielded just four articles. “Since then, there’s been an exponential explosion of literature on various aspects of bullying,” he said. Now there is ample evidence in the peer-reviewed literature to show the increased risk for bullying/cyberbullying in children/teens, not just with neurodevelopmental disorders, but also for kids with other medical disorders such as obesity, asthma, and allergies.

“We’ve had a good number of kids over the years with peanut allergy who were literally threatened physically with peanut butter at school,” he said. “It’s incredible how callous some kids can be. Kids with oppositional defiant disorder, impulse control disorder, and callous/unemotional traits from a psychological standpoint are hardest to reach when it comes to getting them to stop bullying. You’d be surprised how frequently bullies use the phrase [to their victims], ‘You should kill yourself.’ They don’t realize the damage they’re doing to people. Bullying can lead to severe psychological but also long-term medical problems, including suicidal ideation.”

Published studies show that the highest incidences of bullying occur in children with neurodevelopmental conditions such as ADHD, autistic spectrum disorders, Tourette syndrome, and other learning disabilities (Eur J Spec Needs Ed. 2010;25[1]:77-91). This population of children is overrepresented in bullying “because the services they receive at school make their disabilities more visible,” explained Dr. Raffalli, who is also an assistant professor of neurology at Harvard Medical School, Boston. “They stand out, and they have social information–processing deficits or distortions that exacerbate bullying involvement. They also have difficulty interpreting social cues or attributing hostile characteristics to their peer’s behavior.”
 

The consequences of bullying

The psychological and educational consequences of bullying among children in general include being more likely to develop depression, loneliness, low self-esteem, alcohol and drug abuse, sleeping difficulties, self-harm, and suicidal ideation and attempts. “We’re social creatures, and when we don’t have those social connections, we get very depressed.”

Bullying victims also are more likely to develop school avoidance and absence, decreased school performance, poor concentration, high anxiety, and social withdrawal – all of which limit their opportunities to learn. “The No. 1 thing you can do to help these kids is to believe their story – to explain to them that it’s not their fault, and to explain that you are there for them and that you support them,” he said. “When a kid gets the feeling that someone is willing to listen to them and believe them, it does an enormous good for their emotional state.”

Doug Brunk/MDedge News

Dr. Raffalli added that a toxic stress response can occur when a child experiences strong, frequent, and/or prolonged adversity – such as physical or emotional abuse, chronic neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship – without adequate adult support. This kind of prolonged activation of the stress response systems can disrupt the development of brain architecture and other organ systems, and increase the risk for stress-related disease and cognitive impairment well into the adult years.

In the Harvard Review of Psychiatry, researchers set out to investigate what’s known about the long-term health effects of childhood bullying. They found that bullying can induce “aspects of the stress response, via epigenetic, inflammatory, and metabolic mediators [that] have the capacity to compromise mental and physical health, and to increase the risk of disease.” The researchers advised clinicians who care for children to assess the mental and physical health effects of bullying (Harv Rev Psychiatry. 2017;25[2]:89-95).

Additional vulnerabilities for bullying victims include parents and children whose primary language is not English, as well as parents with mental illness or substance abuse and families living in poverty. “We have to keep in mind how much additional stress they may be dealing with. This can make it harder for them to cope. Bullies also are shown to be at higher risk for psychological and legal trouble into adulthood, so we should be trying to help them too. We have to keep in mind that these are all developing kids.”
 

Cyberbullying

In Dr. Raffalli’s clinical experience, cyberbullying has become the bully’s weapon of choice. “I call it the stealth bomber of bullying,” he said. “Cyberbullying can start as early as the second or third grade. Most parents are not giving phones to second-graders. I’m worried that it’s going to get worse, though, with the excuse that ‘I feel safer if they have a cell phone so they can call me.’ I tell parents that they still make flip phones. You don’t have to get a smartphone for a second- or third-grader, or even for a sixth-grader.”

By the time kids reach fourth and fifth grade, he continued, they begin to form their opinion “about what they believe is cool and not cool, and they begin to get into cliques that have similar beliefs, and support each other, and may break off from old friends.” He added that, while adult predation “makes the news and is certainly something we should all be concerned about, the incidence of being harassed and bullied by someone in your own age group at school is actually much higher and still has serious outcomes, including the possibility of death.”

The Massachusetts antibullying law stipulates that all teachers and all school personnel have to participate in mandatory bullying training. Schools also are required to draft and follow a bullying investigative protocol.

“Apparently the schools have all done this, yet the number of times that schools use interventions that are not advisable, such as mediation, is incredible to me,” Dr. Raffalli said. “Bringing the bully and the victim together for a ‘cup of coffee and a handshake’ is not advisable. Mediation has been shown in a number of studies to be detrimental in bullying situations. Things can easily get worse.”

Often, family members who bring their child to the BACPAC “feel that their child’s school is not helping them,” he said. “We should try to figure out why those schools are having such a hard time and see if we can help them.”

Dr. Raffalli reported having no financial disclosures.

[email protected]

NEW ORLEANS – After Massachusetts passed antibullying legislation in 2009, Peter C. Raffalli, MD, saw an opportunity to improve care for the increasing numbers of children presenting to his neurology practice at Boston Children’s Hospital who were victims of bullying – especially those with developmental disabilities.

omgimages/thinkstockphotos.com

“I had been thinking of a clinic to help kids with these issues, aside from just helping them deal with the fallout: the depression, anxiety, et cetera, that comes with being bullied,” Dr. Raffalli recalled at the annual meeting of the American Academy of Pediatrics. “I wanted to do something to help present to families the evidence-based strategies regarding bullying prevention, detection, and intervention that might help to stop the bullying.”

This led him to launch the Bullying and Cyberbullying Prevention and Advocacy Collaborative (BACPAC) at Boston Children’s Hospital, which began in 2009 as an educational resource for families, medical colleagues, and schools. Dr. Raffalli also formed an alliance with the Massachusetts Aggression Reduction Center at Bridgewater State University (Ann Neurol. 2016;79[2]:167-8).

Two years later in 2011, BACPAC became a formal clinic at Boston Children’s that serves as a subspecialty consult service for victims of bullying and their families. The clinic team consists of a child neurologist, a social worker, and an education resource specialist who meet with the bullying victim and his/her family in initial consultation for 90 minutes. The goal is to develop an evidence-based plan for bullying prevention, detection, and intervention that is individualized to the patient’s developmental and social needs.

“We tell families that bullying is recognized medically and legally as a form of abuse,” said Dr. Raffalli. “The medical and psychological consequences are similar to other forms of abuse. In the clinic, I explain to families that bullying is never the victim’s fault, and they should not blame themselves for the bullying. You’d be surprised how often patients do think the bullying is their fault.”
 

The extent of the problem

Researchers estimate that 25%-30% of children will experience some form of bullying between kindergarten and grade 12, and about 8% will engage in bullying themselves. When BACPAC began in 2009, Dr. Raffalli conducted an informal search of peer-reviewed literature on bullying in children with special needs; it yielded just four articles. “Since then, there’s been an exponential explosion of literature on various aspects of bullying,” he said. Now there is ample evidence in the peer-reviewed literature to show the increased risk for bullying/cyberbullying in children/teens, not just with neurodevelopmental disorders, but also for kids with other medical disorders such as obesity, asthma, and allergies.

“We’ve had a good number of kids over the years with peanut allergy who were literally threatened physically with peanut butter at school,” he said. “It’s incredible how callous some kids can be. Kids with oppositional defiant disorder, impulse control disorder, and callous/unemotional traits from a psychological standpoint are hardest to reach when it comes to getting them to stop bullying. You’d be surprised how frequently bullies use the phrase [to their victims], ‘You should kill yourself.’ They don’t realize the damage they’re doing to people. Bullying can lead to severe psychological but also long-term medical problems, including suicidal ideation.”

Published studies show that the highest incidences of bullying occur in children with neurodevelopmental conditions such as ADHD, autistic spectrum disorders, Tourette syndrome, and other learning disabilities (Eur J Spec Needs Ed. 2010;25[1]:77-91). This population of children is overrepresented in bullying “because the services they receive at school make their disabilities more visible,” explained Dr. Raffalli, who is also an assistant professor of neurology at Harvard Medical School, Boston. “They stand out, and they have social information–processing deficits or distortions that exacerbate bullying involvement. They also have difficulty interpreting social cues or attributing hostile characteristics to their peer’s behavior.”
 

The consequences of bullying

The psychological and educational consequences of bullying among children in general include being more likely to develop depression, loneliness, low self-esteem, alcohol and drug abuse, sleeping difficulties, self-harm, and suicidal ideation and attempts. “We’re social creatures, and when we don’t have those social connections, we get very depressed.”

Bullying victims also are more likely to develop school avoidance and absence, decreased school performance, poor concentration, high anxiety, and social withdrawal – all of which limit their opportunities to learn. “The No. 1 thing you can do to help these kids is to believe their story – to explain to them that it’s not their fault, and to explain that you are there for them and that you support them,” he said. “When a kid gets the feeling that someone is willing to listen to them and believe them, it does an enormous good for their emotional state.”

Doug Brunk/MDedge News

Dr. Raffalli added that a toxic stress response can occur when a child experiences strong, frequent, and/or prolonged adversity – such as physical or emotional abuse, chronic neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship – without adequate adult support. This kind of prolonged activation of the stress response systems can disrupt the development of brain architecture and other organ systems, and increase the risk for stress-related disease and cognitive impairment well into the adult years.

In the Harvard Review of Psychiatry, researchers set out to investigate what’s known about the long-term health effects of childhood bullying. They found that bullying can induce “aspects of the stress response, via epigenetic, inflammatory, and metabolic mediators [that] have the capacity to compromise mental and physical health, and to increase the risk of disease.” The researchers advised clinicians who care for children to assess the mental and physical health effects of bullying (Harv Rev Psychiatry. 2017;25[2]:89-95).

Additional vulnerabilities for bullying victims include parents and children whose primary language is not English, as well as parents with mental illness or substance abuse and families living in poverty. “We have to keep in mind how much additional stress they may be dealing with. This can make it harder for them to cope. Bullies also are shown to be at higher risk for psychological and legal trouble into adulthood, so we should be trying to help them too. We have to keep in mind that these are all developing kids.”
 

Cyberbullying

In Dr. Raffalli’s clinical experience, cyberbullying has become the bully’s weapon of choice. “I call it the stealth bomber of bullying,” he said. “Cyberbullying can start as early as the second or third grade. Most parents are not giving phones to second-graders. I’m worried that it’s going to get worse, though, with the excuse that ‘I feel safer if they have a cell phone so they can call me.’ I tell parents that they still make flip phones. You don’t have to get a smartphone for a second- or third-grader, or even for a sixth-grader.”

By the time kids reach fourth and fifth grade, he continued, they begin to form their opinion “about what they believe is cool and not cool, and they begin to get into cliques that have similar beliefs, and support each other, and may break off from old friends.” He added that, while adult predation “makes the news and is certainly something we should all be concerned about, the incidence of being harassed and bullied by someone in your own age group at school is actually much higher and still has serious outcomes, including the possibility of death.”

The Massachusetts antibullying law stipulates that all teachers and all school personnel have to participate in mandatory bullying training. Schools also are required to draft and follow a bullying investigative protocol.

“Apparently the schools have all done this, yet the number of times that schools use interventions that are not advisable, such as mediation, is incredible to me,” Dr. Raffalli said. “Bringing the bully and the victim together for a ‘cup of coffee and a handshake’ is not advisable. Mediation has been shown in a number of studies to be detrimental in bullying situations. Things can easily get worse.”

Often, family members who bring their child to the BACPAC “feel that their child’s school is not helping them,” he said. “We should try to figure out why those schools are having such a hard time and see if we can help them.”

Dr. Raffalli reported having no financial disclosures.

[email protected]

The unusually high levels of flu activity seen at the end of November have been followed by a decrease in activity, according to the Centers for Disease Control and Prevention.

Nationally, 3.2% of outpatient visits were for influenza-like illness (ILI) during the week of Dec. 1-7, the CDC reported. That is down from 3.4% the week before, which was the highest November rate in 10 years. The national baseline rate is 2.4%, and the current 3.2% marks the fifth consecutive week that the outpatient ILI rate has been at or above the baseline level, the CDC report noted.

The drop in activity “may be influenced in part by a reduction in routine healthcare visits surrounding the Thanksgiving holiday. … as has occurred during previous seasons,” the CDC influenza division said Dec. 13 in its weekly flu report.

The early spike in “activity is being caused mostly by influenza B/Victoria viruses, which is unusual for this time of year,” the report said. Since the beginning of the 2019-2020 season a little over 2 months ago, almost 70% of specimens that have been positive for influenza have been identified as type B.

The nationwide decline in activity doesn’t, however, show up at the state level. For the week ending Dec. 7, there were eight states along with Puerto Rico at level 10 on the CDC’s 1-10 scale of flu activity, as there were the previous week. Washington state moved up from 9 to 10, but Louisiana, which was at level 10 last week, had insufficient data to be included this week, the CDC data show.

There were four flu-related pediatric deaths reported to the CDC during the week ending Dec. 7, all occurring in previous weeks, which brings the total to 10 for the season. In 2018-2019, there were 143 pediatric deaths caused by influenza, the CDC said.

[email protected]

The unusually high levels of flu activity seen at the end of November have been followed by a decrease in activity, according to the Centers for Disease Control and Prevention.

Nationally, 3.2% of outpatient visits were for influenza-like illness (ILI) during the week of Dec. 1-7, the CDC reported. That is down from 3.4% the week before, which was the highest November rate in 10 years. The national baseline rate is 2.4%, and the current 3.2% marks the fifth consecutive week that the outpatient ILI rate has been at or above the baseline level, the CDC report noted.

The drop in activity “may be influenced in part by a reduction in routine healthcare visits surrounding the Thanksgiving holiday. … as has occurred during previous seasons,” the CDC influenza division said Dec. 13 in its weekly flu report.

The early spike in “activity is being caused mostly by influenza B/Victoria viruses, which is unusual for this time of year,” the report said. Since the beginning of the 2019-2020 season a little over 2 months ago, almost 70% of specimens that have been positive for influenza have been identified as type B.

The nationwide decline in activity doesn’t, however, show up at the state level. For the week ending Dec. 7, there were eight states along with Puerto Rico at level 10 on the CDC’s 1-10 scale of flu activity, as there were the previous week. Washington state moved up from 9 to 10, but Louisiana, which was at level 10 last week, had insufficient data to be included this week, the CDC data show.

There were four flu-related pediatric deaths reported to the CDC during the week ending Dec. 7, all occurring in previous weeks, which brings the total to 10 for the season. In 2018-2019, there were 143 pediatric deaths caused by influenza, the CDC said.

[email protected]

The unusually high levels of flu activity seen at the end of November have been followed by a decrease in activity, according to the Centers for Disease Control and Prevention.

Nationally, 3.2% of outpatient visits were for influenza-like illness (ILI) during the week of Dec. 1-7, the CDC reported. That is down from 3.4% the week before, which was the highest November rate in 10 years. The national baseline rate is 2.4%, and the current 3.2% marks the fifth consecutive week that the outpatient ILI rate has been at or above the baseline level, the CDC report noted.

The drop in activity “may be influenced in part by a reduction in routine healthcare visits surrounding the Thanksgiving holiday. … as has occurred during previous seasons,” the CDC influenza division said Dec. 13 in its weekly flu report.

The early spike in “activity is being caused mostly by influenza B/Victoria viruses, which is unusual for this time of year,” the report said. Since the beginning of the 2019-2020 season a little over 2 months ago, almost 70% of specimens that have been positive for influenza have been identified as type B.

The nationwide decline in activity doesn’t, however, show up at the state level. For the week ending Dec. 7, there were eight states along with Puerto Rico at level 10 on the CDC’s 1-10 scale of flu activity, as there were the previous week. Washington state moved up from 9 to 10, but Louisiana, which was at level 10 last week, had insufficient data to be included this week, the CDC data show.

There were four flu-related pediatric deaths reported to the CDC during the week ending Dec. 7, all occurring in previous weeks, which brings the total to 10 for the season. In 2018-2019, there were 143 pediatric deaths caused by influenza, the CDC said.

[email protected]

LOS ANGELES – Until the recent approval of liraglutide for the treatment of children and adolescents with type 2 diabetes, investigators like Sonia Caprio, MD, were at their wits’ end watching the beta-cell function of their patients decline on metformin treatment.

Doug Brunk/MDedge News

“The kids were not doing well. It was like they were being treated with water,” Dr. Caprio, a pediatric endocrinologist at Yale University, New Haven, Conn., said at the annual World Congress on Insulin Resistance, Diabetes and Cardiovascular Disease.

For example, in the NIH-funded TODAY (Treatment Options for Type 2 Diabetes in Adolescents and Youth) study that began enrollment in 2004, 699 patients aged between 10 and 17 years and with type 2 diabetes were treated with metformin (1,000 mg, twice daily) to attain a glycated hemoglobin level of less than 8% and were then randomly assigned to continued treatment with metformin alone or to metformin combined with rosiglitazone (4 mg, twice a day) or a lifestyle-intervention program that focused on weight loss through modifying eating and activity behaviors (N Engl J Med. 2012;366:2247-56).

Over the course of 11 months, the researchers found that 46% of the children were failing treatment. “The worst arm was the metformin arm,” said Dr. Caprio, who was involved with the study. “Kids were not responding to the drug at all. About 52% of children failed to do better using metformin – a classic drug that we all start kids on when we diagnose them with type 2 diabetes.”

Findings from a follow-up study, TODAY2, showed that these young patients were prone to serious diabetes-related events, such as heart attacks, chronic kidney disease, retinal disease, neuropathy, and complications in the offspring of pregnancies.

In addition, results from the RISE (Restoring Insulin Secretion) Pediatric Medication Study found that, in youth with impaired glucose tolerance or recently diagnosed type 2 diabetes, neither 3 months of insulin glargine followed by 9 months of metformin nor 12 months of metformin alone halted the progressive deterioration of beta-cell function (Diabetes Care. 2018 Aug; 41[8]:1717-25).

“The uniqueness of RISE is that we employed very sophisticated techniques to measure insulin secretion and sensitivity while they were being treated with these usual drugs,” said Dr. Caprio, who was one of the study investigators. “The beta cell is unresponsive to metformin and other treatments. The question is, why?”

Despite these findings, 2018 consensus guidelines from the American Diabetes Association on the evaluation and management of youth-onset diabetes (Diabetes Care. 2018;41:2648-68) call for the administration of metformin twice daily in youth with new-onset diabetes who have a hemoglobin A_1c (HbA_1c) level of less than 8.5%. “I argue that is not the way. We need better ways to treat [these patients] because they are moving fast to having complications,” she said.

Enter the Ellipse Trial, a pivotal multicenter, randomized study that evaluated the effect of the glucagonlike peptide-1 receptor agonist liraglutide in children and adolescents with type 2 diabetes (N Engl J Med. 2019;381:637-46).

Researchers, led by William V. Tamborlane, MD, chief of Yale Medicine Pediatric Endocrinology, also in New Haven, randomized 135 patients to one of two arms: 66 to subcutaneous liraglutide (up to 1.8 mg/day) and 69 to placebo for a 26-week, double-blind period, followed by a 26-week open-label extension period. All patients received metformin during the trial. More than half of the study participants (62%) were female, the mean age was 15 years, 65% were white, the mean body mass index was 33.9 kg/m², their mean fasting glucose was 8.4 mmol/L, and their mean HbA_1c was 7.8%.

At 26 weeks, the mean glycated hemoglobin level had decreased by 0.64 percentage points with liraglutide and increased by 0.42 percentage points with placebo, for an estimated treatment difference of −1.06 percentage points (P less than .001). By 52 weeks, the difference increased to −1.30 percentage points.

“There was also a significant drop in BMI z score in patients treated with liraglutide, which is important,” Dr. Caprio said. “This medication is having an impact on weight, which is a key driver of the onset of type 2 diabetes in youth. This is a remarkable achievement because weight loss is hard to achieve in obese adolescents, as we showed in the TODAY study.”

The number of adverse events reported by patients was similar in the treatment and placebo groups (85% and 81%, respectively), but the overall rates of adverse events and gastrointestinal adverse events were higher with liraglutide.

“I use liraglutide just for weight reduction because I mainly see a lot of kids with obesity. Many kids are not responding because of the GI effects of this drug. I think the weight loss could have been better had the investigators moved to a dose of 1.8 mg, which we use in adults.”

A fasting plasma glucose of 6.1 mmol/L was the primary reason for participants remaining on a lower dose of liraglutide, she said. At the same time, liraglutide concentration data indicated a high rate of noncompliance, which was expected in this population. “That’s a big problem we face with children,” Dr. Caprio said. “Some of them are not constantly taking the medication. They skip doses a lot. But that happens with patients in this age group.”

“Finally, we have something else to help children and teenagers to delay the complications we are seeing,” Dr. Caprio said. “To me, I think this is a new era. I have hope. It will be interesting to see whether liraglutide and perhaps SGLT2 [sodium-glucose transporter 2] inhibitors can delay the onset of type 2 diabetes in children. In my view, we will be doing this with drugs. I don’t think the weight loss [concerns are] going to go away without medication, unfortunately.”

Dr. Caprio reported having no financial disclosures.

LOS ANGELES – Until the recent approval of liraglutide for the treatment of children and adolescents with type 2 diabetes, investigators like Sonia Caprio, MD, were at their wits’ end watching the beta-cell function of their patients decline on metformin treatment.

Doug Brunk/MDedge News

“The kids were not doing well. It was like they were being treated with water,” Dr. Caprio, a pediatric endocrinologist at Yale University, New Haven, Conn., said at the annual World Congress on Insulin Resistance, Diabetes and Cardiovascular Disease.

For example, in the NIH-funded TODAY (Treatment Options for Type 2 Diabetes in Adolescents and Youth) study that began enrollment in 2004, 699 patients aged between 10 and 17 years and with type 2 diabetes were treated with metformin (1,000 mg, twice daily) to attain a glycated hemoglobin level of less than 8% and were then randomly assigned to continued treatment with metformin alone or to metformin combined with rosiglitazone (4 mg, twice a day) or a lifestyle-intervention program that focused on weight loss through modifying eating and activity behaviors (N Engl J Med. 2012;366:2247-56).

Over the course of 11 months, the researchers found that 46% of the children were failing treatment. “The worst arm was the metformin arm,” said Dr. Caprio, who was involved with the study. “Kids were not responding to the drug at all. About 52% of children failed to do better using metformin – a classic drug that we all start kids on when we diagnose them with type 2 diabetes.”

Findings from a follow-up study, TODAY2, showed that these young patients were prone to serious diabetes-related events, such as heart attacks, chronic kidney disease, retinal disease, neuropathy, and complications in the offspring of pregnancies.

In addition, results from the RISE (Restoring Insulin Secretion) Pediatric Medication Study found that, in youth with impaired glucose tolerance or recently diagnosed type 2 diabetes, neither 3 months of insulin glargine followed by 9 months of metformin nor 12 months of metformin alone halted the progressive deterioration of beta-cell function (Diabetes Care. 2018 Aug; 41[8]:1717-25).

“The uniqueness of RISE is that we employed very sophisticated techniques to measure insulin secretion and sensitivity while they were being treated with these usual drugs,” said Dr. Caprio, who was one of the study investigators. “The beta cell is unresponsive to metformin and other treatments. The question is, why?”

Despite these findings, 2018 consensus guidelines from the American Diabetes Association on the evaluation and management of youth-onset diabetes (Diabetes Care. 2018;41:2648-68) call for the administration of metformin twice daily in youth with new-onset diabetes who have a hemoglobin A_1c (HbA_1c) level of less than 8.5%. “I argue that is not the way. We need better ways to treat [these patients] because they are moving fast to having complications,” she said.

Enter the Ellipse Trial, a pivotal multicenter, randomized study that evaluated the effect of the glucagonlike peptide-1 receptor agonist liraglutide in children and adolescents with type 2 diabetes (N Engl J Med. 2019;381:637-46).

Researchers, led by William V. Tamborlane, MD, chief of Yale Medicine Pediatric Endocrinology, also in New Haven, randomized 135 patients to one of two arms: 66 to subcutaneous liraglutide (up to 1.8 mg/day) and 69 to placebo for a 26-week, double-blind period, followed by a 26-week open-label extension period. All patients received metformin during the trial. More than half of the study participants (62%) were female, the mean age was 15 years, 65% were white, the mean body mass index was 33.9 kg/m², their mean fasting glucose was 8.4 mmol/L, and their mean HbA_1c was 7.8%.

At 26 weeks, the mean glycated hemoglobin level had decreased by 0.64 percentage points with liraglutide and increased by 0.42 percentage points with placebo, for an estimated treatment difference of −1.06 percentage points (P less than .001). By 52 weeks, the difference increased to −1.30 percentage points.

“There was also a significant drop in BMI z score in patients treated with liraglutide, which is important,” Dr. Caprio said. “This medication is having an impact on weight, which is a key driver of the onset of type 2 diabetes in youth. This is a remarkable achievement because weight loss is hard to achieve in obese adolescents, as we showed in the TODAY study.”

The number of adverse events reported by patients was similar in the treatment and placebo groups (85% and 81%, respectively), but the overall rates of adverse events and gastrointestinal adverse events were higher with liraglutide.

“I use liraglutide just for weight reduction because I mainly see a lot of kids with obesity. Many kids are not responding because of the GI effects of this drug. I think the weight loss could have been better had the investigators moved to a dose of 1.8 mg, which we use in adults.”

A fasting plasma glucose of 6.1 mmol/L was the primary reason for participants remaining on a lower dose of liraglutide, she said. At the same time, liraglutide concentration data indicated a high rate of noncompliance, which was expected in this population. “That’s a big problem we face with children,” Dr. Caprio said. “Some of them are not constantly taking the medication. They skip doses a lot. But that happens with patients in this age group.”

“Finally, we have something else to help children and teenagers to delay the complications we are seeing,” Dr. Caprio said. “To me, I think this is a new era. I have hope. It will be interesting to see whether liraglutide and perhaps SGLT2 [sodium-glucose transporter 2] inhibitors can delay the onset of type 2 diabetes in children. In my view, we will be doing this with drugs. I don’t think the weight loss [concerns are] going to go away without medication, unfortunately.”

Dr. Caprio reported having no financial disclosures.

LOS ANGELES – Until the recent approval of liraglutide for the treatment of children and adolescents with type 2 diabetes, investigators like Sonia Caprio, MD, were at their wits’ end watching the beta-cell function of their patients decline on metformin treatment.

Doug Brunk/MDedge News

“The kids were not doing well. It was like they were being treated with water,” Dr. Caprio, a pediatric endocrinologist at Yale University, New Haven, Conn., said at the annual World Congress on Insulin Resistance, Diabetes and Cardiovascular Disease.

For example, in the NIH-funded TODAY (Treatment Options for Type 2 Diabetes in Adolescents and Youth) study that began enrollment in 2004, 699 patients aged between 10 and 17 years and with type 2 diabetes were treated with metformin (1,000 mg, twice daily) to attain a glycated hemoglobin level of less than 8% and were then randomly assigned to continued treatment with metformin alone or to metformin combined with rosiglitazone (4 mg, twice a day) or a lifestyle-intervention program that focused on weight loss through modifying eating and activity behaviors (N Engl J Med. 2012;366:2247-56).

Over the course of 11 months, the researchers found that 46% of the children were failing treatment. “The worst arm was the metformin arm,” said Dr. Caprio, who was involved with the study. “Kids were not responding to the drug at all. About 52% of children failed to do better using metformin – a classic drug that we all start kids on when we diagnose them with type 2 diabetes.”

Findings from a follow-up study, TODAY2, showed that these young patients were prone to serious diabetes-related events, such as heart attacks, chronic kidney disease, retinal disease, neuropathy, and complications in the offspring of pregnancies.

In addition, results from the RISE (Restoring Insulin Secretion) Pediatric Medication Study found that, in youth with impaired glucose tolerance or recently diagnosed type 2 diabetes, neither 3 months of insulin glargine followed by 9 months of metformin nor 12 months of metformin alone halted the progressive deterioration of beta-cell function (Diabetes Care. 2018 Aug; 41[8]:1717-25).

“The uniqueness of RISE is that we employed very sophisticated techniques to measure insulin secretion and sensitivity while they were being treated with these usual drugs,” said Dr. Caprio, who was one of the study investigators. “The beta cell is unresponsive to metformin and other treatments. The question is, why?”

Despite these findings, 2018 consensus guidelines from the American Diabetes Association on the evaluation and management of youth-onset diabetes (Diabetes Care. 2018;41:2648-68) call for the administration of metformin twice daily in youth with new-onset diabetes who have a hemoglobin A_1c (HbA_1c) level of less than 8.5%. “I argue that is not the way. We need better ways to treat [these patients] because they are moving fast to having complications,” she said.

Enter the Ellipse Trial, a pivotal multicenter, randomized study that evaluated the effect of the glucagonlike peptide-1 receptor agonist liraglutide in children and adolescents with type 2 diabetes (N Engl J Med. 2019;381:637-46).

Researchers, led by William V. Tamborlane, MD, chief of Yale Medicine Pediatric Endocrinology, also in New Haven, randomized 135 patients to one of two arms: 66 to subcutaneous liraglutide (up to 1.8 mg/day) and 69 to placebo for a 26-week, double-blind period, followed by a 26-week open-label extension period. All patients received metformin during the trial. More than half of the study participants (62%) were female, the mean age was 15 years, 65% were white, the mean body mass index was 33.9 kg/m², their mean fasting glucose was 8.4 mmol/L, and their mean HbA_1c was 7.8%.

At 26 weeks, the mean glycated hemoglobin level had decreased by 0.64 percentage points with liraglutide and increased by 0.42 percentage points with placebo, for an estimated treatment difference of −1.06 percentage points (P less than .001). By 52 weeks, the difference increased to −1.30 percentage points.

“There was also a significant drop in BMI z score in patients treated with liraglutide, which is important,” Dr. Caprio said. “This medication is having an impact on weight, which is a key driver of the onset of type 2 diabetes in youth. This is a remarkable achievement because weight loss is hard to achieve in obese adolescents, as we showed in the TODAY study.”

The number of adverse events reported by patients was similar in the treatment and placebo groups (85% and 81%, respectively), but the overall rates of adverse events and gastrointestinal adverse events were higher with liraglutide.

“I use liraglutide just for weight reduction because I mainly see a lot of kids with obesity. Many kids are not responding because of the GI effects of this drug. I think the weight loss could have been better had the investigators moved to a dose of 1.8 mg, which we use in adults.”

A fasting plasma glucose of 6.1 mmol/L was the primary reason for participants remaining on a lower dose of liraglutide, she said. At the same time, liraglutide concentration data indicated a high rate of noncompliance, which was expected in this population. “That’s a big problem we face with children,” Dr. Caprio said. “Some of them are not constantly taking the medication. They skip doses a lot. But that happens with patients in this age group.”

“Finally, we have something else to help children and teenagers to delay the complications we are seeing,” Dr. Caprio said. “To me, I think this is a new era. I have hope. It will be interesting to see whether liraglutide and perhaps SGLT2 [sodium-glucose transporter 2] inhibitors can delay the onset of type 2 diabetes in children. In my view, we will be doing this with drugs. I don’t think the weight loss [concerns are] going to go away without medication, unfortunately.”

Dr. Caprio reported having no financial disclosures.

Women with asthma who suffer asthma exacerbation while pregnant are at increased risk for complications during pregnancy and delivery, and their infants are at increased risk for respiratory problems, according to data from a longitudinal study of 58,524 women with asthma.

Vesnaandjic/E+/Getty Images

“Asthma exacerbation during pregnancy has been found to be associated with adverse perinatal and pregnancy outcomes such as low birth weight, small for gestational age, preterm delivery, congenital malformation, preeclampsia, and perinatal mortality,” but previous studies have been small and limited to comparisons of asthmatic and nonasthmatic women, wrote Kawsari Abdullah, PhD, of Children’s Hospital of Eastern Ontario, Ottawa, and colleagues.

To determine the impact of asthma exacerbation on maternal and fetal outcomes, the researchers analyzed data from the Ontario Asthma Surveillance Information System to identify women with asthma who had at least one pregnancy resulting in a live or still birth between 2006 and 2012.

Overall, significantly more women with exacerbated asthma had preeclampsia or pregnancy-induced hypertension, compared with asthmatic women who had no exacerbations, at 5% vs. 4% and 7% vs. 5%, respectively (P less than .001), according to the study published in the European Respiratory Journal.

Adverse perinatal outcomes were significantly more likely among babies of mothers with exacerbated asthma, compared with those who had no exacerbations, including low birth weight (7% vs. 5%), small for gestational age (3% vs. 2%), preterm birth (8% vs. 7%), and congenital malformation (6% vs. 5%). All P values were less than .001, except for small for gestational age, which was P = .008.

In addition, significantly more babies of asthmatic women with exacerbated asthma during pregnancy had respiratory problems including asthma and pneumonia, compared with those of asthmatic women who had no exacerbations during pregnancy, at 38% vs. 31% and 24% vs. 22% (P less than .001 for both). The researchers found no significant interactions between maternal age and smoking and asthma exacerbations.

The findings were limited by several factors, including the lack of a validated algorithm for asthma exacerbation, which the researchers defined as five or more visits to a general practice clinician for asthma during pregnancy. Other limitations included the lack of categorizing asthma exacerbation by severity, and the inability to include the potential effects of asthma medication on maternal and fetal outcomes, Dr. Abdullah and colleagues noted.

However, the results were strengthened by the large sample size and ability to follow babies from birth until 5 years of age, they said.

“Targeting women with asthma during pregnancy and ensuring appropriate asthma management and postpartum follow-up may help to reduce the risk of pregnancy complications, adverse perinatal outcomes, and early childhood respiratory disorders,” they concluded.

This study is important because asthma is a common, potentially serious medical condition that complicates approximately 4%-8% of pregnancies, and one in three women with asthma experience an exacerbation during pregnancy, Iris Krishna, MD, a specialist in maternal/fetal medicine at Emory University, Atlanta, said in an interview.

“This study is unique in that it uses population-level data to assess the association between an asthma exacerbation during pregnancy and adverse perinatal outcomes,” Dr. Krishna said. “After adjusting for confounders, and consistent with previous studies, study findings suggest an increased risk for women with asthma who have an asthma exacerbation during pregnancy for preeclampsia [odds ratio, 1.3; P less than .001], pregnancy-induced hypertension [OR, 1.17; P less than .05], low-birth-weight infant [OR, 1.14; P less than .05], preterm birth [OR, 1.14; P less than .05], and congenital malformations [OR, 1.21; P less than .001].”

Dr. Krishna also noted the impact on early childhood outcomes. “In this study, children born to women who had an asthma exacerbation during pregnancy had a 23% higher risk of developing asthma before 5 years of age, which is consistent with previous studies. [The] investigators also reported a 12% higher risk of having pneumonia during the first 5 years of life for children born to women who had an asthma exacerbation during pregnancy.”

“Previous studies have suggested children born to mothers with uncontrolled asthma have an increased risk for respiratory infections, but this study is the first to report an association with pneumonia,” she said. This increased risk for childhood respiratory disorders warrants further study.

Consequently, “Women with asthma during pregnancy should have appropriate management to ensure good control to optimize pregnancy outcome,” Dr. Krishna emphasized. “Women who experience asthma exacerbations in pregnancy are at increased risk for preeclampsia, [pregnancy-induced hypertension], low birth weight, and preterm delivery and may require closer monitoring.”

The study was supported by the Institute for Clinical Evaluative Sciences. The researchers and Dr. Krishna had no financial conflicts to disclose.

SOURCE: Abdullah K et al. Eur Respir J. 2019 Nov 26. doi: 10.1183/13993003.01335-2019.

Women with asthma who suffer asthma exacerbation while pregnant are at increased risk for complications during pregnancy and delivery, and their infants are at increased risk for respiratory problems, according to data from a longitudinal study of 58,524 women with asthma.

Vesnaandjic/E+/Getty Images

“Asthma exacerbation during pregnancy has been found to be associated with adverse perinatal and pregnancy outcomes such as low birth weight, small for gestational age, preterm delivery, congenital malformation, preeclampsia, and perinatal mortality,” but previous studies have been small and limited to comparisons of asthmatic and nonasthmatic women, wrote Kawsari Abdullah, PhD, of Children’s Hospital of Eastern Ontario, Ottawa, and colleagues.

To determine the impact of asthma exacerbation on maternal and fetal outcomes, the researchers analyzed data from the Ontario Asthma Surveillance Information System to identify women with asthma who had at least one pregnancy resulting in a live or still birth between 2006 and 2012.

Overall, significantly more women with exacerbated asthma had preeclampsia or pregnancy-induced hypertension, compared with asthmatic women who had no exacerbations, at 5% vs. 4% and 7% vs. 5%, respectively (P less than .001), according to the study published in the European Respiratory Journal.

Adverse perinatal outcomes were significantly more likely among babies of mothers with exacerbated asthma, compared with those who had no exacerbations, including low birth weight (7% vs. 5%), small for gestational age (3% vs. 2%), preterm birth (8% vs. 7%), and congenital malformation (6% vs. 5%). All P values were less than .001, except for small for gestational age, which was P = .008.

In addition, significantly more babies of asthmatic women with exacerbated asthma during pregnancy had respiratory problems including asthma and pneumonia, compared with those of asthmatic women who had no exacerbations during pregnancy, at 38% vs. 31% and 24% vs. 22% (P less than .001 for both). The researchers found no significant interactions between maternal age and smoking and asthma exacerbations.

The findings were limited by several factors, including the lack of a validated algorithm for asthma exacerbation, which the researchers defined as five or more visits to a general practice clinician for asthma during pregnancy. Other limitations included the lack of categorizing asthma exacerbation by severity, and the inability to include the potential effects of asthma medication on maternal and fetal outcomes, Dr. Abdullah and colleagues noted.

However, the results were strengthened by the large sample size and ability to follow babies from birth until 5 years of age, they said.

“Targeting women with asthma during pregnancy and ensuring appropriate asthma management and postpartum follow-up may help to reduce the risk of pregnancy complications, adverse perinatal outcomes, and early childhood respiratory disorders,” they concluded.

This study is important because asthma is a common, potentially serious medical condition that complicates approximately 4%-8% of pregnancies, and one in three women with asthma experience an exacerbation during pregnancy, Iris Krishna, MD, a specialist in maternal/fetal medicine at Emory University, Atlanta, said in an interview.

“This study is unique in that it uses population-level data to assess the association between an asthma exacerbation during pregnancy and adverse perinatal outcomes,” Dr. Krishna said. “After adjusting for confounders, and consistent with previous studies, study findings suggest an increased risk for women with asthma who have an asthma exacerbation during pregnancy for preeclampsia [odds ratio, 1.3; P less than .001], pregnancy-induced hypertension [OR, 1.17; P less than .05], low-birth-weight infant [OR, 1.14; P less than .05], preterm birth [OR, 1.14; P less than .05], and congenital malformations [OR, 1.21; P less than .001].”

Dr. Krishna also noted the impact on early childhood outcomes. “In this study, children born to women who had an asthma exacerbation during pregnancy had a 23% higher risk of developing asthma before 5 years of age, which is consistent with previous studies. [The] investigators also reported a 12% higher risk of having pneumonia during the first 5 years of life for children born to women who had an asthma exacerbation during pregnancy.”

“Previous studies have suggested children born to mothers with uncontrolled asthma have an increased risk for respiratory infections, but this study is the first to report an association with pneumonia,” she said. This increased risk for childhood respiratory disorders warrants further study.

Consequently, “Women with asthma during pregnancy should have appropriate management to ensure good control to optimize pregnancy outcome,” Dr. Krishna emphasized. “Women who experience asthma exacerbations in pregnancy are at increased risk for preeclampsia, [pregnancy-induced hypertension], low birth weight, and preterm delivery and may require closer monitoring.”

The study was supported by the Institute for Clinical Evaluative Sciences. The researchers and Dr. Krishna had no financial conflicts to disclose.

SOURCE: Abdullah K et al. Eur Respir J. 2019 Nov 26. doi: 10.1183/13993003.01335-2019.

Women with asthma who suffer asthma exacerbation while pregnant are at increased risk for complications during pregnancy and delivery, and their infants are at increased risk for respiratory problems, according to data from a longitudinal study of 58,524 women with asthma.

Vesnaandjic/E+/Getty Images

“Asthma exacerbation during pregnancy has been found to be associated with adverse perinatal and pregnancy outcomes such as low birth weight, small for gestational age, preterm delivery, congenital malformation, preeclampsia, and perinatal mortality,” but previous studies have been small and limited to comparisons of asthmatic and nonasthmatic women, wrote Kawsari Abdullah, PhD, of Children’s Hospital of Eastern Ontario, Ottawa, and colleagues.

To determine the impact of asthma exacerbation on maternal and fetal outcomes, the researchers analyzed data from the Ontario Asthma Surveillance Information System to identify women with asthma who had at least one pregnancy resulting in a live or still birth between 2006 and 2012.

Overall, significantly more women with exacerbated asthma had preeclampsia or pregnancy-induced hypertension, compared with asthmatic women who had no exacerbations, at 5% vs. 4% and 7% vs. 5%, respectively (P less than .001), according to the study published in the European Respiratory Journal.

Adverse perinatal outcomes were significantly more likely among babies of mothers with exacerbated asthma, compared with those who had no exacerbations, including low birth weight (7% vs. 5%), small for gestational age (3% vs. 2%), preterm birth (8% vs. 7%), and congenital malformation (6% vs. 5%). All P values were less than .001, except for small for gestational age, which was P = .008.

In addition, significantly more babies of asthmatic women with exacerbated asthma during pregnancy had respiratory problems including asthma and pneumonia, compared with those of asthmatic women who had no exacerbations during pregnancy, at 38% vs. 31% and 24% vs. 22% (P less than .001 for both). The researchers found no significant interactions between maternal age and smoking and asthma exacerbations.

The findings were limited by several factors, including the lack of a validated algorithm for asthma exacerbation, which the researchers defined as five or more visits to a general practice clinician for asthma during pregnancy. Other limitations included the lack of categorizing asthma exacerbation by severity, and the inability to include the potential effects of asthma medication on maternal and fetal outcomes, Dr. Abdullah and colleagues noted.

However, the results were strengthened by the large sample size and ability to follow babies from birth until 5 years of age, they said.

“Targeting women with asthma during pregnancy and ensuring appropriate asthma management and postpartum follow-up may help to reduce the risk of pregnancy complications, adverse perinatal outcomes, and early childhood respiratory disorders,” they concluded.

This study is important because asthma is a common, potentially serious medical condition that complicates approximately 4%-8% of pregnancies, and one in three women with asthma experience an exacerbation during pregnancy, Iris Krishna, MD, a specialist in maternal/fetal medicine at Emory University, Atlanta, said in an interview.

“This study is unique in that it uses population-level data to assess the association between an asthma exacerbation during pregnancy and adverse perinatal outcomes,” Dr. Krishna said. “After adjusting for confounders, and consistent with previous studies, study findings suggest an increased risk for women with asthma who have an asthma exacerbation during pregnancy for preeclampsia [odds ratio, 1.3; P less than .001], pregnancy-induced hypertension [OR, 1.17; P less than .05], low-birth-weight infant [OR, 1.14; P less than .05], preterm birth [OR, 1.14; P less than .05], and congenital malformations [OR, 1.21; P less than .001].”

Dr. Krishna also noted the impact on early childhood outcomes. “In this study, children born to women who had an asthma exacerbation during pregnancy had a 23% higher risk of developing asthma before 5 years of age, which is consistent with previous studies. [The] investigators also reported a 12% higher risk of having pneumonia during the first 5 years of life for children born to women who had an asthma exacerbation during pregnancy.”

“Previous studies have suggested children born to mothers with uncontrolled asthma have an increased risk for respiratory infections, but this study is the first to report an association with pneumonia,” she said. This increased risk for childhood respiratory disorders warrants further study.

Consequently, “Women with asthma during pregnancy should have appropriate management to ensure good control to optimize pregnancy outcome,” Dr. Krishna emphasized. “Women who experience asthma exacerbations in pregnancy are at increased risk for preeclampsia, [pregnancy-induced hypertension], low birth weight, and preterm delivery and may require closer monitoring.”

The study was supported by the Institute for Clinical Evaluative Sciences. The researchers and Dr. Krishna had no financial conflicts to disclose.

SOURCE: Abdullah K et al. Eur Respir J. 2019 Nov 26. doi: 10.1183/13993003.01335-2019.

The day wouldn’t be so bad if he would just go to sleep at night! How many times have you heard this plea from parents of your patients with ADHD? Sleep is important for everyone, but getting enough is both more important and more difficult for children with ADHD. About three-quarters of children with ADHD have significant problems with sleep, most even before any medication treatment. And inadequate sleep can exacerbate or even cause ADHD symptoms!

SeventyFour/iStock/Getty Images

Solving sleep problems for children with ADHD is not always simple. The kinds of sleep issues that are more common in children (and adults) with ADHD, compared with typical children, include behavioral bedtime resistance, circadian rhythm sleep disorder (CRSD), insomnia, morning sleepiness, night waking, periodic limb movement disorder (PLMD), restless leg syndrome (RLS), and sleep disordered breathing (SDB). Such a broad differential means a careful history and sometimes even lab studies may be needed.

Both initial and follow-up visits for ADHD should include a sleep history or, ideally, a tool such as BEARS sleep screening tool or Children’s Sleep Habits Questionnaire and a 2-week sleep diary (http://www.sleepfoundation.org/). These are good ways to collect signs of allergies or apnea (for SDB), limb movements or limb pain (for RLS or PLMD), mouth breathing, night waking, and snoring.

You also need to ask about alcohol, drugs, caffeine, and nicotine; asthma; comorbid conditions such as mental health disorders or their treatments; and enuresis (alone or part of nocturnal seizures).

Do I need to remind you to find out about electronics activating the child before bedtime – hidden under the covers, or signaling messages from friends in the middle of the night – and to encourage limits on these? Some sleep disorders warrant polysomnography in a sleep lab or from MyZeo.com (for PLMD and some SDB) or ferritin less than 50 mg/L (for RLS) for diagnosis and to guide treatment. Nasal steroids, antihistamines, or montelukast may help SDB when there are enlarged tonsils or adenoids, but adenotonsillectomy is usually curative.

The first line and most effective treatment for sleep problems in children with or without ADHD is improving sleep hygiene. Improved sleep “hygiene” sounds easy, but for children with ADHD and their parents, who often have ADHD too, changing behaviors can be tough! The key component is establishing habits for the entire sleep cycle: a steady pattern of reduced stimulation in the hour before bedtime (sans electronics); a friendly rather than irritated bedtime routine; and the same bedtime and wake up time, ideally 7 days per week. Bedtime stories read to the child can soothe at any age, not just toddlers! Of course, both children and families want fun and special occasions. For most, varying bedtime by up to 1 hour won’t mess up their biological clock, but for some even this should be avoided. Sleeping alone in a cool, dark, quiet room, nightly in the same bed (not used for other activities), is considered the ideal. Earplugs, white noise generators, and eye masks may be helpful. If sleeping with siblings is a necessity, bedtimes can be staggered to put the child to bed earlier or after others are asleep.

Struggles postponing bedtime may be part of a pattern of oppositionality common in ADHD, but the child may not be tired due to being off schedule (from CRSD), napping on the bus or after school, sleeping in mornings, or unrealistic parent expectations for sleep duration. Parents may want their hyperactive children to give them a break and go to bed at 8 p.m., but children aged 6-10 years need only 10-11 hours and those aged 10-17 years need 8.5-9.25 hours of sleep.

Not tired may instead be “wired” from lingering stimulant effects or even lack of such medication leaving the child overactive or rebounding from earlier medications. Lower afternoon doses or shorter-acting medication may solve lasting medication issues, but sometimes an additional low dose of stimulants actually will help a child with ADHD settle at bedtime. All stimulant medications can prolong sleep onset, often by 30 minutes, but this varies by individual and tends to resolve on its own a few weeks after a new or changed medicine. Switching medication category may allow a child to fall asleep faster. Atomoxetine and alpha agonists are less likely to delay sleep than methylphenidate (MPH).

What if sleep hygiene, behavioral methods, and adjusting ADHD medications is not enough? If sleep issues are causing significant problems, medication for sleep is worth a try. Controlled-release melatonin 1-2 hours before bedtime has data for effectiveness. There is no defined dose, so the lowest effective dose should be used, but 3-6 mg may be needed. Because many families with a child with ADHD are not organized enough to give medicine on this schedule, sublingual melatonin that acts in 15-20 minutes is a good alternative or even first choice. Clonidine 0.05-0.2 mg 1 hour before bedtime speeds sleep onset, lasts 3 hours, and does not carry over to sedation the next day. Stronger psychopharmaceuticals can assist sleep onset, including low dose mirtazapine or trazodone, but have the side effect of daytime sleepiness.

Management of waking in the middle of the night can be more difficult to treat as sleep drive has been dissipated. First, consider whether trips out of bed reflect a sleep association that has not been extinguished. Daytime atomoxetine or, better yet, MPH may improve night waking, and sometimes even a low-dose evening, long-acting medication, such as osmotic release oral system (OROS) extended release methylphenidate HCL (OROS MPH), helps. Short-acting clonidine or melatonin in the middle of the night or bedtime mirtazapine or trazodone also may be worth a try.

When dealing with sleep, keep in mind that 50% or more of children with ADHD have a coexisting mental health disorder. Anxiety, separation anxiety, depression, and dysthymia all often affect sleep onset, night waking, and sometimes early morning waking. The child or teen may need extra reassurance or company at bedtime (siblings or pets may suffice). Reading positive stories or playing soft music may be better at setting a positive mood and sense of safety for sleep, certainly more so than social media, which should be avoided.

Keep in mind that substance use is more common in ADHD as well as with those other mental health conditions and can interfere with restful sleep and make RLS worse. Bipolar disorder can be mistaken for ADHD as it often presents with hyperactivity but also can be comorbid. Sleep problems are increased sixfold when both are present. Prolonged periods awake at night and diminished need for sleep are signs that help differentiate bipolar from ADHD. Medication management for the bipolar disorder with atypicals can reduce sleep latency and reduce REM sleep, but also causes morning fatigue. Medications to treat other mental health problems can help sleep onset (for example, anticonvulsants, atypicals), or prolong it (SSRIs), change REM states (atypicals), and even exacerbate RLS (SSRIs). You can make changes or work with the child’s mental health specialist if medications are causing significant sleep problems.

When we help improve sleep for children with ADHD, it can lessen not only ADHD symptoms but also some symptoms of other mental health disorders, improve learning and behavior, and greatly improve family quality of life!
 

Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at [email protected].

The day wouldn’t be so bad if he would just go to sleep at night! How many times have you heard this plea from parents of your patients with ADHD? Sleep is important for everyone, but getting enough is both more important and more difficult for children with ADHD. About three-quarters of children with ADHD have significant problems with sleep, most even before any medication treatment. And inadequate sleep can exacerbate or even cause ADHD symptoms!

SeventyFour/iStock/Getty Images

Solving sleep problems for children with ADHD is not always simple. The kinds of sleep issues that are more common in children (and adults) with ADHD, compared with typical children, include behavioral bedtime resistance, circadian rhythm sleep disorder (CRSD), insomnia, morning sleepiness, night waking, periodic limb movement disorder (PLMD), restless leg syndrome (RLS), and sleep disordered breathing (SDB). Such a broad differential means a careful history and sometimes even lab studies may be needed.

Both initial and follow-up visits for ADHD should include a sleep history or, ideally, a tool such as BEARS sleep screening tool or Children’s Sleep Habits Questionnaire and a 2-week sleep diary (http://www.sleepfoundation.org/). These are good ways to collect signs of allergies or apnea (for SDB), limb movements or limb pain (for RLS or PLMD), mouth breathing, night waking, and snoring.

You also need to ask about alcohol, drugs, caffeine, and nicotine; asthma; comorbid conditions such as mental health disorders or their treatments; and enuresis (alone or part of nocturnal seizures).

Do I need to remind you to find out about electronics activating the child before bedtime – hidden under the covers, or signaling messages from friends in the middle of the night – and to encourage limits on these? Some sleep disorders warrant polysomnography in a sleep lab or from MyZeo.com (for PLMD and some SDB) or ferritin less than 50 mg/L (for RLS) for diagnosis and to guide treatment. Nasal steroids, antihistamines, or montelukast may help SDB when there are enlarged tonsils or adenoids, but adenotonsillectomy is usually curative.

The first line and most effective treatment for sleep problems in children with or without ADHD is improving sleep hygiene. Improved sleep “hygiene” sounds easy, but for children with ADHD and their parents, who often have ADHD too, changing behaviors can be tough! The key component is establishing habits for the entire sleep cycle: a steady pattern of reduced stimulation in the hour before bedtime (sans electronics); a friendly rather than irritated bedtime routine; and the same bedtime and wake up time, ideally 7 days per week. Bedtime stories read to the child can soothe at any age, not just toddlers! Of course, both children and families want fun and special occasions. For most, varying bedtime by up to 1 hour won’t mess up their biological clock, but for some even this should be avoided. Sleeping alone in a cool, dark, quiet room, nightly in the same bed (not used for other activities), is considered the ideal. Earplugs, white noise generators, and eye masks may be helpful. If sleeping with siblings is a necessity, bedtimes can be staggered to put the child to bed earlier or after others are asleep.

Struggles postponing bedtime may be part of a pattern of oppositionality common in ADHD, but the child may not be tired due to being off schedule (from CRSD), napping on the bus or after school, sleeping in mornings, or unrealistic parent expectations for sleep duration. Parents may want their hyperactive children to give them a break and go to bed at 8 p.m., but children aged 6-10 years need only 10-11 hours and those aged 10-17 years need 8.5-9.25 hours of sleep.

Not tired may instead be “wired” from lingering stimulant effects or even lack of such medication leaving the child overactive or rebounding from earlier medications. Lower afternoon doses or shorter-acting medication may solve lasting medication issues, but sometimes an additional low dose of stimulants actually will help a child with ADHD settle at bedtime. All stimulant medications can prolong sleep onset, often by 30 minutes, but this varies by individual and tends to resolve on its own a few weeks after a new or changed medicine. Switching medication category may allow a child to fall asleep faster. Atomoxetine and alpha agonists are less likely to delay sleep than methylphenidate (MPH).

What if sleep hygiene, behavioral methods, and adjusting ADHD medications is not enough? If sleep issues are causing significant problems, medication for sleep is worth a try. Controlled-release melatonin 1-2 hours before bedtime has data for effectiveness. There is no defined dose, so the lowest effective dose should be used, but 3-6 mg may be needed. Because many families with a child with ADHD are not organized enough to give medicine on this schedule, sublingual melatonin that acts in 15-20 minutes is a good alternative or even first choice. Clonidine 0.05-0.2 mg 1 hour before bedtime speeds sleep onset, lasts 3 hours, and does not carry over to sedation the next day. Stronger psychopharmaceuticals can assist sleep onset, including low dose mirtazapine or trazodone, but have the side effect of daytime sleepiness.

Management of waking in the middle of the night can be more difficult to treat as sleep drive has been dissipated. First, consider whether trips out of bed reflect a sleep association that has not been extinguished. Daytime atomoxetine or, better yet, MPH may improve night waking, and sometimes even a low-dose evening, long-acting medication, such as osmotic release oral system (OROS) extended release methylphenidate HCL (OROS MPH), helps. Short-acting clonidine or melatonin in the middle of the night or bedtime mirtazapine or trazodone also may be worth a try.

When dealing with sleep, keep in mind that 50% or more of children with ADHD have a coexisting mental health disorder. Anxiety, separation anxiety, depression, and dysthymia all often affect sleep onset, night waking, and sometimes early morning waking. The child or teen may need extra reassurance or company at bedtime (siblings or pets may suffice). Reading positive stories or playing soft music may be better at setting a positive mood and sense of safety for sleep, certainly more so than social media, which should be avoided.

Keep in mind that substance use is more common in ADHD as well as with those other mental health conditions and can interfere with restful sleep and make RLS worse. Bipolar disorder can be mistaken for ADHD as it often presents with hyperactivity but also can be comorbid. Sleep problems are increased sixfold when both are present. Prolonged periods awake at night and diminished need for sleep are signs that help differentiate bipolar from ADHD. Medication management for the bipolar disorder with atypicals can reduce sleep latency and reduce REM sleep, but also causes morning fatigue. Medications to treat other mental health problems can help sleep onset (for example, anticonvulsants, atypicals), or prolong it (SSRIs), change REM states (atypicals), and even exacerbate RLS (SSRIs). You can make changes or work with the child’s mental health specialist if medications are causing significant sleep problems.

When we help improve sleep for children with ADHD, it can lessen not only ADHD symptoms but also some symptoms of other mental health disorders, improve learning and behavior, and greatly improve family quality of life!
 

Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at [email protected].

The day wouldn’t be so bad if he would just go to sleep at night! How many times have you heard this plea from parents of your patients with ADHD? Sleep is important for everyone, but getting enough is both more important and more difficult for children with ADHD. About three-quarters of children with ADHD have significant problems with sleep, most even before any medication treatment. And inadequate sleep can exacerbate or even cause ADHD symptoms!

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Solving sleep problems for children with ADHD is not always simple. The kinds of sleep issues that are more common in children (and adults) with ADHD, compared with typical children, include behavioral bedtime resistance, circadian rhythm sleep disorder (CRSD), insomnia, morning sleepiness, night waking, periodic limb movement disorder (PLMD), restless leg syndrome (RLS), and sleep disordered breathing (SDB). Such a broad differential means a careful history and sometimes even lab studies may be needed.

Both initial and follow-up visits for ADHD should include a sleep history or, ideally, a tool such as BEARS sleep screening tool or Children’s Sleep Habits Questionnaire and a 2-week sleep diary (http://www.sleepfoundation.org/). These are good ways to collect signs of allergies or apnea (for SDB), limb movements or limb pain (for RLS or PLMD), mouth breathing, night waking, and snoring.

You also need to ask about alcohol, drugs, caffeine, and nicotine; asthma; comorbid conditions such as mental health disorders or their treatments; and enuresis (alone or part of nocturnal seizures).

Do I need to remind you to find out about electronics activating the child before bedtime – hidden under the covers, or signaling messages from friends in the middle of the night – and to encourage limits on these? Some sleep disorders warrant polysomnography in a sleep lab or from MyZeo.com (for PLMD and some SDB) or ferritin less than 50 mg/L (for RLS) for diagnosis and to guide treatment. Nasal steroids, antihistamines, or montelukast may help SDB when there are enlarged tonsils or adenoids, but adenotonsillectomy is usually curative.

The first line and most effective treatment for sleep problems in children with or without ADHD is improving sleep hygiene. Improved sleep “hygiene” sounds easy, but for children with ADHD and their parents, who often have ADHD too, changing behaviors can be tough! The key component is establishing habits for the entire sleep cycle: a steady pattern of reduced stimulation in the hour before bedtime (sans electronics); a friendly rather than irritated bedtime routine; and the same bedtime and wake up time, ideally 7 days per week. Bedtime stories read to the child can soothe at any age, not just toddlers! Of course, both children and families want fun and special occasions. For most, varying bedtime by up to 1 hour won’t mess up their biological clock, but for some even this should be avoided. Sleeping alone in a cool, dark, quiet room, nightly in the same bed (not used for other activities), is considered the ideal. Earplugs, white noise generators, and eye masks may be helpful. If sleeping with siblings is a necessity, bedtimes can be staggered to put the child to bed earlier or after others are asleep.

Struggles postponing bedtime may be part of a pattern of oppositionality common in ADHD, but the child may not be tired due to being off schedule (from CRSD), napping on the bus or after school, sleeping in mornings, or unrealistic parent expectations for sleep duration. Parents may want their hyperactive children to give them a break and go to bed at 8 p.m., but children aged 6-10 years need only 10-11 hours and those aged 10-17 years need 8.5-9.25 hours of sleep.

Not tired may instead be “wired” from lingering stimulant effects or even lack of such medication leaving the child overactive or rebounding from earlier medications. Lower afternoon doses or shorter-acting medication may solve lasting medication issues, but sometimes an additional low dose of stimulants actually will help a child with ADHD settle at bedtime. All stimulant medications can prolong sleep onset, often by 30 minutes, but this varies by individual and tends to resolve on its own a few weeks after a new or changed medicine. Switching medication category may allow a child to fall asleep faster. Atomoxetine and alpha agonists are less likely to delay sleep than methylphenidate (MPH).

What if sleep hygiene, behavioral methods, and adjusting ADHD medications is not enough? If sleep issues are causing significant problems, medication for sleep is worth a try. Controlled-release melatonin 1-2 hours before bedtime has data for effectiveness. There is no defined dose, so the lowest effective dose should be used, but 3-6 mg may be needed. Because many families with a child with ADHD are not organized enough to give medicine on this schedule, sublingual melatonin that acts in 15-20 minutes is a good alternative or even first choice. Clonidine 0.05-0.2 mg 1 hour before bedtime speeds sleep onset, lasts 3 hours, and does not carry over to sedation the next day. Stronger psychopharmaceuticals can assist sleep onset, including low dose mirtazapine or trazodone, but have the side effect of daytime sleepiness.

Management of waking in the middle of the night can be more difficult to treat as sleep drive has been dissipated. First, consider whether trips out of bed reflect a sleep association that has not been extinguished. Daytime atomoxetine or, better yet, MPH may improve night waking, and sometimes even a low-dose evening, long-acting medication, such as osmotic release oral system (OROS) extended release methylphenidate HCL (OROS MPH), helps. Short-acting clonidine or melatonin in the middle of the night or bedtime mirtazapine or trazodone also may be worth a try.

When dealing with sleep, keep in mind that 50% or more of children with ADHD have a coexisting mental health disorder. Anxiety, separation anxiety, depression, and dysthymia all often affect sleep onset, night waking, and sometimes early morning waking. The child or teen may need extra reassurance or company at bedtime (siblings or pets may suffice). Reading positive stories or playing soft music may be better at setting a positive mood and sense of safety for sleep, certainly more so than social media, which should be avoided.

Keep in mind that substance use is more common in ADHD as well as with those other mental health conditions and can interfere with restful sleep and make RLS worse. Bipolar disorder can be mistaken for ADHD as it often presents with hyperactivity but also can be comorbid. Sleep problems are increased sixfold when both are present. Prolonged periods awake at night and diminished need for sleep are signs that help differentiate bipolar from ADHD. Medication management for the bipolar disorder with atypicals can reduce sleep latency and reduce REM sleep, but also causes morning fatigue. Medications to treat other mental health problems can help sleep onset (for example, anticonvulsants, atypicals), or prolong it (SSRIs), change REM states (atypicals), and even exacerbate RLS (SSRIs). You can make changes or work with the child’s mental health specialist if medications are causing significant sleep problems.

When we help improve sleep for children with ADHD, it can lessen not only ADHD symptoms but also some symptoms of other mental health disorders, improve learning and behavior, and greatly improve family quality of life!
 

Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at [email protected].

ATLANTA – Adenosine deaminase 2 above the upper limit of normal is 86% sensitive and 94% specific for distinguishing macrophage activation syndrome from active systemic juvenile idiopathic arthritis, making it perhaps the most potent blood marker yet identified to differentiate the two, according to a report presented at the annual meeting of the American College of Rheumatology.

The upper limit of normal was 27.8 U/L, two standard deviations above the median of 13 U/L (interquartile range, 10.6-16.1) in 174 healthy children. The work was published simultaneously in Annals of the Rheumatic Diseases.

In children with active systemic juvenile idiopathic arthritis (JIA), adenosine deaminase 2 (ADA2) “beyond the upper limit of normal is strong evidence for concomitant” macrophage activation syndrome (MAS). “Our work represents a new method to diagnose this condition,” said lead investigator Pui Y. Lee, MD, PhD, a pediatric rheumatologist at Boston Children’s Hospital.

The hope, he said, is that the finding will lead to quicker recognition and treatment of MAS, a devastating complication of systemic JIA in which rampant inflammation begets further inflammation in a downward spiral that ultimately proves fatal in about 20% of cases. The problem is that the clinical features of MAS overlap with those of active systemic JIA, which makes early diagnosis difficult.

Ferritin and other common markers are not very specific unless “the cutoff is raised significantly to distinguish MAS from general inflammation. Most labs will not tell you ‘this is an active systemic JIA range; this is an MAS-like range.’ It’s hard for them to define that for you. ADA2 is more black and white; if you go above the upper limit, you most likely have MAS,” Dr. Lee explained at the meeting.

Potentially, “we can combine this test with other tests to define a single MAS panel,” he said.

ADA2 is measured by a simple, inexpensive enzyme assay that’s been around for 20 years, but it hasn’t caught on because the protein’s function is unknown and the clinical relevance of ADA2 levels has been uncertain. With the new findings, “it is our hope that ADA2 testing will become more available,” Dr. Lee said.

The protein appears to be a product of monocytes and macrophages, and a genetic deficiency has recently been linked to congenital vasculitis, which made Dr. Lee and colleagues curious about ADA2 in other rheumatic diseases. The first step was to define normal limits in healthy controls; the 13 U/L median in children proved to be a bit higher than in 150 healthy adults.

The team then found that levels were completely normal in 25 children with active Kawasaki disease, and only mildly elevated in 13 children with systemic lupus and 13 with juvenile dermatomyositis. The Kawasaki children, in particular “were highly inflamed, so this protein is not just simply a marker of inflammation,” Dr. Lee said.

They next turned to 120 children with JIA, with a mix of systemic and nonsystemic cases. “The ones with very high levels, far beyond the upper limit of normal, were” almost exclusively the 23 children with systemic JIA and clinically diagnosed MAS. “As long as [JIA children] didn’t have MAS, their levels were pretty much close to normal,” he said.

In eight MAS children with repeat testing, levels fell below the upper limit of normal with treatment and remission, but children prone to repeat MAS seemed to hover closer to the limit even when they were well.

Blood sample testing showed that interleukin-18 and interferon-gamma were the main drivers of ADA2 expression in the periphery, “which makes sense because these two cytokines are very involved in the process of MAS,” Dr. Lee said.

The work was funded by the National Institutes of Health, among others. Dr. Lee didn’t have any disclosures.

[email protected]

SOURCE: Lee PY et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 920.

ATLANTA – Adenosine deaminase 2 above the upper limit of normal is 86% sensitive and 94% specific for distinguishing macrophage activation syndrome from active systemic juvenile idiopathic arthritis, making it perhaps the most potent blood marker yet identified to differentiate the two, according to a report presented at the annual meeting of the American College of Rheumatology.

The upper limit of normal was 27.8 U/L, two standard deviations above the median of 13 U/L (interquartile range, 10.6-16.1) in 174 healthy children. The work was published simultaneously in Annals of the Rheumatic Diseases.

In children with active systemic juvenile idiopathic arthritis (JIA), adenosine deaminase 2 (ADA2) “beyond the upper limit of normal is strong evidence for concomitant” macrophage activation syndrome (MAS). “Our work represents a new method to diagnose this condition,” said lead investigator Pui Y. Lee, MD, PhD, a pediatric rheumatologist at Boston Children’s Hospital.

The hope, he said, is that the finding will lead to quicker recognition and treatment of MAS, a devastating complication of systemic JIA in which rampant inflammation begets further inflammation in a downward spiral that ultimately proves fatal in about 20% of cases. The problem is that the clinical features of MAS overlap with those of active systemic JIA, which makes early diagnosis difficult.

Ferritin and other common markers are not very specific unless “the cutoff is raised significantly to distinguish MAS from general inflammation. Most labs will not tell you ‘this is an active systemic JIA range; this is an MAS-like range.’ It’s hard for them to define that for you. ADA2 is more black and white; if you go above the upper limit, you most likely have MAS,” Dr. Lee explained at the meeting.

Potentially, “we can combine this test with other tests to define a single MAS panel,” he said.

ADA2 is measured by a simple, inexpensive enzyme assay that’s been around for 20 years, but it hasn’t caught on because the protein’s function is unknown and the clinical relevance of ADA2 levels has been uncertain. With the new findings, “it is our hope that ADA2 testing will become more available,” Dr. Lee said.

The protein appears to be a product of monocytes and macrophages, and a genetic deficiency has recently been linked to congenital vasculitis, which made Dr. Lee and colleagues curious about ADA2 in other rheumatic diseases. The first step was to define normal limits in healthy controls; the 13 U/L median in children proved to be a bit higher than in 150 healthy adults.

The team then found that levels were completely normal in 25 children with active Kawasaki disease, and only mildly elevated in 13 children with systemic lupus and 13 with juvenile dermatomyositis. The Kawasaki children, in particular “were highly inflamed, so this protein is not just simply a marker of inflammation,” Dr. Lee said.

They next turned to 120 children with JIA, with a mix of systemic and nonsystemic cases. “The ones with very high levels, far beyond the upper limit of normal, were” almost exclusively the 23 children with systemic JIA and clinically diagnosed MAS. “As long as [JIA children] didn’t have MAS, their levels were pretty much close to normal,” he said.

In eight MAS children with repeat testing, levels fell below the upper limit of normal with treatment and remission, but children prone to repeat MAS seemed to hover closer to the limit even when they were well.

Blood sample testing showed that interleukin-18 and interferon-gamma were the main drivers of ADA2 expression in the periphery, “which makes sense because these two cytokines are very involved in the process of MAS,” Dr. Lee said.

The work was funded by the National Institutes of Health, among others. Dr. Lee didn’t have any disclosures.

[email protected]

SOURCE: Lee PY et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 920.

ATLANTA – Adenosine deaminase 2 above the upper limit of normal is 86% sensitive and 94% specific for distinguishing macrophage activation syndrome from active systemic juvenile idiopathic arthritis, making it perhaps the most potent blood marker yet identified to differentiate the two, according to a report presented at the annual meeting of the American College of Rheumatology.

The upper limit of normal was 27.8 U/L, two standard deviations above the median of 13 U/L (interquartile range, 10.6-16.1) in 174 healthy children. The work was published simultaneously in Annals of the Rheumatic Diseases.

In children with active systemic juvenile idiopathic arthritis (JIA), adenosine deaminase 2 (ADA2) “beyond the upper limit of normal is strong evidence for concomitant” macrophage activation syndrome (MAS). “Our work represents a new method to diagnose this condition,” said lead investigator Pui Y. Lee, MD, PhD, a pediatric rheumatologist at Boston Children’s Hospital.

The hope, he said, is that the finding will lead to quicker recognition and treatment of MAS, a devastating complication of systemic JIA in which rampant inflammation begets further inflammation in a downward spiral that ultimately proves fatal in about 20% of cases. The problem is that the clinical features of MAS overlap with those of active systemic JIA, which makes early diagnosis difficult.

Ferritin and other common markers are not very specific unless “the cutoff is raised significantly to distinguish MAS from general inflammation. Most labs will not tell you ‘this is an active systemic JIA range; this is an MAS-like range.’ It’s hard for them to define that for you. ADA2 is more black and white; if you go above the upper limit, you most likely have MAS,” Dr. Lee explained at the meeting.

Potentially, “we can combine this test with other tests to define a single MAS panel,” he said.

ADA2 is measured by a simple, inexpensive enzyme assay that’s been around for 20 years, but it hasn’t caught on because the protein’s function is unknown and the clinical relevance of ADA2 levels has been uncertain. With the new findings, “it is our hope that ADA2 testing will become more available,” Dr. Lee said.

The protein appears to be a product of monocytes and macrophages, and a genetic deficiency has recently been linked to congenital vasculitis, which made Dr. Lee and colleagues curious about ADA2 in other rheumatic diseases. The first step was to define normal limits in healthy controls; the 13 U/L median in children proved to be a bit higher than in 150 healthy adults.

The team then found that levels were completely normal in 25 children with active Kawasaki disease, and only mildly elevated in 13 children with systemic lupus and 13 with juvenile dermatomyositis. The Kawasaki children, in particular “were highly inflamed, so this protein is not just simply a marker of inflammation,” Dr. Lee said.

They next turned to 120 children with JIA, with a mix of systemic and nonsystemic cases. “The ones with very high levels, far beyond the upper limit of normal, were” almost exclusively the 23 children with systemic JIA and clinically diagnosed MAS. “As long as [JIA children] didn’t have MAS, their levels were pretty much close to normal,” he said.

In eight MAS children with repeat testing, levels fell below the upper limit of normal with treatment and remission, but children prone to repeat MAS seemed to hover closer to the limit even when they were well.

Blood sample testing showed that interleukin-18 and interferon-gamma were the main drivers of ADA2 expression in the periphery, “which makes sense because these two cytokines are very involved in the process of MAS,” Dr. Lee said.

The work was funded by the National Institutes of Health, among others. Dr. Lee didn’t have any disclosures.

[email protected]

SOURCE: Lee PY et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 920.