Pulmonary Health Hub

Idiopathic pulmonary fibrosis (IPF) progressed at similar rates in patients who did and did not receive antacid therapy, based on a post hoc analysis of 52-week data from patients in three placebo-controlled trials.

“We found no association between antacid therapy and progression-free survival, mortality, or adverse events, reported Dr. Michael Krueter of the University of Heidelberg, Germany, and his colleagues (Lancet Respir Med. 2016 Mar 31;S2213-2600[16]00067-9). Further, patients who took antacids and had less than 70% forced vital capacity (FVC) had higher rates of pulmonary and nonpulmonary infections than did patients who did not receive antacid therapy.

“Long-term double-blind randomized studies are urgently needed to further investigate the potential benefit (and possible harms) of antacid therapy in patients with different stages of IPF, especially those with advanced disease,” the researchers said.

The findings challenge the conditional recommendation for antacid use in the American Thoracic Society/European Respiratory Society/Japanese Respiratory Society/Latin American Thoracic Association guidelines on the treatment of IPF. That advice was based on previous retrospective studies that indicated antacid users had slower IPF progression, fewer acute exacerbations, and improved survival compared to patients who did not take antacids.

The new study looked at IPF patients in the placebo groups in three large, phase III trials of pirfenidone. In the placebo groups of those studies, 291 patients were receiving antacid therapy and 333 patients were not receiving antacid therapy at baseline. At 1 year, the rates of disease progression in the placebo group were not significantly different – 38% in the antacid users and 42% in those not using antacids. Disease progression was the composite endpoint of death, an absolute FVC decrease of at least 10%, and a decrease of 50 meters or more in the 6-minute walk distance (6MWD). In both groups of patients, the rates of all-cause mortality were also similar.

The risk of death from IPF at 1 year also was not significantly different; 3.9% for antacid users and 5.2% for those not using antacids.

When patients were grouped on the basis of FVC at baseline – either less than 70% FVC or at least 70% FVC or greater – little or no difference was seen in disease mortality, disease progression, changes in FVC, 6MWD, and all-cause hospital admission between patients who received antacids and those who did not receive antacids at baseline.

Prior to stratification by baseline FVC, the rates of all-cause hospital admissions, gastrointestinal adverse effects, infections, and pulmonary infections were similar for the two groups of patients. At 52 weeks, however, infections and pulmonary infections were significantly higher in patients who received antacid therapy at baseline compared with those patients who did not receive antacids at baseline (74% vs. 62%; P = .0174 and 14% vs. 6%; P = .0214, respectively).

Unlike the patients in the previous retrospective studies, few patients in the placebo arms of the clinical trials had advanced IPF and low FVC, the researchers noted. All had IPF that had been diagnosed within 48 months of entering a trial, no evidence of improvement in disease severity in the year preceding trial entry, a predicted FVC of 50% or more, and a 6MWD of 150 meters or more. Among the patients receiving antacid therapy at baseline, 88% used proton-pump inhibitors, 8% used H2 blockers and 4% used proton-pump inhibitors and H2 blockers. Of the 291 patients receiving antacid therapy, 38 stopped after baseline; of the 333 not receiving antacid therapy, 83 started receiving the therapy after baseline.

Dr. Kreuter disclosed ties with Boehringer Ingelheim and InterMune/Roche. Two coauthors disclosed ties with F. Hoffmann-La Roche, which funded the study: Derek Weycker, Ph.D., reported receiving funding from the company, and Dr. Klaus-Uwe Kirchgaessler is an employee.

[email protected]

Idiopathic pulmonary fibrosis (IPF) progressed at similar rates in patients who did and did not receive antacid therapy, based on a post hoc analysis of 52-week data from patients in three placebo-controlled trials.

“We found no association between antacid therapy and progression-free survival, mortality, or adverse events, reported Dr. Michael Krueter of the University of Heidelberg, Germany, and his colleagues (Lancet Respir Med. 2016 Mar 31;S2213-2600[16]00067-9). Further, patients who took antacids and had less than 70% forced vital capacity (FVC) had higher rates of pulmonary and nonpulmonary infections than did patients who did not receive antacid therapy.

“Long-term double-blind randomized studies are urgently needed to further investigate the potential benefit (and possible harms) of antacid therapy in patients with different stages of IPF, especially those with advanced disease,” the researchers said.

The findings challenge the conditional recommendation for antacid use in the American Thoracic Society/European Respiratory Society/Japanese Respiratory Society/Latin American Thoracic Association guidelines on the treatment of IPF. That advice was based on previous retrospective studies that indicated antacid users had slower IPF progression, fewer acute exacerbations, and improved survival compared to patients who did not take antacids.

The new study looked at IPF patients in the placebo groups in three large, phase III trials of pirfenidone. In the placebo groups of those studies, 291 patients were receiving antacid therapy and 333 patients were not receiving antacid therapy at baseline. At 1 year, the rates of disease progression in the placebo group were not significantly different – 38% in the antacid users and 42% in those not using antacids. Disease progression was the composite endpoint of death, an absolute FVC decrease of at least 10%, and a decrease of 50 meters or more in the 6-minute walk distance (6MWD). In both groups of patients, the rates of all-cause mortality were also similar.

The risk of death from IPF at 1 year also was not significantly different; 3.9% for antacid users and 5.2% for those not using antacids.

When patients were grouped on the basis of FVC at baseline – either less than 70% FVC or at least 70% FVC or greater – little or no difference was seen in disease mortality, disease progression, changes in FVC, 6MWD, and all-cause hospital admission between patients who received antacids and those who did not receive antacids at baseline.

Prior to stratification by baseline FVC, the rates of all-cause hospital admissions, gastrointestinal adverse effects, infections, and pulmonary infections were similar for the two groups of patients. At 52 weeks, however, infections and pulmonary infections were significantly higher in patients who received antacid therapy at baseline compared with those patients who did not receive antacids at baseline (74% vs. 62%; P = .0174 and 14% vs. 6%; P = .0214, respectively).

Unlike the patients in the previous retrospective studies, few patients in the placebo arms of the clinical trials had advanced IPF and low FVC, the researchers noted. All had IPF that had been diagnosed within 48 months of entering a trial, no evidence of improvement in disease severity in the year preceding trial entry, a predicted FVC of 50% or more, and a 6MWD of 150 meters or more. Among the patients receiving antacid therapy at baseline, 88% used proton-pump inhibitors, 8% used H2 blockers and 4% used proton-pump inhibitors and H2 blockers. Of the 291 patients receiving antacid therapy, 38 stopped after baseline; of the 333 not receiving antacid therapy, 83 started receiving the therapy after baseline.

Dr. Kreuter disclosed ties with Boehringer Ingelheim and InterMune/Roche. Two coauthors disclosed ties with F. Hoffmann-La Roche, which funded the study: Derek Weycker, Ph.D., reported receiving funding from the company, and Dr. Klaus-Uwe Kirchgaessler is an employee.

[email protected]

Idiopathic pulmonary fibrosis (IPF) progressed at similar rates in patients who did and did not receive antacid therapy, based on a post hoc analysis of 52-week data from patients in three placebo-controlled trials.

“We found no association between antacid therapy and progression-free survival, mortality, or adverse events, reported Dr. Michael Krueter of the University of Heidelberg, Germany, and his colleagues (Lancet Respir Med. 2016 Mar 31;S2213-2600[16]00067-9). Further, patients who took antacids and had less than 70% forced vital capacity (FVC) had higher rates of pulmonary and nonpulmonary infections than did patients who did not receive antacid therapy.

“Long-term double-blind randomized studies are urgently needed to further investigate the potential benefit (and possible harms) of antacid therapy in patients with different stages of IPF, especially those with advanced disease,” the researchers said.

The findings challenge the conditional recommendation for antacid use in the American Thoracic Society/European Respiratory Society/Japanese Respiratory Society/Latin American Thoracic Association guidelines on the treatment of IPF. That advice was based on previous retrospective studies that indicated antacid users had slower IPF progression, fewer acute exacerbations, and improved survival compared to patients who did not take antacids.

The new study looked at IPF patients in the placebo groups in three large, phase III trials of pirfenidone. In the placebo groups of those studies, 291 patients were receiving antacid therapy and 333 patients were not receiving antacid therapy at baseline. At 1 year, the rates of disease progression in the placebo group were not significantly different – 38% in the antacid users and 42% in those not using antacids. Disease progression was the composite endpoint of death, an absolute FVC decrease of at least 10%, and a decrease of 50 meters or more in the 6-minute walk distance (6MWD). In both groups of patients, the rates of all-cause mortality were also similar.

The risk of death from IPF at 1 year also was not significantly different; 3.9% for antacid users and 5.2% for those not using antacids.

When patients were grouped on the basis of FVC at baseline – either less than 70% FVC or at least 70% FVC or greater – little or no difference was seen in disease mortality, disease progression, changes in FVC, 6MWD, and all-cause hospital admission between patients who received antacids and those who did not receive antacids at baseline.

Prior to stratification by baseline FVC, the rates of all-cause hospital admissions, gastrointestinal adverse effects, infections, and pulmonary infections were similar for the two groups of patients. At 52 weeks, however, infections and pulmonary infections were significantly higher in patients who received antacid therapy at baseline compared with those patients who did not receive antacids at baseline (74% vs. 62%; P = .0174 and 14% vs. 6%; P = .0214, respectively).

Unlike the patients in the previous retrospective studies, few patients in the placebo arms of the clinical trials had advanced IPF and low FVC, the researchers noted. All had IPF that had been diagnosed within 48 months of entering a trial, no evidence of improvement in disease severity in the year preceding trial entry, a predicted FVC of 50% or more, and a 6MWD of 150 meters or more. Among the patients receiving antacid therapy at baseline, 88% used proton-pump inhibitors, 8% used H2 blockers and 4% used proton-pump inhibitors and H2 blockers. Of the 291 patients receiving antacid therapy, 38 stopped after baseline; of the 333 not receiving antacid therapy, 83 started receiving the therapy after baseline.

Dr. Kreuter disclosed ties with Boehringer Ingelheim and InterMune/Roche. Two coauthors disclosed ties with F. Hoffmann-La Roche, which funded the study: Derek Weycker, Ph.D., reported receiving funding from the company, and Dr. Klaus-Uwe Kirchgaessler is an employee.

[email protected]

The findings of a new, international study of 6,685 mothers and their newborns may explain why certain infant and child health problems frequently have been seen in the offspring of mothers who smoked during pregnancy, Kendall Morgan, Ph.D., wrote in the National Institutes of Health Director’s Blog.

The study, published in the American Journal of Human Genetics, “found significant differences between the epigenetic patterns of babies born to women who smoked during pregnancy and those born to nonsmokers, with many of the differences affecting genes known to play key roles in the development of the lungs, face, and nervous system,” Dr. Morgan wrote in the April 12 blog entry.

©Christian Jasiuk/Thinkstock

Smaller studies show there is evidence that maternal smoking can have epigenetic effects on a fetus. The new research from 13 research cohorts reaffirms and renders this finding more statistically powerful, Dr. Morgan wrote. In the infants of women who smoked every day during pregnancy, the researchers found more than 6,000 places where chemical marks on the DNA differed from those of babies born to mothers who did not smoke during pregnancy. The researchers also observed more than 4,600 epigenetic modifications in the DNA of babies of mothers who self-identified as falling under the broad category of having engaged in “any smoking during pregnancy.”

The genes thought to cause a cleft lip and/or palate were among the others to have been epigenetically modified in the fetuses of women who smoked while pregnant. The study also suggested that thousands of the epigenetic modifications seen affected children until at least age 4 years.

Read the study in the American Journal of Human Genetics (doi: 10.1016/j.ajhg.2016.02.019).

[email protected]

The findings of a new, international study of 6,685 mothers and their newborns may explain why certain infant and child health problems frequently have been seen in the offspring of mothers who smoked during pregnancy, Kendall Morgan, Ph.D., wrote in the National Institutes of Health Director’s Blog.

The study, published in the American Journal of Human Genetics, “found significant differences between the epigenetic patterns of babies born to women who smoked during pregnancy and those born to nonsmokers, with many of the differences affecting genes known to play key roles in the development of the lungs, face, and nervous system,” Dr. Morgan wrote in the April 12 blog entry.

©Christian Jasiuk/Thinkstock

Smaller studies show there is evidence that maternal smoking can have epigenetic effects on a fetus. The new research from 13 research cohorts reaffirms and renders this finding more statistically powerful, Dr. Morgan wrote. In the infants of women who smoked every day during pregnancy, the researchers found more than 6,000 places where chemical marks on the DNA differed from those of babies born to mothers who did not smoke during pregnancy. The researchers also observed more than 4,600 epigenetic modifications in the DNA of babies of mothers who self-identified as falling under the broad category of having engaged in “any smoking during pregnancy.”

The genes thought to cause a cleft lip and/or palate were among the others to have been epigenetically modified in the fetuses of women who smoked while pregnant. The study also suggested that thousands of the epigenetic modifications seen affected children until at least age 4 years.

Read the study in the American Journal of Human Genetics (doi: 10.1016/j.ajhg.2016.02.019).

[email protected]

The findings of a new, international study of 6,685 mothers and their newborns may explain why certain infant and child health problems frequently have been seen in the offspring of mothers who smoked during pregnancy, Kendall Morgan, Ph.D., wrote in the National Institutes of Health Director’s Blog.

The study, published in the American Journal of Human Genetics, “found significant differences between the epigenetic patterns of babies born to women who smoked during pregnancy and those born to nonsmokers, with many of the differences affecting genes known to play key roles in the development of the lungs, face, and nervous system,” Dr. Morgan wrote in the April 12 blog entry.

©Christian Jasiuk/Thinkstock

Smaller studies show there is evidence that maternal smoking can have epigenetic effects on a fetus. The new research from 13 research cohorts reaffirms and renders this finding more statistically powerful, Dr. Morgan wrote. In the infants of women who smoked every day during pregnancy, the researchers found more than 6,000 places where chemical marks on the DNA differed from those of babies born to mothers who did not smoke during pregnancy. The researchers also observed more than 4,600 epigenetic modifications in the DNA of babies of mothers who self-identified as falling under the broad category of having engaged in “any smoking during pregnancy.”

The genes thought to cause a cleft lip and/or palate were among the others to have been epigenetically modified in the fetuses of women who smoked while pregnant. The study also suggested that thousands of the epigenetic modifications seen affected children until at least age 4 years.

Read the study in the American Journal of Human Genetics (doi: 10.1016/j.ajhg.2016.02.019).

[email protected]

Children with better adherence to asthma treatments tended to have more severe asthma symptoms, according to Dr. Marjolein Engelkes of Erasmus University, Rotterdam (The Netherlands) and her associates.

Of the 14,303 children with asthma included in the study, short-acting beta2-agonists and inhaled corticosteroids were the most commonly prescribed treatments at 38 users/100 person-years and 31 users/100 person-years, respectively. Inhaled corticosteroid prescriptions were most common during the winter and in September, and decreased as children increased in age.

©tupungato/Thinkstock.com

The median medication possession ratio (MPR) for inhaled corticosteroids was 56%. Children with an MPR over 87% were significantly more likely to be younger at the start of inhaled corticosteroid treatment, visit specialists more often, and to have more exacerbations than children with an MPR less than 37%.

“These findings indicate that there is room for improvement of adherence to treatment, especially in children with milder forms of asthma,” the investigators concluded.

Find the full study in Pediatric Allergy and Immunology (2016 Mar. doi: 10.1111/pai.12507).

Children with better adherence to asthma treatments tended to have more severe asthma symptoms, according to Dr. Marjolein Engelkes of Erasmus University, Rotterdam (The Netherlands) and her associates.

Of the 14,303 children with asthma included in the study, short-acting beta2-agonists and inhaled corticosteroids were the most commonly prescribed treatments at 38 users/100 person-years and 31 users/100 person-years, respectively. Inhaled corticosteroid prescriptions were most common during the winter and in September, and decreased as children increased in age.

©tupungato/Thinkstock.com

The median medication possession ratio (MPR) for inhaled corticosteroids was 56%. Children with an MPR over 87% were significantly more likely to be younger at the start of inhaled corticosteroid treatment, visit specialists more often, and to have more exacerbations than children with an MPR less than 37%.

“These findings indicate that there is room for improvement of adherence to treatment, especially in children with milder forms of asthma,” the investigators concluded.

Find the full study in Pediatric Allergy and Immunology (2016 Mar. doi: 10.1111/pai.12507).

Children with better adherence to asthma treatments tended to have more severe asthma symptoms, according to Dr. Marjolein Engelkes of Erasmus University, Rotterdam (The Netherlands) and her associates.

Of the 14,303 children with asthma included in the study, short-acting beta2-agonists and inhaled corticosteroids were the most commonly prescribed treatments at 38 users/100 person-years and 31 users/100 person-years, respectively. Inhaled corticosteroid prescriptions were most common during the winter and in September, and decreased as children increased in age.

©tupungato/Thinkstock.com

The median medication possession ratio (MPR) for inhaled corticosteroids was 56%. Children with an MPR over 87% were significantly more likely to be younger at the start of inhaled corticosteroid treatment, visit specialists more often, and to have more exacerbations than children with an MPR less than 37%.

“These findings indicate that there is room for improvement of adherence to treatment, especially in children with milder forms of asthma,” the investigators concluded.

Find the full study in Pediatric Allergy and Immunology (2016 Mar. doi: 10.1111/pai.12507).

Chronic illnesses such as otitis media, respiratory disease, and epilepsy increase the likelihood that children will be developmentally at risk for difficulties at school entry, a study showed.

The authors’ findings indicated “that chronically poor health in early childhood is a risk for school readiness, over and above the disadvantage conferred by socioeconomic factors,” Megan F. Bell of the University of Western Australia in Perth and her associates reported online (Pediatrics. 2016 April 13. doi: 10.1542/peds.2015-2475). “This increased risk was particularly evident for social and emotional capacities.”

Courtesy Wikimedia Commons/Mar10029/Creative Commons License

The researchers analyzed developmental school readiness among 22,890 children (average age, 5 years), within the context of having chronic illness. The children were born in Western Australia in 2003-2004, underwent an early development assessment for school readiness in 2009, and did not have special needs, cerebral palsy, or a diagnosed developmental disorder. The assessments’ five domains included physical health and well-being, social competence, emotional maturity, language and cognitive skills, and communication skills and general knowledge. Children were designated “developmentally vulnerable” if they scored in the bottom 10% of a domain and “at risk” if they scored in the bottom 10%-25%. The top 75% were classified as “on track.”

Among 2,879 children with chronic illness, involving 13% of the overall sample, 93% of these children had one chronic illness diagnosis, and 7% had at least two. The most common illnesses were chronic otitis media (71%), chronic respiratory disease (27%), and epilepsy (3%).

Using health and demographic data for 19,227 mothers and 19,030 fathers of the children, the researchers accounted for sociodemographic characteristics of each child, their community, and their parents, including parental chronic illness. After these adjustments, children with a chronic illness were approximately 20%-35% more likely to fall within the vulnerable or at-risk categories in all five developmental domains, compared with their healthier peers. Children with multiple diagnoses, however, were not significantly more likely to be less developmentally ready for school in any of the five domains than their peers with one diagnosis, suggesting that “just one chronic illness is enough to increase a child’s risk for lower school readiness,” the authors wrote.

A 15%-35% increase in the risk of developmental vulnerability was seen in all domains for 1,859 children with a single diagnosis of otitis media and a 24%-45% increase was seen for 618 children with a single diagnosis of respiratory disease. However, there was no significant increase in risk for the 63 children with a diagnosis of epilepsy; all probability values were greater than .05.

“School-based programs targeted at enhancing social and emotional abilities have been shown to lead to improvements in behavioral, social, and academic outcomes,” the authors wrote. “This may therefore be an important focus of intervention for chronically ill children.

“Our findings suggest there is a need to broaden the scope of health conditions eligible for additional support at school entry. For instance, the most prevalent diagnosis was chronic otitis media, a common childhood condition that is associated with delayed language development, reading and spelling difficulties, and auditory processing deficits. Although recurrent ear infections may not be associated with significant limitations in daily activities, our study demonstrated that children with this condition are at increased risk of poor school readiness, even without having a more severe comorbid condition,” Ms. Bell and her associates wrote.

The research was funded by the Australian Research Council Linkage Project. The authors reported no relevant financial disclosures.

Chronic illnesses such as otitis media, respiratory disease, and epilepsy increase the likelihood that children will be developmentally at risk for difficulties at school entry, a study showed.

The authors’ findings indicated “that chronically poor health in early childhood is a risk for school readiness, over and above the disadvantage conferred by socioeconomic factors,” Megan F. Bell of the University of Western Australia in Perth and her associates reported online (Pediatrics. 2016 April 13. doi: 10.1542/peds.2015-2475). “This increased risk was particularly evident for social and emotional capacities.”

Courtesy Wikimedia Commons/Mar10029/Creative Commons License

The researchers analyzed developmental school readiness among 22,890 children (average age, 5 years), within the context of having chronic illness. The children were born in Western Australia in 2003-2004, underwent an early development assessment for school readiness in 2009, and did not have special needs, cerebral palsy, or a diagnosed developmental disorder. The assessments’ five domains included physical health and well-being, social competence, emotional maturity, language and cognitive skills, and communication skills and general knowledge. Children were designated “developmentally vulnerable” if they scored in the bottom 10% of a domain and “at risk” if they scored in the bottom 10%-25%. The top 75% were classified as “on track.”

Among 2,879 children with chronic illness, involving 13% of the overall sample, 93% of these children had one chronic illness diagnosis, and 7% had at least two. The most common illnesses were chronic otitis media (71%), chronic respiratory disease (27%), and epilepsy (3%).

Using health and demographic data for 19,227 mothers and 19,030 fathers of the children, the researchers accounted for sociodemographic characteristics of each child, their community, and their parents, including parental chronic illness. After these adjustments, children with a chronic illness were approximately 20%-35% more likely to fall within the vulnerable or at-risk categories in all five developmental domains, compared with their healthier peers. Children with multiple diagnoses, however, were not significantly more likely to be less developmentally ready for school in any of the five domains than their peers with one diagnosis, suggesting that “just one chronic illness is enough to increase a child’s risk for lower school readiness,” the authors wrote.

A 15%-35% increase in the risk of developmental vulnerability was seen in all domains for 1,859 children with a single diagnosis of otitis media and a 24%-45% increase was seen for 618 children with a single diagnosis of respiratory disease. However, there was no significant increase in risk for the 63 children with a diagnosis of epilepsy; all probability values were greater than .05.

“School-based programs targeted at enhancing social and emotional abilities have been shown to lead to improvements in behavioral, social, and academic outcomes,” the authors wrote. “This may therefore be an important focus of intervention for chronically ill children.

“Our findings suggest there is a need to broaden the scope of health conditions eligible for additional support at school entry. For instance, the most prevalent diagnosis was chronic otitis media, a common childhood condition that is associated with delayed language development, reading and spelling difficulties, and auditory processing deficits. Although recurrent ear infections may not be associated with significant limitations in daily activities, our study demonstrated that children with this condition are at increased risk of poor school readiness, even without having a more severe comorbid condition,” Ms. Bell and her associates wrote.

The research was funded by the Australian Research Council Linkage Project. The authors reported no relevant financial disclosures.

Chronic illnesses such as otitis media, respiratory disease, and epilepsy increase the likelihood that children will be developmentally at risk for difficulties at school entry, a study showed.

The authors’ findings indicated “that chronically poor health in early childhood is a risk for school readiness, over and above the disadvantage conferred by socioeconomic factors,” Megan F. Bell of the University of Western Australia in Perth and her associates reported online (Pediatrics. 2016 April 13. doi: 10.1542/peds.2015-2475). “This increased risk was particularly evident for social and emotional capacities.”

Courtesy Wikimedia Commons/Mar10029/Creative Commons License

The researchers analyzed developmental school readiness among 22,890 children (average age, 5 years), within the context of having chronic illness. The children were born in Western Australia in 2003-2004, underwent an early development assessment for school readiness in 2009, and did not have special needs, cerebral palsy, or a diagnosed developmental disorder. The assessments’ five domains included physical health and well-being, social competence, emotional maturity, language and cognitive skills, and communication skills and general knowledge. Children were designated “developmentally vulnerable” if they scored in the bottom 10% of a domain and “at risk” if they scored in the bottom 10%-25%. The top 75% were classified as “on track.”

Among 2,879 children with chronic illness, involving 13% of the overall sample, 93% of these children had one chronic illness diagnosis, and 7% had at least two. The most common illnesses were chronic otitis media (71%), chronic respiratory disease (27%), and epilepsy (3%).

Using health and demographic data for 19,227 mothers and 19,030 fathers of the children, the researchers accounted for sociodemographic characteristics of each child, their community, and their parents, including parental chronic illness. After these adjustments, children with a chronic illness were approximately 20%-35% more likely to fall within the vulnerable or at-risk categories in all five developmental domains, compared with their healthier peers. Children with multiple diagnoses, however, were not significantly more likely to be less developmentally ready for school in any of the five domains than their peers with one diagnosis, suggesting that “just one chronic illness is enough to increase a child’s risk for lower school readiness,” the authors wrote.

A 15%-35% increase in the risk of developmental vulnerability was seen in all domains for 1,859 children with a single diagnosis of otitis media and a 24%-45% increase was seen for 618 children with a single diagnosis of respiratory disease. However, there was no significant increase in risk for the 63 children with a diagnosis of epilepsy; all probability values were greater than .05.

“School-based programs targeted at enhancing social and emotional abilities have been shown to lead to improvements in behavioral, social, and academic outcomes,” the authors wrote. “This may therefore be an important focus of intervention for chronically ill children.

“Our findings suggest there is a need to broaden the scope of health conditions eligible for additional support at school entry. For instance, the most prevalent diagnosis was chronic otitis media, a common childhood condition that is associated with delayed language development, reading and spelling difficulties, and auditory processing deficits. Although recurrent ear infections may not be associated with significant limitations in daily activities, our study demonstrated that children with this condition are at increased risk of poor school readiness, even without having a more severe comorbid condition,” Ms. Bell and her associates wrote.

The research was funded by the Australian Research Council Linkage Project. The authors reported no relevant financial disclosures.

Atopy was not related to development of eczema or asthma in children under age 13 years, according to Ann-Marie Malby Schoos, Ph.D., and her associates at the University of Copenhagen.

Allergic sensitization increased with age in the 399 children tested, rising from 12% at 6 months to 54% at 13 years. The incidence of asthma was highest at age 4 years at 16%, but decreased afterward, falling to 12% at 13 years. The incidence of eczema peaked at 39% in children aged 1.5 years old, but decreased steadily to only 12% in 13-year-olds.

©marekuliasz/Thinkstock

Asthma and allergic sensitization were related only in late childhood, with an odds ratio of 4.49 in 13-year-olds. This pattern was seen throughout allergic sensitization subgroups. There were strong associations between eczema and allergic sensitization at 6 months (OR, 6.02), 1.5 years (OR, 2.06), and 6 years (OR, 2.77), but no association at 13 years. The proportion of children with allergic sensitization who did not have asthma or eczema also increased with age.

“The tradition of using atopy as a particular endotype of asthma and eczema seems unfounded because it depends on the method of testing for sensitization, type of allergens, and age of the patient. This questions the relevance of the terms atopic asthma and atopic eczema as true endotypes,” the investigators concluded.

Find the full study in the Journal of Allergy and Clinical Immunology (doi: 10.1016/j.jaci.2015.10.004).

Atopy was not related to development of eczema or asthma in children under age 13 years, according to Ann-Marie Malby Schoos, Ph.D., and her associates at the University of Copenhagen.

Allergic sensitization increased with age in the 399 children tested, rising from 12% at 6 months to 54% at 13 years. The incidence of asthma was highest at age 4 years at 16%, but decreased afterward, falling to 12% at 13 years. The incidence of eczema peaked at 39% in children aged 1.5 years old, but decreased steadily to only 12% in 13-year-olds.

©marekuliasz/Thinkstock

Asthma and allergic sensitization were related only in late childhood, with an odds ratio of 4.49 in 13-year-olds. This pattern was seen throughout allergic sensitization subgroups. There were strong associations between eczema and allergic sensitization at 6 months (OR, 6.02), 1.5 years (OR, 2.06), and 6 years (OR, 2.77), but no association at 13 years. The proportion of children with allergic sensitization who did not have asthma or eczema also increased with age.

“The tradition of using atopy as a particular endotype of asthma and eczema seems unfounded because it depends on the method of testing for sensitization, type of allergens, and age of the patient. This questions the relevance of the terms atopic asthma and atopic eczema as true endotypes,” the investigators concluded.

Find the full study in the Journal of Allergy and Clinical Immunology (doi: 10.1016/j.jaci.2015.10.004).

Atopy was not related to development of eczema or asthma in children under age 13 years, according to Ann-Marie Malby Schoos, Ph.D., and her associates at the University of Copenhagen.

Allergic sensitization increased with age in the 399 children tested, rising from 12% at 6 months to 54% at 13 years. The incidence of asthma was highest at age 4 years at 16%, but decreased afterward, falling to 12% at 13 years. The incidence of eczema peaked at 39% in children aged 1.5 years old, but decreased steadily to only 12% in 13-year-olds.

©marekuliasz/Thinkstock

Asthma and allergic sensitization were related only in late childhood, with an odds ratio of 4.49 in 13-year-olds. This pattern was seen throughout allergic sensitization subgroups. There were strong associations between eczema and allergic sensitization at 6 months (OR, 6.02), 1.5 years (OR, 2.06), and 6 years (OR, 2.77), but no association at 13 years. The proportion of children with allergic sensitization who did not have asthma or eczema also increased with age.

“The tradition of using atopy as a particular endotype of asthma and eczema seems unfounded because it depends on the method of testing for sensitization, type of allergens, and age of the patient. This questions the relevance of the terms atopic asthma and atopic eczema as true endotypes,” the investigators concluded.

Find the full study in the Journal of Allergy and Clinical Immunology (doi: 10.1016/j.jaci.2015.10.004).