Pediatrics

Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.

While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.

“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”

The findings were published online on May 28 in JAMA Network Open.
 

Large, Longitudinal Study

To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.

Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.

They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.

Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.

Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.

When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.

A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).

After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).

Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
 

Vulnerability of the Developing Brain

The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”

They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.

Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.

“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”

Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.

The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.

While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.

“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”

The findings were published online on May 28 in JAMA Network Open.
 

Large, Longitudinal Study

To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.

Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.

They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.

Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.

Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.

When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.

A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).

After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).

Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
 

Vulnerability of the Developing Brain

The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”

They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.

Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.

“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”

Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.

The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.

While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.

“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”

The findings were published online on May 28 in JAMA Network Open.
 

Large, Longitudinal Study

To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.

Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.

They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.

Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.

Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.

When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.

A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).

After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).

Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
 

Vulnerability of the Developing Brain

The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”

They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.

Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.

“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”

Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.

The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Celiac disease is a chronic, immune-mediated, systemic disorder caused by intolerance to gluten — a protein present in rye, barley, and wheat grains — that affects genetically predisposed individuals.

Due to its wide spectrum of clinical manifestations, celiac disease resembles a multisystemic disorder. Its most common gastrointestinal (GI) symptoms include chronic diarrhea, weight loss, and abdominal distention. However, celiac disease can also manifest in myriad extraintestinal symptoms, ranging from headache and fatigue to delayed puberty and psychiatric disorders, with differing presentations in children and adults.

To date, the only treatment is adopting a gluten-free diet (GFD). Although key to preventing persistent villous atrophy, the main cause of complications in celiac disease, lifelong adherence to GFD is challenging and may not resolve all clinical issues. These shortcomings have driven recent efforts to develop novel therapeutic options for patients with this disease.

Here are five things to know about celiac disease.
 

1. Rising Prevalence of Celiac Disease and Other Autoimmune Disorders Suggests Environmental Factors May Be at Play

Gluten was first identified as the cause of celiac disease in the 1950s. At that time, the condition was thought to be a relatively rare GI disease of childhood that primarily affected people of European descent, but it is now known to be a common disease affecting those of various ages, races, and ethnicities.

A 2018 meta-analysis found the pooled global prevalence of celiac disease was 1.4%. Incidence has increased by as much as 7.5% annually over the past several decades.

Increased awareness among clinicians and improved detection likely play a role in the trend. However, the growth in celiac disease is consistent with that seen for other autoimmune disorders, according to a 2024 update of evidence surrounding celiac disease. Shared environmental factors have been proposed as triggers for celiac disease and other autoimmune diseases and appear to be influencing their rise, the authors noted. These factors include migration and population growth, changing dietary patterns and food processing practices, and altered wheat consumption.
 

2. No-Biopsy Diagnosis Is Accepted for Children and Shows Promise for Adults

It is estimated that almost 60 million people worldwide have celiac disease, but most remain undiagnosed or misdiagnosed, or they experience significant diagnostic delays.

Prospective data indicate that children with first-degree relatives with celiac disease are at a significantly higher risk of developing the condition, which should prompt screening efforts in this population.

The 2023 updated guidelines from the American College of Gastroenterology (ACG) state that serology testing plays a central role in screening. This commonly involves serological testing for positive serological markers of the disease, including immunoglobulin A (IgA), anti-tissue transglutaminase IgA (tTG-IgA), anti-deamidated gliadin peptide, or endomysial antibodies.

To confirm diagnosis, clinicians have relied on intestinal biopsy since the late 1950s. The ACG still recommends esophagogastroduodenoscopy with multiple duodenal biopsies for confirmation of diagnosis in both children and adults with suspicion of celiac disease. However, recent years have seen a shift toward a no-biopsy approach.

For more than a decade in Europe, a no-biopsy approach has been established practice in pediatric patients, for whom the burden of obtaining a histological confirmation is understandably greater. Most guidelines now permit children to be diagnosed with celiac disease in the absence of a biopsy under specific circumstances (eg, characteristic symptoms of celiac disease and tTG-IgA levels > 10 times the upper limit of normal). The ACG guidelines state that “this approach is a reasonable alternative to the standard approach to a [celiac disease] diagnosis in selected children.”

The ACG does not recommend a no-biopsy approach in adults, noting that, in comparison with children, there is a relative lack of data indicating that serology is predictive in this population. However, it does recognize that physicians may encounter patients for whom a biopsy diagnosis may not be safe or practical. In such cases, an “after-the-fact” diagnosis of likely celiac disease can be given to symptomatic adult patients with a ≥ 10-fold elevation of tTG-IgA and a positive endomysial antibody in a second blood sample.

A 2024 meta-analysis of 18 studies involving over 12,103 adult patients from 15 countries concluded that a no-biopsy approach using tTG-IgA antibody levels ≥ 10 times the upper limit of normal was highly specific and predictive of celiac disease.
 

3. Celiac Disease Is Associated With Several Life-Threatening Conditions

Emerging data indicate that gastroenterologists should be vigilant in screening patients with celiac disease for several other GI conditions.

Inflammatory bowel disease and celiac disease have a strong bidirectional association, suggesting a possible genetic link between the conditions and indicating that physicians should consider the alternate diagnosis when symptoms persist after treatment.

Given the hypervigilance around food and diet inherent to celiac disease, patients are at an increased risk of developing avoidant/restrictive food intake disorder, according to a 2022 retrospective study.

In 2023, Italian investigators showed that children with celiac disease have an elevated prevalence of functional GI disorders even after adopting a GFD for a year, regardless of whether they consumed processed or natural foods. It was unclear whether this was due to a chronic inflammatory process or to nutritional factors.

Complications resulting from celiac disease are not limited to GI disorders. For a variety of underlying pathophysiological reasons, including intestinal permeability, hyposplenism, and malabsorption of nutrients, patients with celiac disease may be at a higher risk for non-GI conditions, such as osteopenia, women’s health disorders (eg, ovarian failure, endometriosis, or pregnancy loss), juvenile idiopathic arthritis in children and rheumatoid arthritis in adults, certain forms of cancer, infectious diseases, and cardiomyopathy.
 

4. GFD Is the Only Treatment, but It’s Imperfect and Frustrating for Patients

GFD is the only treatment for celiac disease and must be adhered to without deviation throughout a patient’s life.

Maintaining unwavering adherence reaps considerable benefits: Improved clinical symptoms, robust mucosal healing, and normalization of serological markers. Yet it also takes a considerable toll on patients. Patients with celiac disease struggle with a host of negative physical, psychological, and social impacts. They also report a higher treatment burden than those with gastroesophageal reflux disease or hypertension, and comparable with end-stage renal disease.

GFD also poses financial challenges. Although the price of gluten-free products has decreased in recent years, they still cost significantly more than items with gluten.

Adherence to GFD does not always equate to complete mucosal recovery. While mucosal recovery is achieved in 95% of children within 2 years of the diet’s adoption, only 34% and 66% of adults obtain it within 2 and 5 years, respectively.

GFD may lead to nutrient imbalances because gluten-free foods are typically low in alimentary fiber, micronutrients (eg, vitamin D, vitamin B12, or folate), and minerals (eg, iron, zinc, magnesium, or calcium). With higher sugar and fat content, GFD may leave patients susceptible to unwanted weight gain.

The pervasiveness of gluten in the food production system makes the risk for cross-contamination high. Gluten is often found in both naturally gluten-free foods and products labeled as such. Gluten-sensing technologies, some of which can be used via smartphone apps, have been developed to help patients identify possible cross-contamination. However, the ACG guidelines recommend against the use of these technologies until there is sufficient evidence supporting their ability to improve adherence and clinical outcomes.
 

5. Novel Therapies for Celiac Disease Are in the Pipeline

The limitations of GFD as the standard treatment for celiac disease have led to an increased focus on developing novel therapeutic interventions. They can be sorted into five key categories: Modulation of the immunostimulatory effects of toxic gluten peptides, elimination of toxic gluten peptides before they reach the intestine, induction of gluten tolerance, modulation of intestinal permeability, and restoration of gut microbiota balance.

Three therapies designed to block antigen presentation by HLA-DQ2/8, the gene alleles that predispose people to celiac disease, show promise: TPM502, an agent that contains three gluten-specific antigenic peptides with overlapping T-cell epitopes for the HLA-DQ2.5 gene; KAN-101, designed to induce gluten tolerance by targeting receptors on the liver; and DONQ52, a multi-specific antibody that targets HLA-DQ2. The KAN-101 therapy received Fast Track designation by the US Food and Drug Administration in 2022.

These and several other agents in clinical and preclinical development are discussed in detail in a 2024 review article. Although no therapies have reached phase 3 testing, when they do, it will undoubtedly be welcomed by those with celiac disease.

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

Celiac disease is a chronic, immune-mediated, systemic disorder caused by intolerance to gluten — a protein present in rye, barley, and wheat grains — that affects genetically predisposed individuals.

Due to its wide spectrum of clinical manifestations, celiac disease resembles a multisystemic disorder. Its most common gastrointestinal (GI) symptoms include chronic diarrhea, weight loss, and abdominal distention. However, celiac disease can also manifest in myriad extraintestinal symptoms, ranging from headache and fatigue to delayed puberty and psychiatric disorders, with differing presentations in children and adults.

To date, the only treatment is adopting a gluten-free diet (GFD). Although key to preventing persistent villous atrophy, the main cause of complications in celiac disease, lifelong adherence to GFD is challenging and may not resolve all clinical issues. These shortcomings have driven recent efforts to develop novel therapeutic options for patients with this disease.

Here are five things to know about celiac disease.
 

1. Rising Prevalence of Celiac Disease and Other Autoimmune Disorders Suggests Environmental Factors May Be at Play

Gluten was first identified as the cause of celiac disease in the 1950s. At that time, the condition was thought to be a relatively rare GI disease of childhood that primarily affected people of European descent, but it is now known to be a common disease affecting those of various ages, races, and ethnicities.

A 2018 meta-analysis found the pooled global prevalence of celiac disease was 1.4%. Incidence has increased by as much as 7.5% annually over the past several decades.

Increased awareness among clinicians and improved detection likely play a role in the trend. However, the growth in celiac disease is consistent with that seen for other autoimmune disorders, according to a 2024 update of evidence surrounding celiac disease. Shared environmental factors have been proposed as triggers for celiac disease and other autoimmune diseases and appear to be influencing their rise, the authors noted. These factors include migration and population growth, changing dietary patterns and food processing practices, and altered wheat consumption.
 

2. No-Biopsy Diagnosis Is Accepted for Children and Shows Promise for Adults

It is estimated that almost 60 million people worldwide have celiac disease, but most remain undiagnosed or misdiagnosed, or they experience significant diagnostic delays.

Prospective data indicate that children with first-degree relatives with celiac disease are at a significantly higher risk of developing the condition, which should prompt screening efforts in this population.

The 2023 updated guidelines from the American College of Gastroenterology (ACG) state that serology testing plays a central role in screening. This commonly involves serological testing for positive serological markers of the disease, including immunoglobulin A (IgA), anti-tissue transglutaminase IgA (tTG-IgA), anti-deamidated gliadin peptide, or endomysial antibodies.

To confirm diagnosis, clinicians have relied on intestinal biopsy since the late 1950s. The ACG still recommends esophagogastroduodenoscopy with multiple duodenal biopsies for confirmation of diagnosis in both children and adults with suspicion of celiac disease. However, recent years have seen a shift toward a no-biopsy approach.

For more than a decade in Europe, a no-biopsy approach has been established practice in pediatric patients, for whom the burden of obtaining a histological confirmation is understandably greater. Most guidelines now permit children to be diagnosed with celiac disease in the absence of a biopsy under specific circumstances (eg, characteristic symptoms of celiac disease and tTG-IgA levels > 10 times the upper limit of normal). The ACG guidelines state that “this approach is a reasonable alternative to the standard approach to a [celiac disease] diagnosis in selected children.”

The ACG does not recommend a no-biopsy approach in adults, noting that, in comparison with children, there is a relative lack of data indicating that serology is predictive in this population. However, it does recognize that physicians may encounter patients for whom a biopsy diagnosis may not be safe or practical. In such cases, an “after-the-fact” diagnosis of likely celiac disease can be given to symptomatic adult patients with a ≥ 10-fold elevation of tTG-IgA and a positive endomysial antibody in a second blood sample.

A 2024 meta-analysis of 18 studies involving over 12,103 adult patients from 15 countries concluded that a no-biopsy approach using tTG-IgA antibody levels ≥ 10 times the upper limit of normal was highly specific and predictive of celiac disease.
 

3. Celiac Disease Is Associated With Several Life-Threatening Conditions

Emerging data indicate that gastroenterologists should be vigilant in screening patients with celiac disease for several other GI conditions.

Inflammatory bowel disease and celiac disease have a strong bidirectional association, suggesting a possible genetic link between the conditions and indicating that physicians should consider the alternate diagnosis when symptoms persist after treatment.

Given the hypervigilance around food and diet inherent to celiac disease, patients are at an increased risk of developing avoidant/restrictive food intake disorder, according to a 2022 retrospective study.

In 2023, Italian investigators showed that children with celiac disease have an elevated prevalence of functional GI disorders even after adopting a GFD for a year, regardless of whether they consumed processed or natural foods. It was unclear whether this was due to a chronic inflammatory process or to nutritional factors.

Complications resulting from celiac disease are not limited to GI disorders. For a variety of underlying pathophysiological reasons, including intestinal permeability, hyposplenism, and malabsorption of nutrients, patients with celiac disease may be at a higher risk for non-GI conditions, such as osteopenia, women’s health disorders (eg, ovarian failure, endometriosis, or pregnancy loss), juvenile idiopathic arthritis in children and rheumatoid arthritis in adults, certain forms of cancer, infectious diseases, and cardiomyopathy.
 

4. GFD Is the Only Treatment, but It’s Imperfect and Frustrating for Patients

GFD is the only treatment for celiac disease and must be adhered to without deviation throughout a patient’s life.

Maintaining unwavering adherence reaps considerable benefits: Improved clinical symptoms, robust mucosal healing, and normalization of serological markers. Yet it also takes a considerable toll on patients. Patients with celiac disease struggle with a host of negative physical, psychological, and social impacts. They also report a higher treatment burden than those with gastroesophageal reflux disease or hypertension, and comparable with end-stage renal disease.

GFD also poses financial challenges. Although the price of gluten-free products has decreased in recent years, they still cost significantly more than items with gluten.

Adherence to GFD does not always equate to complete mucosal recovery. While mucosal recovery is achieved in 95% of children within 2 years of the diet’s adoption, only 34% and 66% of adults obtain it within 2 and 5 years, respectively.

GFD may lead to nutrient imbalances because gluten-free foods are typically low in alimentary fiber, micronutrients (eg, vitamin D, vitamin B12, or folate), and minerals (eg, iron, zinc, magnesium, or calcium). With higher sugar and fat content, GFD may leave patients susceptible to unwanted weight gain.

The pervasiveness of gluten in the food production system makes the risk for cross-contamination high. Gluten is often found in both naturally gluten-free foods and products labeled as such. Gluten-sensing technologies, some of which can be used via smartphone apps, have been developed to help patients identify possible cross-contamination. However, the ACG guidelines recommend against the use of these technologies until there is sufficient evidence supporting their ability to improve adherence and clinical outcomes.
 

5. Novel Therapies for Celiac Disease Are in the Pipeline

The limitations of GFD as the standard treatment for celiac disease have led to an increased focus on developing novel therapeutic interventions. They can be sorted into five key categories: Modulation of the immunostimulatory effects of toxic gluten peptides, elimination of toxic gluten peptides before they reach the intestine, induction of gluten tolerance, modulation of intestinal permeability, and restoration of gut microbiota balance.

Three therapies designed to block antigen presentation by HLA-DQ2/8, the gene alleles that predispose people to celiac disease, show promise: TPM502, an agent that contains three gluten-specific antigenic peptides with overlapping T-cell epitopes for the HLA-DQ2.5 gene; KAN-101, designed to induce gluten tolerance by targeting receptors on the liver; and DONQ52, a multi-specific antibody that targets HLA-DQ2. The KAN-101 therapy received Fast Track designation by the US Food and Drug Administration in 2022.

These and several other agents in clinical and preclinical development are discussed in detail in a 2024 review article. Although no therapies have reached phase 3 testing, when they do, it will undoubtedly be welcomed by those with celiac disease.

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

Celiac disease is a chronic, immune-mediated, systemic disorder caused by intolerance to gluten — a protein present in rye, barley, and wheat grains — that affects genetically predisposed individuals.

Due to its wide spectrum of clinical manifestations, celiac disease resembles a multisystemic disorder. Its most common gastrointestinal (GI) symptoms include chronic diarrhea, weight loss, and abdominal distention. However, celiac disease can also manifest in myriad extraintestinal symptoms, ranging from headache and fatigue to delayed puberty and psychiatric disorders, with differing presentations in children and adults.

To date, the only treatment is adopting a gluten-free diet (GFD). Although key to preventing persistent villous atrophy, the main cause of complications in celiac disease, lifelong adherence to GFD is challenging and may not resolve all clinical issues. These shortcomings have driven recent efforts to develop novel therapeutic options for patients with this disease.

Here are five things to know about celiac disease.
 

1. Rising Prevalence of Celiac Disease and Other Autoimmune Disorders Suggests Environmental Factors May Be at Play

Gluten was first identified as the cause of celiac disease in the 1950s. At that time, the condition was thought to be a relatively rare GI disease of childhood that primarily affected people of European descent, but it is now known to be a common disease affecting those of various ages, races, and ethnicities.

A 2018 meta-analysis found the pooled global prevalence of celiac disease was 1.4%. Incidence has increased by as much as 7.5% annually over the past several decades.

Increased awareness among clinicians and improved detection likely play a role in the trend. However, the growth in celiac disease is consistent with that seen for other autoimmune disorders, according to a 2024 update of evidence surrounding celiac disease. Shared environmental factors have been proposed as triggers for celiac disease and other autoimmune diseases and appear to be influencing their rise, the authors noted. These factors include migration and population growth, changing dietary patterns and food processing practices, and altered wheat consumption.
 

2. No-Biopsy Diagnosis Is Accepted for Children and Shows Promise for Adults

It is estimated that almost 60 million people worldwide have celiac disease, but most remain undiagnosed or misdiagnosed, or they experience significant diagnostic delays.

Prospective data indicate that children with first-degree relatives with celiac disease are at a significantly higher risk of developing the condition, which should prompt screening efforts in this population.

The 2023 updated guidelines from the American College of Gastroenterology (ACG) state that serology testing plays a central role in screening. This commonly involves serological testing for positive serological markers of the disease, including immunoglobulin A (IgA), anti-tissue transglutaminase IgA (tTG-IgA), anti-deamidated gliadin peptide, or endomysial antibodies.

To confirm diagnosis, clinicians have relied on intestinal biopsy since the late 1950s. The ACG still recommends esophagogastroduodenoscopy with multiple duodenal biopsies for confirmation of diagnosis in both children and adults with suspicion of celiac disease. However, recent years have seen a shift toward a no-biopsy approach.

For more than a decade in Europe, a no-biopsy approach has been established practice in pediatric patients, for whom the burden of obtaining a histological confirmation is understandably greater. Most guidelines now permit children to be diagnosed with celiac disease in the absence of a biopsy under specific circumstances (eg, characteristic symptoms of celiac disease and tTG-IgA levels > 10 times the upper limit of normal). The ACG guidelines state that “this approach is a reasonable alternative to the standard approach to a [celiac disease] diagnosis in selected children.”

The ACG does not recommend a no-biopsy approach in adults, noting that, in comparison with children, there is a relative lack of data indicating that serology is predictive in this population. However, it does recognize that physicians may encounter patients for whom a biopsy diagnosis may not be safe or practical. In such cases, an “after-the-fact” diagnosis of likely celiac disease can be given to symptomatic adult patients with a ≥ 10-fold elevation of tTG-IgA and a positive endomysial antibody in a second blood sample.

A 2024 meta-analysis of 18 studies involving over 12,103 adult patients from 15 countries concluded that a no-biopsy approach using tTG-IgA antibody levels ≥ 10 times the upper limit of normal was highly specific and predictive of celiac disease.
 

3. Celiac Disease Is Associated With Several Life-Threatening Conditions

Emerging data indicate that gastroenterologists should be vigilant in screening patients with celiac disease for several other GI conditions.

Inflammatory bowel disease and celiac disease have a strong bidirectional association, suggesting a possible genetic link between the conditions and indicating that physicians should consider the alternate diagnosis when symptoms persist after treatment.

Given the hypervigilance around food and diet inherent to celiac disease, patients are at an increased risk of developing avoidant/restrictive food intake disorder, according to a 2022 retrospective study.

In 2023, Italian investigators showed that children with celiac disease have an elevated prevalence of functional GI disorders even after adopting a GFD for a year, regardless of whether they consumed processed or natural foods. It was unclear whether this was due to a chronic inflammatory process or to nutritional factors.

Complications resulting from celiac disease are not limited to GI disorders. For a variety of underlying pathophysiological reasons, including intestinal permeability, hyposplenism, and malabsorption of nutrients, patients with celiac disease may be at a higher risk for non-GI conditions, such as osteopenia, women’s health disorders (eg, ovarian failure, endometriosis, or pregnancy loss), juvenile idiopathic arthritis in children and rheumatoid arthritis in adults, certain forms of cancer, infectious diseases, and cardiomyopathy.
 

4. GFD Is the Only Treatment, but It’s Imperfect and Frustrating for Patients

GFD is the only treatment for celiac disease and must be adhered to without deviation throughout a patient’s life.

Maintaining unwavering adherence reaps considerable benefits: Improved clinical symptoms, robust mucosal healing, and normalization of serological markers. Yet it also takes a considerable toll on patients. Patients with celiac disease struggle with a host of negative physical, psychological, and social impacts. They also report a higher treatment burden than those with gastroesophageal reflux disease or hypertension, and comparable with end-stage renal disease.

GFD also poses financial challenges. Although the price of gluten-free products has decreased in recent years, they still cost significantly more than items with gluten.

Adherence to GFD does not always equate to complete mucosal recovery. While mucosal recovery is achieved in 95% of children within 2 years of the diet’s adoption, only 34% and 66% of adults obtain it within 2 and 5 years, respectively.

GFD may lead to nutrient imbalances because gluten-free foods are typically low in alimentary fiber, micronutrients (eg, vitamin D, vitamin B12, or folate), and minerals (eg, iron, zinc, magnesium, or calcium). With higher sugar and fat content, GFD may leave patients susceptible to unwanted weight gain.

The pervasiveness of gluten in the food production system makes the risk for cross-contamination high. Gluten is often found in both naturally gluten-free foods and products labeled as such. Gluten-sensing technologies, some of which can be used via smartphone apps, have been developed to help patients identify possible cross-contamination. However, the ACG guidelines recommend against the use of these technologies until there is sufficient evidence supporting their ability to improve adherence and clinical outcomes.
 

5. Novel Therapies for Celiac Disease Are in the Pipeline

The limitations of GFD as the standard treatment for celiac disease have led to an increased focus on developing novel therapeutic interventions. They can be sorted into five key categories: Modulation of the immunostimulatory effects of toxic gluten peptides, elimination of toxic gluten peptides before they reach the intestine, induction of gluten tolerance, modulation of intestinal permeability, and restoration of gut microbiota balance.

Three therapies designed to block antigen presentation by HLA-DQ2/8, the gene alleles that predispose people to celiac disease, show promise: TPM502, an agent that contains three gluten-specific antigenic peptides with overlapping T-cell epitopes for the HLA-DQ2.5 gene; KAN-101, designed to induce gluten tolerance by targeting receptors on the liver; and DONQ52, a multi-specific antibody that targets HLA-DQ2. The KAN-101 therapy received Fast Track designation by the US Food and Drug Administration in 2022.

These and several other agents in clinical and preclinical development are discussed in detail in a 2024 review article. Although no therapies have reached phase 3 testing, when they do, it will undoubtedly be welcomed by those with celiac disease.

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

Upadacitinib (Rinvoq) is now indicated for patients aged 2 years or older with active polyarticular juvenile idiopathic arthritis (pJIA) and psoriatic arthritis (PsA) who cannot tolerate or achieve adequate disease response with one or more tumor necrosis factor (TNF) blockers, according to a press release from manufacturer AbbVie. 

For the youngest patients, upadacitinib is also available as a weight-based oral solution (Rinvoq LQ) in addition to the previously available tablets, according to the company. JIA, which includes pJIA and juvenile PsA, affects nearly 300,000 children and adolescents in the United States, and alternatives to TNF inhibitor (TNFi) therapy are limited, according to the company. 

“Pediatric patients with pJIA and PsA can be severely limited in their ability to complete daily physical tasks and participate in everyday activities. Understanding their needs today and knowing the likelihood of disease in adulthood underscores the need for additional treatment options,” Aarat Patel, MD, a pediatric rheumatologist at Bon Secours Rheumatology Center, Richmond, Virginia, said in the press release. “Having a treatment option available for patients who do not respond well to a TNFi addresses a need for the healthcare community, patients, and their families,” he said.

Upadacitinib, a Janus kinase (JAK) inhibitor, is being studied for multiple immune-mediated inflammatory diseases. The new indication was supported by data from adults with rheumatoid arthritis (RA) and PsA, 51 pediatric patients with pJIA and active polyarthritis, and safety data from 83 pediatric patients aged 2 years to younger than 18 years with pJIA and active polyarthritis. 

In the studies, the drug’s safety in pediatric patients was similar to the known safety profile in adults, which includes increased risk for serious infections such as tuberculosis, cancer, immune system problems, blood clots, and serious allergic reactions to components of the drug, according to the press release. However, the safety and effectiveness of upadacitinib for pJIA and PsA in patients younger than 2 years are unknown.

“Upadacitinib plasma exposures in pediatric patients with pJIA and PsA at the recommended dosage are predicted to be comparable to those observed in adults with RA and PsA based on population pharmacokinetic modeling and simulation,” according to the press release.

Currently, upadacitinib’s only other pediatric indication is for moderate to severe atopic dermatitis in children aged 12 years or older. Upadacitinib also is indicated for treatment of adults with moderate to severe RA, active PsA, active ankylosing spondylitis, active nonradiographic axial spondyloarthritis, and moderate to severe ulcerative colitis and Crohn’s disease, but safety and efficacy for its use in treatment of these conditions in children and adolescents is unknown.

Upadacitinib also is being studied in phase 3 trials for treatment of conditions including alopecia areata, ankylosing spondylitis, atopic dermatitis, axial spondyloarthritis, Crohn’s disease, giant cell arteritis, hidradenitis suppurativa, psoriatic arthritis, RA, systemic lupus erythematosus, Takayasu arteritis, ulcerative colitis, and vitiligo, according to the press release. 

Full prescribing information and safety data for upadacitinib are available here. 

A version of this article appeared on Medscape.com.

Upadacitinib (Rinvoq) is now indicated for patients aged 2 years or older with active polyarticular juvenile idiopathic arthritis (pJIA) and psoriatic arthritis (PsA) who cannot tolerate or achieve adequate disease response with one or more tumor necrosis factor (TNF) blockers, according to a press release from manufacturer AbbVie. 

For the youngest patients, upadacitinib is also available as a weight-based oral solution (Rinvoq LQ) in addition to the previously available tablets, according to the company. JIA, which includes pJIA and juvenile PsA, affects nearly 300,000 children and adolescents in the United States, and alternatives to TNF inhibitor (TNFi) therapy are limited, according to the company. 

“Pediatric patients with pJIA and PsA can be severely limited in their ability to complete daily physical tasks and participate in everyday activities. Understanding their needs today and knowing the likelihood of disease in adulthood underscores the need for additional treatment options,” Aarat Patel, MD, a pediatric rheumatologist at Bon Secours Rheumatology Center, Richmond, Virginia, said in the press release. “Having a treatment option available for patients who do not respond well to a TNFi addresses a need for the healthcare community, patients, and their families,” he said.

Upadacitinib, a Janus kinase (JAK) inhibitor, is being studied for multiple immune-mediated inflammatory diseases. The new indication was supported by data from adults with rheumatoid arthritis (RA) and PsA, 51 pediatric patients with pJIA and active polyarthritis, and safety data from 83 pediatric patients aged 2 years to younger than 18 years with pJIA and active polyarthritis. 

In the studies, the drug’s safety in pediatric patients was similar to the known safety profile in adults, which includes increased risk for serious infections such as tuberculosis, cancer, immune system problems, blood clots, and serious allergic reactions to components of the drug, according to the press release. However, the safety and effectiveness of upadacitinib for pJIA and PsA in patients younger than 2 years are unknown.

“Upadacitinib plasma exposures in pediatric patients with pJIA and PsA at the recommended dosage are predicted to be comparable to those observed in adults with RA and PsA based on population pharmacokinetic modeling and simulation,” according to the press release.

Currently, upadacitinib’s only other pediatric indication is for moderate to severe atopic dermatitis in children aged 12 years or older. Upadacitinib also is indicated for treatment of adults with moderate to severe RA, active PsA, active ankylosing spondylitis, active nonradiographic axial spondyloarthritis, and moderate to severe ulcerative colitis and Crohn’s disease, but safety and efficacy for its use in treatment of these conditions in children and adolescents is unknown.

Upadacitinib also is being studied in phase 3 trials for treatment of conditions including alopecia areata, ankylosing spondylitis, atopic dermatitis, axial spondyloarthritis, Crohn’s disease, giant cell arteritis, hidradenitis suppurativa, psoriatic arthritis, RA, systemic lupus erythematosus, Takayasu arteritis, ulcerative colitis, and vitiligo, according to the press release. 

Full prescribing information and safety data for upadacitinib are available here. 

A version of this article appeared on Medscape.com.

Upadacitinib (Rinvoq) is now indicated for patients aged 2 years or older with active polyarticular juvenile idiopathic arthritis (pJIA) and psoriatic arthritis (PsA) who cannot tolerate or achieve adequate disease response with one or more tumor necrosis factor (TNF) blockers, according to a press release from manufacturer AbbVie. 

For the youngest patients, upadacitinib is also available as a weight-based oral solution (Rinvoq LQ) in addition to the previously available tablets, according to the company. JIA, which includes pJIA and juvenile PsA, affects nearly 300,000 children and adolescents in the United States, and alternatives to TNF inhibitor (TNFi) therapy are limited, according to the company. 

“Pediatric patients with pJIA and PsA can be severely limited in their ability to complete daily physical tasks and participate in everyday activities. Understanding their needs today and knowing the likelihood of disease in adulthood underscores the need for additional treatment options,” Aarat Patel, MD, a pediatric rheumatologist at Bon Secours Rheumatology Center, Richmond, Virginia, said in the press release. “Having a treatment option available for patients who do not respond well to a TNFi addresses a need for the healthcare community, patients, and their families,” he said.

Upadacitinib, a Janus kinase (JAK) inhibitor, is being studied for multiple immune-mediated inflammatory diseases. The new indication was supported by data from adults with rheumatoid arthritis (RA) and PsA, 51 pediatric patients with pJIA and active polyarthritis, and safety data from 83 pediatric patients aged 2 years to younger than 18 years with pJIA and active polyarthritis. 

In the studies, the drug’s safety in pediatric patients was similar to the known safety profile in adults, which includes increased risk for serious infections such as tuberculosis, cancer, immune system problems, blood clots, and serious allergic reactions to components of the drug, according to the press release. However, the safety and effectiveness of upadacitinib for pJIA and PsA in patients younger than 2 years are unknown.

“Upadacitinib plasma exposures in pediatric patients with pJIA and PsA at the recommended dosage are predicted to be comparable to those observed in adults with RA and PsA based on population pharmacokinetic modeling and simulation,” according to the press release.

Currently, upadacitinib’s only other pediatric indication is for moderate to severe atopic dermatitis in children aged 12 years or older. Upadacitinib also is indicated for treatment of adults with moderate to severe RA, active PsA, active ankylosing spondylitis, active nonradiographic axial spondyloarthritis, and moderate to severe ulcerative colitis and Crohn’s disease, but safety and efficacy for its use in treatment of these conditions in children and adolescents is unknown.

Upadacitinib also is being studied in phase 3 trials for treatment of conditions including alopecia areata, ankylosing spondylitis, atopic dermatitis, axial spondyloarthritis, Crohn’s disease, giant cell arteritis, hidradenitis suppurativa, psoriatic arthritis, RA, systemic lupus erythematosus, Takayasu arteritis, ulcerative colitis, and vitiligo, according to the press release. 

Full prescribing information and safety data for upadacitinib are available here. 

A version of this article appeared on Medscape.com.

CHICAGO — Genetics and diet have been among the top theories for what may be fueling the troubling rise of colorectal cancer in young adults. Now, an early look at genetic data from people with colorectal cancer further suggests that the cause is linked to what is happening in the gut.

The findings were presented at the annual meeting of the American Society for Clinical Oncology (ASCO) by researchers from Ohio State University. For the analysis, they analyzed genetic data on tumors.

The researchers found signs that a high-fat, low-fiber diet may increase inflammation in the gut that prevents it from naturally suppressing tumors. The cells of young people with colorectal cancer also appeared to have aged more quickly — by 15 years on average — than a person’s actual age. That’s unusual, because older people with colorectal cancer don’t have the same boost in cellular aging.

The rate of colorectal cancer among young people has been rising at an alarming rate, according to a 2023 report from the American Cancer Society. In 2019, one in five colorectal cancer cases were among people younger than 55. That’s up from 1 in 10 in 1995, which means the rate has doubled in less than 30 years.
 

Need Colon Cancer Screening?

Who needs a colorectal cancer screening? Ask colorectal cancer specialist Nancy Kemeny, MD.

A 2017 analysis estimated that a person’s risk of colorectal cancer increased 12% by eating 3.5 ounces of red or processed meat daily, which is the equivalent of the size of a deck of playing cards. The same study also linked colorectal cancer risk to alcohol intake, citing its ethanol content. Eating a diet high in fiber can reduce a person’s risk.

This latest study aligned with previous findings that link bacteria called Fusobacterium to colorectal cancer. It’s not unusual for Fusobacterium to be present in a person’s mouth, but it is more likely to be found in the intestines of colorectal cancer patients, compared with those of healthy people. One study even found that people with colorectal cancer were five times more likely to have Fusobacterium in their stool, compared with healthy people.

Colorectal cancer is more common among men than women, “likely reflecting differences in risk factor prevalence, such as excess body weight and processed meat consumption,” the authors of the 2023 American Cancer Society report explained.

People younger than 45 should alert their medical provider if they have constipation, rectal bleeding, or sudden changes in bowel movements, which can be symptoms of colorectal cancer. Screening for colorectal cancer should begin for most people at age 45.

A version of this article appeared on WebMD.com.

CHICAGO — Genetics and diet have been among the top theories for what may be fueling the troubling rise of colorectal cancer in young adults. Now, an early look at genetic data from people with colorectal cancer further suggests that the cause is linked to what is happening in the gut.

The findings were presented at the annual meeting of the American Society for Clinical Oncology (ASCO) by researchers from Ohio State University. For the analysis, they analyzed genetic data on tumors.

The researchers found signs that a high-fat, low-fiber diet may increase inflammation in the gut that prevents it from naturally suppressing tumors. The cells of young people with colorectal cancer also appeared to have aged more quickly — by 15 years on average — than a person’s actual age. That’s unusual, because older people with colorectal cancer don’t have the same boost in cellular aging.

The rate of colorectal cancer among young people has been rising at an alarming rate, according to a 2023 report from the American Cancer Society. In 2019, one in five colorectal cancer cases were among people younger than 55. That’s up from 1 in 10 in 1995, which means the rate has doubled in less than 30 years.
 

Need Colon Cancer Screening?

Who needs a colorectal cancer screening? Ask colorectal cancer specialist Nancy Kemeny, MD.

A 2017 analysis estimated that a person’s risk of colorectal cancer increased 12% by eating 3.5 ounces of red or processed meat daily, which is the equivalent of the size of a deck of playing cards. The same study also linked colorectal cancer risk to alcohol intake, citing its ethanol content. Eating a diet high in fiber can reduce a person’s risk.

This latest study aligned with previous findings that link bacteria called Fusobacterium to colorectal cancer. It’s not unusual for Fusobacterium to be present in a person’s mouth, but it is more likely to be found in the intestines of colorectal cancer patients, compared with those of healthy people. One study even found that people with colorectal cancer were five times more likely to have Fusobacterium in their stool, compared with healthy people.

Colorectal cancer is more common among men than women, “likely reflecting differences in risk factor prevalence, such as excess body weight and processed meat consumption,” the authors of the 2023 American Cancer Society report explained.

People younger than 45 should alert their medical provider if they have constipation, rectal bleeding, or sudden changes in bowel movements, which can be symptoms of colorectal cancer. Screening for colorectal cancer should begin for most people at age 45.

A version of this article appeared on WebMD.com.

CHICAGO — Genetics and diet have been among the top theories for what may be fueling the troubling rise of colorectal cancer in young adults. Now, an early look at genetic data from people with colorectal cancer further suggests that the cause is linked to what is happening in the gut.

The findings were presented at the annual meeting of the American Society for Clinical Oncology (ASCO) by researchers from Ohio State University. For the analysis, they analyzed genetic data on tumors.

The researchers found signs that a high-fat, low-fiber diet may increase inflammation in the gut that prevents it from naturally suppressing tumors. The cells of young people with colorectal cancer also appeared to have aged more quickly — by 15 years on average — than a person’s actual age. That’s unusual, because older people with colorectal cancer don’t have the same boost in cellular aging.

The rate of colorectal cancer among young people has been rising at an alarming rate, according to a 2023 report from the American Cancer Society. In 2019, one in five colorectal cancer cases were among people younger than 55. That’s up from 1 in 10 in 1995, which means the rate has doubled in less than 30 years.
 

Need Colon Cancer Screening?

Who needs a colorectal cancer screening? Ask colorectal cancer specialist Nancy Kemeny, MD.

A 2017 analysis estimated that a person’s risk of colorectal cancer increased 12% by eating 3.5 ounces of red or processed meat daily, which is the equivalent of the size of a deck of playing cards. The same study also linked colorectal cancer risk to alcohol intake, citing its ethanol content. Eating a diet high in fiber can reduce a person’s risk.

This latest study aligned with previous findings that link bacteria called Fusobacterium to colorectal cancer. It’s not unusual for Fusobacterium to be present in a person’s mouth, but it is more likely to be found in the intestines of colorectal cancer patients, compared with those of healthy people. One study even found that people with colorectal cancer were five times more likely to have Fusobacterium in their stool, compared with healthy people.

Colorectal cancer is more common among men than women, “likely reflecting differences in risk factor prevalence, such as excess body weight and processed meat consumption,” the authors of the 2023 American Cancer Society report explained.

People younger than 45 should alert their medical provider if they have constipation, rectal bleeding, or sudden changes in bowel movements, which can be symptoms of colorectal cancer. Screening for colorectal cancer should begin for most people at age 45.

A version of this article appeared on WebMD.com.

Early education is right up there with motherhood and apple pie as unarguable positive concepts. How could exposing young children to a school-like atmosphere not be a benefit, particularly in communities dominated by socioeconomic challenges? While there are some questions about the value of playing Mozart to infants, early education in the traditional sense continues to be viewed as a key strategy for providing young children a preschool foundation on which a successful academic career can be built. Several oft-cited randomized controlled trials have fueled both private and public interest and funding.

However, a recent commentary published in Science suggests that all programs are “not unequivocally positive and much more research is needed.” “Worrisome results in Tennessee,” “Success in Boston,” and “Largely null results for Headstart” are just a few of the article’s section titles and convey a sense of the inconsistency the investigators found as they reviewed early education systems around the country.

While there may be some politicians who may attempt to use the results of this investigation as a reason to cancel public funding of underperforming early education programs, the authors avoid this baby-and-the-bathwater conclusion. Instead, they urge more rigorous research “to understand how effective programs can be designed and implemented.”

The kind of re-thinking and brainstorming these investigators suggest takes time. While we’re waiting for this process to gain traction, this might be a good time to consider some of the benefits of early education that we don’t usually consider when our focus is on academic metrics.

A recent paper in Children’s Health Care by investigators at the Boston University Medical Center and School of Medicine considered the diet of children attending preschool. Looking at the dietary records of more than 300 children attending 30 childcare centers, the researchers found that the children’s diets before arrival at daycare was less healthy than while they were in daycare. “The hour after pickup appeared to be the least healthful” of any of the time periods surveyed. Of course, we will all conjure up images of what this chaotic post-daycare pickup may look like and cut the harried parents and grandparents some slack when it comes to nutritional choices. However, the bottom line is that for the group of children surveyed being in preschool or daycare protected them from a less healthy diet they were being provided outside of school hours.

Our recent experience with pandemic-related school closures provides more evidence that being in school was superior to any remote experience academically. School-age children and adolescents gained weight when school closures were the norm. Play patterns for children shifted from outdoor play to indoor play — often dominated by more sedentary video games. Both fatal and non-fatal gun-related injuries surged during the pandemic and, by far, the majority of these occur in the home and not at school.

Stepping back to look at this broader picture that includes diet, physical activity, and safety — not to mention the benefits of socialization — leads one to arrive at the unfortunate conclusion that for many children in this country, being at home is considerably less healthy than being in school. Of course there will be those who point to the belief that schools are petri dishes putting children at greater risk for respiratory infections. On the other hand, we must accept that schools haven’t proved to be a major factor in the spread of COVID that many had feared.

The authors of the study in Science are certainly correct in recommending a more thorough investigation into the academic benefits of preschool education. However, we must keep in mind that preschool offers an environment that can be a positive influence on young children.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Early education is right up there with motherhood and apple pie as unarguable positive concepts. How could exposing young children to a school-like atmosphere not be a benefit, particularly in communities dominated by socioeconomic challenges? While there are some questions about the value of playing Mozart to infants, early education in the traditional sense continues to be viewed as a key strategy for providing young children a preschool foundation on which a successful academic career can be built. Several oft-cited randomized controlled trials have fueled both private and public interest and funding.

However, a recent commentary published in Science suggests that all programs are “not unequivocally positive and much more research is needed.” “Worrisome results in Tennessee,” “Success in Boston,” and “Largely null results for Headstart” are just a few of the article’s section titles and convey a sense of the inconsistency the investigators found as they reviewed early education systems around the country.

While there may be some politicians who may attempt to use the results of this investigation as a reason to cancel public funding of underperforming early education programs, the authors avoid this baby-and-the-bathwater conclusion. Instead, they urge more rigorous research “to understand how effective programs can be designed and implemented.”

The kind of re-thinking and brainstorming these investigators suggest takes time. While we’re waiting for this process to gain traction, this might be a good time to consider some of the benefits of early education that we don’t usually consider when our focus is on academic metrics.

A recent paper in Children’s Health Care by investigators at the Boston University Medical Center and School of Medicine considered the diet of children attending preschool. Looking at the dietary records of more than 300 children attending 30 childcare centers, the researchers found that the children’s diets before arrival at daycare was less healthy than while they were in daycare. “The hour after pickup appeared to be the least healthful” of any of the time periods surveyed. Of course, we will all conjure up images of what this chaotic post-daycare pickup may look like and cut the harried parents and grandparents some slack when it comes to nutritional choices. However, the bottom line is that for the group of children surveyed being in preschool or daycare protected them from a less healthy diet they were being provided outside of school hours.

Our recent experience with pandemic-related school closures provides more evidence that being in school was superior to any remote experience academically. School-age children and adolescents gained weight when school closures were the norm. Play patterns for children shifted from outdoor play to indoor play — often dominated by more sedentary video games. Both fatal and non-fatal gun-related injuries surged during the pandemic and, by far, the majority of these occur in the home and not at school.

Stepping back to look at this broader picture that includes diet, physical activity, and safety — not to mention the benefits of socialization — leads one to arrive at the unfortunate conclusion that for many children in this country, being at home is considerably less healthy than being in school. Of course there will be those who point to the belief that schools are petri dishes putting children at greater risk for respiratory infections. On the other hand, we must accept that schools haven’t proved to be a major factor in the spread of COVID that many had feared.

The authors of the study in Science are certainly correct in recommending a more thorough investigation into the academic benefits of preschool education. However, we must keep in mind that preschool offers an environment that can be a positive influence on young children.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Early education is right up there with motherhood and apple pie as unarguable positive concepts. How could exposing young children to a school-like atmosphere not be a benefit, particularly in communities dominated by socioeconomic challenges? While there are some questions about the value of playing Mozart to infants, early education in the traditional sense continues to be viewed as a key strategy for providing young children a preschool foundation on which a successful academic career can be built. Several oft-cited randomized controlled trials have fueled both private and public interest and funding.

However, a recent commentary published in Science suggests that all programs are “not unequivocally positive and much more research is needed.” “Worrisome results in Tennessee,” “Success in Boston,” and “Largely null results for Headstart” are just a few of the article’s section titles and convey a sense of the inconsistency the investigators found as they reviewed early education systems around the country.

While there may be some politicians who may attempt to use the results of this investigation as a reason to cancel public funding of underperforming early education programs, the authors avoid this baby-and-the-bathwater conclusion. Instead, they urge more rigorous research “to understand how effective programs can be designed and implemented.”

The kind of re-thinking and brainstorming these investigators suggest takes time. While we’re waiting for this process to gain traction, this might be a good time to consider some of the benefits of early education that we don’t usually consider when our focus is on academic metrics.

A recent paper in Children’s Health Care by investigators at the Boston University Medical Center and School of Medicine considered the diet of children attending preschool. Looking at the dietary records of more than 300 children attending 30 childcare centers, the researchers found that the children’s diets before arrival at daycare was less healthy than while they were in daycare. “The hour after pickup appeared to be the least healthful” of any of the time periods surveyed. Of course, we will all conjure up images of what this chaotic post-daycare pickup may look like and cut the harried parents and grandparents some slack when it comes to nutritional choices. However, the bottom line is that for the group of children surveyed being in preschool or daycare protected them from a less healthy diet they were being provided outside of school hours.

Our recent experience with pandemic-related school closures provides more evidence that being in school was superior to any remote experience academically. School-age children and adolescents gained weight when school closures were the norm. Play patterns for children shifted from outdoor play to indoor play — often dominated by more sedentary video games. Both fatal and non-fatal gun-related injuries surged during the pandemic and, by far, the majority of these occur in the home and not at school.

Stepping back to look at this broader picture that includes diet, physical activity, and safety — not to mention the benefits of socialization — leads one to arrive at the unfortunate conclusion that for many children in this country, being at home is considerably less healthy than being in school. Of course there will be those who point to the belief that schools are petri dishes putting children at greater risk for respiratory infections. On the other hand, we must accept that schools haven’t proved to be a major factor in the spread of COVID that many had feared.

The authors of the study in Science are certainly correct in recommending a more thorough investigation into the academic benefits of preschool education. However, we must keep in mind that preschool offers an environment that can be a positive influence on young children.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Children with concomitant atopic dermatitis (AD) and alopecia areata (AA) who were treated with dupilumab demonstrated significant hair regrowth over a mean of nearly 68 weeks, preliminary results from a small case series showed.

“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”

When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”

Courtesy Mount Sinai Health System

“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
 

Case Series of 20 Pediatric Patients

As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.

At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.

In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”

She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.

Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.

Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.

A version of this article appeared on Medscape.com.

Children with concomitant atopic dermatitis (AD) and alopecia areata (AA) who were treated with dupilumab demonstrated significant hair regrowth over a mean of nearly 68 weeks, preliminary results from a small case series showed.

“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”

When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”

Courtesy Mount Sinai Health System

“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
 

Case Series of 20 Pediatric Patients

As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.

At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.

In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”

She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.

Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.

Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.

A version of this article appeared on Medscape.com.

Children with concomitant atopic dermatitis (AD) and alopecia areata (AA) who were treated with dupilumab demonstrated significant hair regrowth over a mean of nearly 68 weeks, preliminary results from a small case series showed.

“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”

When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”

Courtesy Mount Sinai Health System

“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
 

Case Series of 20 Pediatric Patients

As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.

At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.

In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”

She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.

Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.

Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.

A version of this article appeared on Medscape.com.

Maternal in utero exposure to antibiotics was associated with an increased risk for infantile seborrheic dermatitis (SD) regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD.

The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.

SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”

“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”

She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.

Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.

A version of this article appeared on Medscape.com .

Maternal in utero exposure to antibiotics was associated with an increased risk for infantile seborrheic dermatitis (SD) regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD.

The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.

SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”

“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”

She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.

Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.

A version of this article appeared on Medscape.com .

Maternal in utero exposure to antibiotics was associated with an increased risk for infantile seborrheic dermatitis (SD) regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD.

The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.

SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”

“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”

She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.

Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.

A version of this article appeared on Medscape.com .

Teenagers who use cannabis have a dramatic increased risk for a psychotic disorder, compared with their counterparts who don’t use the drug, new research showed.

Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.

“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.

“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.

The study was published online in Psychological Medicine.


 

Increased Potency

“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.

The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.

To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.

They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.

Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.

The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.

Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
 

Perception of Harm Declining

When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).

“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.

The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.

The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.

Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.

Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.

This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

Teenagers who use cannabis have a dramatic increased risk for a psychotic disorder, compared with their counterparts who don’t use the drug, new research showed.

Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.

“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.

“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.

The study was published online in Psychological Medicine.


 

Increased Potency

“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.

The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.

To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.

They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.

Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.

The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.

Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
 

Perception of Harm Declining

When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).

“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.

The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.

The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.

Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.

Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.

This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

Teenagers who use cannabis have a dramatic increased risk for a psychotic disorder, compared with their counterparts who don’t use the drug, new research showed.

Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.

“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.

“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.

The study was published online in Psychological Medicine.


 

Increased Potency

“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.

The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.

To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.

They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.

Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.

The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.

Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
 

Perception of Harm Declining

When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).

“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.

The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.

The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.

Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.

Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.

This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved Onyda XR (clonidine hydrochloride) for the treatment of attention-deficit/hyperactivity disorder (ADHD), drug manufacturer Tris Pharma announced in a statement.

The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.

“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release. 

“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.

The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.

Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine. 

The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.

Onyda XR should be available in pharmacies in the second half of 2024.
 

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved Onyda XR (clonidine hydrochloride) for the treatment of attention-deficit/hyperactivity disorder (ADHD), drug manufacturer Tris Pharma announced in a statement.

The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.

“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release. 

“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.

The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.

Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine. 

The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.

Onyda XR should be available in pharmacies in the second half of 2024.
 

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved Onyda XR (clonidine hydrochloride) for the treatment of attention-deficit/hyperactivity disorder (ADHD), drug manufacturer Tris Pharma announced in a statement.

The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.

“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release. 

“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.

The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.

Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine. 

The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.

Onyda XR should be available in pharmacies in the second half of 2024.
 

A version of this article appeared on Medscape.com.

AIRWAYS DISORDERS NETWORK

Pediatric Chest Medicine Section

Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.¹ Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.^2,3,4Using a case-control design, researchers analyzed data from 2,962 children enrolled in the Boston Birth Cohort (BBC): 235 children with severe LRTIs and 2,333 controls. They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.

CHEST

Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.

Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.

– Agnes S. Montgomery, MD

Fellow-in-Training


References

1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.

2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.

3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.

4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.
 

AIRWAYS DISORDERS NETWORK

Pediatric Chest Medicine Section

Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.¹ Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.^2,3,4Using a case-control design, researchers analyzed data from 2,962 children enrolled in the Boston Birth Cohort (BBC): 235 children with severe LRTIs and 2,333 controls. They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.

CHEST

Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.

Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.

– Agnes S. Montgomery, MD

Fellow-in-Training


References

1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.

2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.

3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.

4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.
 

AIRWAYS DISORDERS NETWORK

Pediatric Chest Medicine Section

Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.¹ Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.^2,3,4Using a case-control design, researchers analyzed data from 2,962 children enrolled in the Boston Birth Cohort (BBC): 235 children with severe LRTIs and 2,333 controls. They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.

CHEST

Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.

Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.

– Agnes S. Montgomery, MD

Fellow-in-Training


References

1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.

2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.

3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.

4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.