Atopic Sensitization and Inflammation in Depressed versus Non-depressed Asthmatic Children
Monday, March 5, 2018
South Hall A2 (Convention Center)
Vivian T. Aranez, MD, Heather K. Lehman, MD FAAAAI, Bruce Miller, MD, Beatrice L Wood, PhD, ABPP, Hannah Elsinghorst, Kristel McGuire, Rachel Rainey, Brian Wrotniak

RATIONALE: Asthma is the most prevalent chronic disease of childhood. While most child asthmatics are atopic, a small subset are non-allergic. Depression is seen more frequently in asthmatics compared to the general population and is associated with unfavorable asthma outcomes, including medication nonadherence, increased emergency room visits, hospitalizations, and even asthma-related death. Comorbid depression may be associated with decreased response of asthma to bronchodilators or corticosteroids. We assessed atopic sensitization and inflammation in depressed vs non-depressed asthmatics to investigate whether children with depression have evidence of distinct underlying asthma pathology.

METHODS: Eighteen children with asthma ages 7 to 17 years were evaluated for depressive symptoms using the Children’s Depression Inventory (CDI). Markers of inflammation including exhaled nitric oxide (FeNO) and peripheral blood eosinophils (PBE) were compared in depressed vs non-depressed groups. Atopic status and allergic sensitization were evaluated by total serum IgE (TSE) and skin prick testing (SPT) to environmental allergens.

RESULTS: There was no significant association between depressive symptom score and in the degree of inflammation measured by FeNO or PBE. TSE and number of SPT was not significantly different in depressed versus non-depressed child asthmatics in our study population.

CONCLUSIONS: Evidence exists that depression worsens asthma outcomes and predicts non-responsive to typical asthma therapies. Children with high CDI scores, suggestive of depression, have similar markers of inflammation and atopic sensitization as children without evidence of depression on the CDI. However, larger sample sizes will be needed to truly differentiate whether the inflammation in depressed asthmatics is distinct from that in non-depressed asthmatics.