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Anxiety and Atopic Disease: Comorbidity in a Youth Mental Health Setting

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Abstract

Anxiety frequently co-occurs with atopic diseases (e.g., allergies) in community samples, although data are limited to community and pediatric medical samples. Little work has examined atopy rates among mental health treatment seeking youth or whether youth with comorbid anxiety and atopy present similarly to non-comorbid youth. Using initial intake data from a University-based specialty youth clinic for anxiety and depressive disorders (n = 189), rates of atopic comorbidity were benchmarked against lifetime prevalence estimates in epidemiological samples. Anxiety severity and parental stress were compared between youth with and without atopy. Results indicated high rates of atopy in the clinical sample (51.3 %) relative to population atopy estimates (34.5 %). Anxious youth with atopy exhibited more overall and generalized anxiety symptoms relative to non-atopic youth (ps < .05); parental stress was comparable between atopic and non-atopic anxious youth. This suggests potentially heightened clinical severity for youth with co-occurring anxiety and atopy.

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Notes

  1. Briefly, in response to an antigen (any molecule that activates an immune response), the immune system produces antibodies called immunoglobulins, intended to neutralize pathogens. Helper T cells work to regulate the immune response. Popular immunological theory points toward two differing immunologic responses that are in constant balance to control the other: T-helper 1 (Th1) cells, which mediate a cellular immunity, are often activated to fight intracellular pathogens such as viruses, while T-helper 2 (Th2) cells upregulate antibody production to fight extracellular organisms. In atopic disease, the immune system activates to fight what are typically innocuous antigens (“allergens”) and releases immunoglobulin E (IgE). Exposure to an allergen causes a shift toward a predominance of Th2-mediated immune responses, leading to a release of inflammatory cytokines and histamines that produce IgE, and ultimately, the allergic response. Lasting exposure to an antigen can lead to increased Th2 shift leading to chronic allergic inflammation [22] (see [23] for a review of the immunological response in atopic disease).

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Correspondence to Emily M. Becker-Haimes.

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Becker-Haimes, E.M., Diaz, K.I., Haimes, B.A. et al. Anxiety and Atopic Disease: Comorbidity in a Youth Mental Health Setting. Child Psychiatry Hum Dev 48, 528–536 (2017). https://doi.org/10.1007/s10578-016-0678-8

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