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Salivary Cortisol Response to Stress in Young Children with Atopic Dermatitis
Author(s) -
Kojima Reiji,
Matsuda Akio,
Nomura Ichiro,
Matsubara Osamu,
oyama Shigeaki,
Ohya Yukihiro,
Saito Hirohisa,
Matsumoto Kenji
Publication year - 2012
Publication title -
pediatric dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.542
H-Index - 73
eISSN - 1525-1470
pISSN - 0736-8046
DOI - 10.1111/j.1525-1470.2012.01770.x
Subject(s) - medicine , atopic dermatitis , corticosteroid , young adult , exacerbation , hydrocortisone , eczema area and severity index , provocation test , hypothalamic–pituitary–adrenal axis , endocrinology , dermatology , hormone , alternative medicine , pathology
Poor responsiveness of the hypothalamic–pituitary–adrenal (HPA) axis under stress may be one explanation for stress‐induced exacerbation of atopic dermatitis (AD) symptoms. In previous studies, children and adults with AD showed attenuated salivary cortisol responses to psychosocial stress, suggesting hyporesponsiveness of the HPA axis, but few studies have been conducted in young children, who are vulnerable to systemic side effects of topical corticosteroid (TCS) therapy. We evaluated whether salivary cortisol responses to the stress of venipuncture in young children with AD were related to the severity of AD or performance of TCS therapy. We studied 38 young children with AD (median age 16.5 mos, range 3–66 mos) being treated at our outpatient unit. Patients were divided into three groups according to the scoring of atopic dermatitis index: mild ( n = 12), moderate ( n = 14), and severe ( n = 12). To evaluate the responsiveness of the HPA axis to stress, salivary cortisol was determined before and after venipuncture. Salivary cortisol responsiveness to stress correlated negatively with severity of AD (p = 0.048) but not with previous use of TCS (p = 0.43) in young children with AD. Our findings suggest that the disease activity of AD, rather than TCS use, is responsible for HPA axis dysfunction in children with AD.