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Low basal serum cortisol in patients with severe atopic dermatitis: potent topical corticosteroids wrongfully accused
Author(s) -
Haeck I.M.,
Timmerde Mik L.,
Lentjes E.G.W.M.,
Buskens E.,
Hijnen D.J.,
Guikers C.,
BruijnzeelKoomen C.A.F.M.,
De BruinWeller M.S.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2007.07753.x
Subject(s) - medicine , dermatology , family medicine
Summary Background Topical corticosteroids are used extensively to treat inflammatory skin disorders including atopic dermatitis (AD). Several studies have described temporary reversible suppression of hypothalamic–pituitary–adrenal function. However, sound evidence of permanent disturbance of adrenal gland function is lacking. Objectives To relate basal cortisol levels to prior use of topical corticosteroids and disease activity in patients with moderate to severe AD and to investigate the effect on basal serum cortisol levels of topical corticosteroid treatment during hospitalization. Methods Two groups of patients with AD were evaluated: 25 inpatients with severe AD who required hospitalization (group 1) and 28 outpatients with moderate to severe AD (group 2). In group 1, morning basal serum cortisol levels were measured twice, at admission and at discharge; in group 2, morning basal serum cortisol levels were measured once. Use of topical corticosteroids in the 3 months prior to the cortisol measurement was recorded and disease activity was monitored using the Six Area, Six Sign Atopic Dermatitis (SASSAD) score and serum thymus and activation‐regulated chemokine (TARC) levels. Results On admission, basal cortisol levels in group 1 were significantly ( P < 0·001) decreased in 80% of the patients. In group 2, the basal cortisol levels were normal in all but three patients. Comparing the two groups, group 1 on admission had a significantly lower cortisol level than that of group 2 ( P < 0·001). Disease activity in group 1 on admission was significantly higher than that of group 2 ( P < 0·001). There was no difference in use of topical corticosteroids in the 3 months before cortisol measurement. At discharge in group 1 there was a significant increase ( P < 0·0001) of basal cortisol levels and a significant ( P < 0·001) decrease in disease activity reflected by the decrease in serum TARC levels and SASSAD score. Conclusions Disease activity, rather than the use of topical corticosteroids, is responsible for the low basal cortisol values in patients with severe AD.