Hypothalamic-pituitary-adrenal (HPA) response to topical glucocorticoids(GC) in atopic dermatitis (AD) and GC sensitivity in patients with refractory disease was assessed.

27 patients (0.7-18.7 years) with moderate or severe AD had a low dose adrenocorticotrophic hormone (ACTH) test (500ng/1.73m2) to assess their adrenal function. 14 healthy subjects (3.8-17.3 years) served as controls. All patients had used topical GC over 0.5-17.7 years. Group I (8 patients) used mildly potent, Group II (15 patients) moderately potent and Group III (4 patients) potent or very potent (British National Formulary classification) topical GC. None had received inhaled or systemic GC in the preceding 6 months. A group of 8 boys (2.6-16.5 years) with severe AD, also had daytime plasma cortisol profile and measurement of plasma ACTH and its precursors in addition to the ACTH test. All had received mildly and moderately potent GC from infancy. 5 had received other GC preparations (3 used potent topical GC, 1 had repeated courses of oral GC treatment and 1 had continuous oral GC treatment).

Results Cortisol parameters for Groups I and II did not differ from controls but Group III had lower peak (275 vs 495 nmol/l;p<0.03) and increment cortisol levels (105 vs 285nmol/l;p<0.005). The patient on oral GC had severe HPA suppression (all cortisol levels <20 nmol/l, ACTH <5ng/l and ACTH precursors 7pmol/l). Only 2 of the remaining 7 patients had 08:00 hrs cortisol above 300nmol/l. These 7 patients had lower baseline (100 nmol/l; p<0.01), peak(340 nmol/l; p<0.01) and area-under-the-curve cortisol (13600 nmol.min/l; p<0.01) responses to the ACTH test than did the controls (275nmol/l, 565nmol/l and 26800nmol.min/l respectively) but the increment from baseline to peak cortisol did not differ. ACTH levels were inappropriately low for the cortisol concentrations. The ratio of ACTH precursor:ACTH at 08:00 hrs was 2.8 compared to 5.3 in normal adults.

Conclusion Use of potent (but not mild or moderately potent) topical GC alone caused adrenal suppression, indicating systemic effects with their use. The lack of clinical response with evidence of HPA suppression in the severely affected patients suggests local skin resistance but preserved systemic responsiveness to GC.