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Developmental Endocrinology Branch, National Institute of Child Health, National Institutes of Health Bethesda, Maryland 20892
Human Development, National Institutes of Health Bethesda, Maryland 20892
The Dermatology Branch, National Cancer Institute, National Institutes of Health Bethesda, Maryland 20892
Department of Pediatrics, Georgetown University Childrens Medical Center Washington, D.C. 20007
Address requests for reprints to: Louisa Laue, M.D., Department of Pediatrics, Georgetown University Childrens Medical Center, 3800 Reservoir Road NW, Washington, D.C. 20007.
Basal and ACTH-stimulated plasma levels of cortisol,
4-androstenedione, and dehydroepiandrosterone (DHEA) were measured in a group of 11 female patients with postadolescent acne resistant to or relapsing after conventional therapy and in a group of 10 normal women without acne or hirsutism. Each patient received, in a blinded random fashion, a series of 5 1-h ACTH tests. For each test a different dose of ACTH-(l–24) was administered, ranging from 0–1 µg/kg, given as an iv bolus. Blood samples were collected 0, 10, 30, and 60 min after ACTH bolus injection. Patients with acne had slightly higher concentrations of basal cortisol,
4-androstenedione, and DHEA than normal controls (P <0.05). After ACTH-(l–24) stimulation, the same patients had greater peak and time-integrated DHEA concentrations (P <0.03). The ED50 values of the cortisol dose-response curves were similar in patients and normal women (P <0.05), suggesting that there are no differences in the sensitivity of the adrenal cortex to ACTH between the acne patients and the controls studied. The ratio of DHEA to cortisol response was significantly elevated in women with acne compared to that in control women, suggesting some preponderance of the
5 pathway of steroidogenesis in acne (P <0.05). These findings of basal and ACTH-stimulated hypersecretion of
5-androgens in patients with postadolescent acne are consistent with an increased volume of androgen-secreting tissue, rather than hypersensitivity of the adrenal zona reticularis to ACTH.
Received June 6, 1990.
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