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Adrenal Androgen Hyperresponsiveness to Adrenocorticotropin in Women with Acne and/or Hirsutism: Adrenal Enzyme Defects and Exaggerated Adrenarche^*

Departments of Dermatology and Pediatrics, University of Cincinnati College of Medicine and Children's Hospital Medical Center Cincinnati, Ohio 45267
Departments of Pediatrics and Medicine, University of Chicago Chicago, Illinois 60637
Department of Dermatology, Yale University School of Medicine New Haven, Connecticut 06510

Address requests for reprints to: Dr. Anne W. Lucky, Department of Dermatology, University of Cincinnati Medical Center, Mail Location 592, 231 Bethesda Avenue, Cincinnati, Ohio 45267.

To determine the adrenal contribution to elevated plasma androgens in 31 young hyperandrogenemic women with acne and/or hirsutism, we compared their responses to ACTH with those of 14 normal women. Each subject was given a low dose (10 µg/m²) of synthetic ACTH-(l–24) (Cortrosyn) after administration of 1.5 mg dexamethasone the night before the test. Thirty and 60 min responses of plasma 17-hydroxy-pregnenolone (17-Preg), 17-hydroxyprogesterone, (17-prog), dehydroepiandrosterone (DHEA), androstenedione, 11-deoxycortisol, and cortisol were measured.

Eighteen (58%) patients had increased responses of at least one 17-ketosteroid or adrenal androgen precursor. All patients had cortisol responses within the range of those of the 14 normal subjects. Nine patients (29%) had evidence of steroid biosynthetic enzyme deficiencies, either mild congenital adrenal hyperplasia or the heterozygote state; after ACTH, 4 of these patients had elevated 17-prog in the range of values in heterozygote carriers of 21-hydroxylase deficiency, 2 had elevated levels of 11-deoxycortisol compatible with llβ-hydroxylase deficiency, and 3 had elevated levels of 17-Preg and DHEA, suggestive of 3β-hydroxysteroid dehydrogenase deficiency. Another 9 subjects (29%) had 17-ketosteroid (DHEA and/or androstenedione) hyperresponsivenesshyperresponsiveness to ACTH with associated elevated 17-Preg responses. As a group, their patterns suggested relatively deficient 3β-hydroxysteroid dehydrogenase and relatively hyperactive C_17–20 lyase without impairment of cortisol secretion. This pattern resembles exaggerated adrenarche, and we postulate that these 9 patients have hyperplasia of the zona reticularis.

Neither basal levels of plasma androgens (free testosterone and DHEA sulfate) nor menstrual history predicted which patients would have abnormal ACTH responses. Although 5 of 11 (45%) patients with acne alone had abnormal responses to ACTH, 10 of 14 patients with acne and hirsutism (71%) had abnormal responses to ACTH.

We conclude that an adrenal contribution is found in about half of hyperandrogenemic women with acne and/or hirsutism. This adrenal androgen hyperresponsiveness is heterogeneous. Some patients may have mild forms of congenital adrenal hyperplasia. However, functional androgenic hyperresponsiveness to ACTH, which resembles an exaggeration of adrenarche, is the most common abnormality found. Such findings may provide an explanation for the clinical observation of exacerbations of acne with stress.

^* Presented in part at the 53rd annual meeting of the Societyfor Pediatric Research, San Francisco, CA, May 2–4, 1984

Received May 31, 1985.

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