Acanthosis Nigricans and Obesity

Historical findings, physical characteristics, and results of laboratory evaluation of adrenocortical function were studied in 14 massively obese patients with benign acanthosis nigricans and a comparably obese group of 14 patients without the skin lesion. The baseline level of adrenocortical function was high in both groups as compared with normal controls, and there was a tendency to hyperresponsiveness to corticotropin (adrenocorticotropic hormone). Urinary 17-ketogenic steroids were suppressed poorly by the administration of dexamethasone, regardless of whether the patient did or did not have acanthosis. In striking contrast, there was normal suppression of 17-hydroxycorticosteroids (Porter-Silber chromogens) in response to dexamethasone in every patient. Except for four female patients with acanthosis, hirsutism, menstrual irregularities, and loss of the diurnal variation in plasma levels of 11-hydroxycorticosteroids, there was no abnormality of pituitary-adrenal function in massively obese patients with or without acanthosis nigricans.