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THE development of gynecomastia is an uncommon result of excessive steroid hormone production by adrenocortical tumors. The present report concerns the thirty-fourth occurrence of this phenomenon recorded in the world literature (1–16). The findings of relative adrenocortical insufficiency, increased excretion of estrogen-like materials in the urine and the successful isolation of steroids from the tumor (17) are of special interest in this patient. A 28-year-old radio announcer noted the onset of intermittently tender nipples in March 1953 and of bilateral breast enlargement in September 1953. There was progressive increase in size during the next twelve months. The patient was sufficiently embarrassed by this cosmetic defect to request admission to the Salt Lake Veterans Administration Hospital in March 1955 for evaluation and treatment. He had noted a veiy gradual decline in libido and potency during the two years prior to admission. There were no other symptoms and no fluctuations in weight. The past history was negative. There was no history of gynecomastia during puberty, or of jaundice, liver disease, alcoholism or exposure to hepatoxins or estrogens.
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Wallach et al. (1957) studied this question.
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