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A Gonadotropin-Responsive Adrenocortical Adenoma
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1974
Year
FertilityReproductive HealthGynecologyFemale Reproductive FunctionOvarian AgingOvarian CancerReproductive EndocrinologyAdrenal GlandFemale InfertilityReproductive MedicinePeripheral Plasma TestosteronePlasma TPublic HealthReproductive HormoneInfertilityAndrologyGonadotropin-responsive Adrenocortical AdenomaAdrenal DiseaseEndocrinologyActh InfusionOvarian HormoneUrologyAdrenal HealthMedicineEndocrine ResearchWomen's HealthGonadotropin Biology
A 49-yr-old virilized woman had a peripheral plasma testosterone (T) concentration of 783–911 ng/100 ml with a normal plasma concentration of androstenedione (A) and normal urinary 17-ketosteroids (17-KS). Plasma LH was below normal and FSH was low normal. Plasma T was not changed by dexamethasone 2 mg/day and the 17-KS were not normally suppressible. The administration of 5,000 units of human chorionic gonadotropin (hCG) increased plasma T to 3,744 ng/100 ml and also increased A and the 17-KS. Based on these results an ovarian source of T was suspected and bilateral oophorectomy was performed. Bilateral ovarian cortical stromal hyperplasia was found. Removal of both ovaries did not correct the hypertestosteronemia. Because an adrenal lesion was suspected, an 8-hr ACTH infusion test was done. Plasma T was decreased 42% and LH 31% at the sixth hour of the ACTH infusion. Plasma T was again increased by hCG to 2,379 ng/100 ml after the ovaries were removed. Both adrenals were explored and a 4 cm × 3 cm × 2 cm brown adrenocortical adenoma weighing 21 g was removed from the right adrenal. Plasma T was 17 ng/100 ml after the removal of the tumor and was now not increased by hCG. This gonadotropin-responsive adrenal adenoma further emphasizes that the results of hormonal manipulative procedures may be misleading in determining the source of excess androgen production.