Abstract
important etiologic cause. In this work, 12 patients were studied under basal conditions and during tests of pituitary and adrenal function with the objective of making a differential diagnosis. The 12 patients were divided by age into two subgroups of six patients each. The prepubertal group had tumors, with the exception of one child with bilateral hyperplasia: one basophil adenoma, one adenocarcinoma, two ectopic ACTH-producing tumors (thymoma and embryoma), and one adrenal adenoma. The pubertal group consisted of five with bilateral hyperplasia and one with an adrenal adenoma. The tumors did not respond to stimulation or suppression tests, except for the adrenal adenoma which showed a hyperresponsiver}ess to the infusion of ACTH. The results of attempts at inhibition of the bilateral hyperplasia were as follows: four inhibited with a small dose of dexamethasone, one partially inhibited with a large dose, and no inhibition in one patient. The last patient also did not respond to intravenous ACTH stimulus, presenting with a very high secretion of cortisol (156 mg/day/m2). This marked adrenal hyperactivity explains its tumor-like behavior. TREATMENT. Two patients with bilateral hyperplasia received conventional 4,000 r pituitary radiotherapy with no result; five patients had bilateral adrenalectomy with no deaths. The three 9 patients with adrenalectomy who had had no previous hypophyseal radiotherapy developed a syndrome of hyperpigmentation, one with enlargement of the sella turcica and diplopia. All patients received rotating 5,000 r pituitary cobalt therapy. The results suggest that optimum therapy would be bilateral adrenalectomy plus radiotherapy.
Published Version
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