naloxone and Adrenal-Hyperplasia--Congenital

The effect of a high (5.4 mg/h) and a low (0.8 mg/h) dose of naloxone (i.v. over a period of 90 min) on ACTH secretion was compared with placebo in patients with Addison's disease, congenital adrenal hyperplasia, Cushing's disease or Nelson's syndrome. In seven patients with primary adrenal insufficiency the high dose of naloxone provoked a significant increase of plasma ACTH concentrations (P less than 0.02) whereas the low dose of naloxone failed to influence ACTH secretion. In six patients with ACTH dependent Cushing's disease or Nelson's syndrome both doses failed to alter plasma ACTH levels. These results support the concept of inhibitory delta- or kappa-opiate receptors in the regulation of ACTH secretion. In patients with Cushing's disease or Nelson's syndrome ACTH secretion is insensitive to naloxone, presumably because of an autonomous pituitary adenoma or hypothalamic derangement.

Topics: Adrenal Gland Diseases; Adrenal Hyperplasia, Congenital; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Drug Administration Schedule; Female; Humans; Male; Middle Aged; Naloxone; Nelson Syndrome

A woman with a schizophreniform syndrome, drug-induced dyskinetic movements, and partial adrenocortical 21-hydroxylase deficiency was given short-term treatment with naloxone, which ameliorated the psychiatric symptoms and eliminated the dyskinetic movements.

Topics: Adrenal Hyperplasia, Congenital; Adult; Dyskinesia, Drug-Induced; Female; Humans; Naloxone; Psychiatric Status Rating Scales; Psychotic Disorders; Steroid 21-Hydroxylase; Steroid Hydroxylases