Autoantibodies to cell surface antigens of human somatotropinoma (ASAS), human prolactinoma (ASAP) and rat adenohypophysis (ASARA) were assayed in the serum of patients with pituitary diseases associated with GH deficiency (GHD), such as pituitary dwarfism and primary empty sella syndrome (ESS), and in the serum of patients with hyperprolactinaemia of different etiologies: idiopathic hyperprolactinaemia, prolactinoma and ESS. The investigation was carried out with a cellular variant of an ELISA. Among children with GHD, the highest percentage of antibody-positive patients was found in the group with idiopathic isolated GHD (89% of ASAS + patients and 30% of ASARA + patients vs 33·3% and 0% respectively in the group with idiopathic combined pituitary hormone deficiency, and 33·3% and 9% in patients with pituitary hypoplasia associated with isolated GHD or combined pituitary hormone deficiency). Among hyperprolactinaemic patients, the highest ASAP and ASARA frequency was observed in patients with idiopathic hyperprolactinaemia (67·7% and 41·9% respectively) where it was twice as high as in the group of patients with prolactinoma.

OBJECTIVE: The purpose of this study was to evaluate the direct action of desmopressin (agonist of vasopressin) on the hypophysis and the three zones of the adrenal cortex in patients with different forms of hypercortisolism. DESIGN: Forty-three patients with hypercortisolism-21 with Cushing's disease (14 females, 7 males), 11 with extrapituitary, ectopic tumours (5 females, 6 males), and 11 with ACTH-independent Cushing's syndrome (6 females, 5 males)-were evaluated. The response of the pituitary and adrenal glands was assessed by measuring plasma levels of Adrenocorticotropic Hormone (ACTH), cortisol, aldosterone, and dehydroepiandrosterone sulfate (DHEAS) at baseline and at 15, 30, 60, 90, and 120 min after the administration of desmopressin. RESULTS: We observed two main modes of secretory response: (1) elevation of the ACTH level followed by a rise of one, two or all three adrenal steroids, and (2) ACTH-independent elevation of adrenal steroids in various combinations. CONCLUSION: In a number of patients with hypercortisolism, the adrenal cortex responded to desmopressin administration by enhanced synthesis and secretion of glucocorticoids (cortisol), mineralocorticoids (aldosterone), and adrenal androgens (DHEAS) without a concomitant rise in ACTH. These findings suggest the presence of "ectopic" vasopressin receptors in the human adrenal cortex.

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