HYPERGASTRINEMIA IN CUSHINGS-SYNDROME - PITUITARY ORIGIN OR GLUCOCORTICOID-INDUCED

OBJECTIVES Several reports have shown an increase in serum gastrin lev els in patients with Gushing's syndrome (CS). However, the actual orig in of this hypergastrinaemia is not known. Two hypotheses have been pr oposed: concomitant ACTH and gastrin secretion by corticotrophic pitui tary adenomas or hypergastrinaemia induced by hypercortisolism. DESIGN AND PATIENTS We performed simultaneous, bilateral inferior petrosal s inus (IFS) sampling in nine patients with Gushing's disease (GO), prov en by histological studies. In all of them, blood samples were taken f rom both IFS and a peripheral vein to measure plasma ACTH and serum ga strin. In addition, we measured peripheral serum gastrin levels after an overnight fast in 10 patients with GS (seven with pituitary tumours and three with adrenal tumours) before and after surgical treatment. RESULTS Petrosal-peripheral and interpetrosal gradients of ACTH were h igher than 2.0 and 1.4, respectively, confirming the pituitary origin of AGTH. Mean serum gastrin levels were 149.1 +/- 53.6 ng/l in periphe ral vein, 183.4 +/- 71.7 ng/l in dominant IFS and 181.4 +/- 68.9 ng/l in non-dominant IFS. No significant differences in gastrin concentrati ons in these locations were found. Mean preoperative gastrin level in patients with GD was 194.6 +/- 47.9 ng/l, whereas in patients with adr enal tumours it was 247.3 +/- 125.9 ng/l. After surgical treatment, th e gastrin levels decreased to 62.1 +/- 13.2 ng/l (P < 0.05) and 90.3 /- 50.3 ng/l (NS), respectively. CONCLUSIONS These results suggest tha t hypergastrinaemia is a common finding in patients with Gushing's syn drome. The lack of significant petrosal-peripheral gradient in individ uals with Gushing's disease and the reduction in gastrin level followi ng adrenal tumour resection argues against the hypothesis of a predomi nantly pituitary source of gastrin, suggesting a glucocorticoid relate d mechanism as an explanation for the hypergastrinaemia.