Lopez-Guzman A, Salvador J, Frutos R, Diez JJ, Iglesias P, Sastre J et al
Hypergastrinaemia in Cushing's syndrome: pituitary origin or glucocorticoid-induced?

Clin Endocrinol (Oxford), 44(3): 335-339, 1996
ISSN: 0300-0664 Clinical Endocrinology (Oxford) (PubMed)

Abstract
OBJECTIVES: Several reports have shown an increase in serum gastrin levels in patients with Cushing's syndrome (CS). However, the actual origin of this hypergastrinaemia is not known. Two hypotheses have been proposed: concomitant ACTH and gastrin secretion by corticotrophic pituitary adenomas or hypergastrinaemia induced by hypercortisolism. DESIGN AND PATIENTS: We performed simultaneous, bilateral inferior petrosal sinus (IPS) sampling in nine patients with Cushing's disease (CD), proven by histological studies. In all of them, blood samples were taken from both IPS and a peripheral vein to measure plasma ACTH and serum gastrin. In addition, we measured peripheral serum gastrin levels after an overnight fast in 10 patients with CS (seven with pituitary tumours and three with adrenal tumours) before and after surgical treatment. RESULTS: Petrosal-peripheral and interpetrosal gradients of ACTH were higher than 2.0 and 1.4, respectively, confirming the pituitary origin of ACTH. Mean serum gastrin levels were 149.1 +/- 53.6 ng/l in peripheral vein, 183.4 +/- 71.7 ng/l in dominant IPS and 181.4 +/- 68.9 ng/l in non-dominant IPS. No significant differences in gastrin concentrations in these locations were found. Mean preoperative gastrin level in patients with CD was 194.6 +/- 47.9 ng/l, whereas in patients with adrenal tumours it was 247.3 +/- 125.9 ng/l. After surgical treatment, the 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 that hypergastrinaemia is a common finding in patients with Cushing's syndrome. The lack of significant petrosal-peripheral gradient in individuals with Cushing's disease and the reduction in gastrin level following adrenal tumour resection argues against the hypothesis of a predominantly pituitary source of gastrin, suggesting a glucocorticoid related mechanism as an explanation for the hypergastrinaemia.