CALCIUM REVERSES OCTREOTIDE INHIBITION OF INSULIN AND GLUCAGON-LEVELSIN PATIENTS WITH INSULINOMA AND GLUCAGONOMA

Excessive secretion of peptides causes the clinical syndromes associat ed with functional gastro-intestinal tumours. The somatostatin analogu e octreotide acetate inhibits peptide release from a variety of tumour s. This study investigated the interactions of calcium and somatostati n analogues on peptide release in two patients, one with a glucagonoma (patient A) and one with an insulinoma (patient B). Peptide responses were evaluated before (fasting levels) and after pravocative tests (a 4-hour calcium infusion, an intravenous tolbutamide infusion, a secre tin bolus and a standard test meal) in the absence and presence of oct reotide acetate treatment (100 mu g subcutaneously every 8 h). Patient s A and B had elevated fasting plasma levels of glucagon and insulin, respectively, which were reduced by octreotide therapy by 73 and 50%, respectively. The peak provoked levels and calculated values for pepti de synthesis were lower after octreotide therapy. In both patients. to lbutamide provoked most peptide release, and calcium infusion was the least susceptible to the effects of octreotide therapy. Calcium appear s to inhibit octreotide suppression of glucagon and insulin secretion in patients with glucagonoma and insulinoma, respectively. Calcium may stimulate peptide release From endocrine tumours by suppressing the i nhibitory effects of endogenous somatostatin. Normalisation of serum c alcium, either surgically or pharmacologically, may improve the effect iveness of somatostatin analogue therapy.