Secretin-Stimulated Serum Gastrin Levels in Hyperparathyroid Patients from Families with Multiple Endocrine Adenomatosis Type I

Abstract

Twenty-three patients with hyperparathyroidism from six families with the multiple endocrine adenomatosis (MEA) I-syndrome were tested by secretin provocation. In nine cases this led to increases in serum gastrin ranging from 298 to 13 300 pg/ml, whereas the maximum rise in gastrin in the other 14 patients was 32 pg/ml. In all nine patients with marked gastrin responses to secretin, the Zollinger-Ellison syndrome was diagnosed by gastric acid hypersecretion and large increases in gastrin after calcium administration. Six of these nine patients had, at most, minor postprandial rises in gastin and two had demonstrable tumors. In 34 normal subjects, 23 nonaffected members of families with MEA I-syndrome, and 42 patients with various diseases the maximum gastrin response to secretin was 21 pg/ml. We conclude that secretin provocation is helpful in the diagnosis of the Zollinger-Ellison syndrome, especially when basal serum gastrin levels are only slightly elevated.

Comparative study of the value of the calcium, secretin, and meal stimulated increase in serum gastrin to the diagnosis of the Zollinger-Ellison syndrome.

“…The reason for the marked increase in serum gastrin after a test meal in some ZE patients is not clear. Several mechanisms may be put forward to account for the pronounced meal stimulated increase in serum gastrin in these patients, as direct interaction between food and a tumour originated in the duodenal wall, the release of a gastrin stimulating agent-for example, secretin-from the small intestine and co-existing antral G-cell hyperplasia and pancreatic tumours (Polak et al, 1972 (Korman et al, 1973b;Lamers et al, 1977), excluded gastric antrum (Korman et al, 1972b), non-tumorous hypergastrinaemic hyperchlorhydria (Straus and Yalow, 1975), and postprandial conditions (Thompson et al, 1972b). In patients with achlorhydria and excluded gastric antrum, marked increases in serum gastrin after calcium infusion have been found (Straus and Yalow, 1975;Lamers and van Tongeren 1976).…”

“…However, the exact reason for the negative stimulation tests in ZE patients has so far been obscure. Moreover, the frequency in the literature of negative stimulation tests in ZE patients is difficult to evaluate, because different amounts of provocative agents of different potency over different periods of time have been administered (Lamers et al, 1977).…”

“…Both in acute hypercalcaemia after calcium infusion (see Fig. 4) and in chronic hypercalcaemia, as in coexisting hyperparathyroidism and ZE syndrome, secretin is effective in increasing serum gastrin levels (Lamers et al, 1977). How far calcium or secretin administration stimulates not only the release but also the synthesis of gastrin by the tumour has still to be investigated.…”

Pancreatic endocrine tumors

“…This technique involves the fusion of octreotide to a beta-emitting radionuclide resulting in 90 Yttrium-DOTA-labeled or 111 Indium-DTPA, D-Phe1. The side effects of this therapy are similar to those for more traditional radiation therapies including nausea, vomiting, and renal toxicity.…”

“…Many other tissues unrelated to PETs, such as lung granulomas, postoperative sites, accessory spleens, and thyroid tissue, can express these receptors [73,74]. A somatostatin analogue, 111 In-DTPA-D-Phe1 octreotide is administered and binds to all tissues expressing a significant concentration of somatostatin subtype 2 receptors. The abundance of these receptors on certain PETs makes this a good test for identifying gastrinomas, glucagonomas, nonfunctioning tumors, and pancreatic carcinoids [75][76][77].…”