Higher Gastrin Concentrations Research Articles

Family studies in patients with primary parathyroid hyperplasia

The relatives of 25 index patients with primary parathyroid hyperplasia were tested for hypercalcemia. At least 13 of these patients had one or more first degree relatives with hypercalcemia. Two familial syndromes each with autosomal dominant transmission were recognized. Two index patients were part of large kindreds categorized as having familial hypocalciuric hypercalcemia (FHH). Manifestations of multiple endocrine neoplasia type I were present in the kindreds of at least four other index patients (FMEN I). In seven other kindreds there were too few affected members to allow definitive classification. Differences between manifestations of FHH and FMEN I were described. Among offspring of affected persons in kindreds with FHH, as distinct from FMEN I, the prevalence of hypercalcemia approached the theoretic maximum of 50 per cent during the first two decades. In FHH, nephrolithiasis and peptic disease were unusual; moderate hypercalcemia occurred without hypercalciuria; and subtotal parathyroidectomy did not abolish hypercalcemia. Concentrations of peptide hormones other than parathyroid hormone (PTH) were normal in those with FHH; in FMEN I high concentrations of glucagon in plasma were found in five of six patients tested, and high concentrations of gastrin were found in three of 12 patients. Hypergastrinemia generally accompanied obvious peptic disease. Distinction of the two conditions is important since patients with FHH may not benefit from subtotal parathyroidectomy, but they generally have a better clinical prognosis than do patients with FMEN I.

Effects of somatostatin and human gastrin I on the lower esophageal sphincter in man.

The influence of gastrin and somatostatin on the lower esophageal sphincter was investigated in a total of ten metabolically healthy volunteers and one patient with Zollinger-Ellison syndrome. It could be shown that only unphysiologically high concentrations of gastrin produce a rise in pressure in the lower esophageal sphincter, while somatostatin has neither an effect on the lower esophageal sphincter pressure, nor is it able to inhibit the pharmacological effect of exogenic gastrin administration. The results of this study demonstrate that normal levels of serum gastrin do not seem to have much effect of resting LES pressure, nor does somatostatin. (Gastrin, in fact, in pharmacologic dosage does have an effecton the tonicity of the lower esophageal sphincter.)

Plasma Gastrin and Gastric Acid Responses to Sham Feeding and Feeding in Dogs

Gastric acid secretion and plasma gastrin concentrations were determined during fasting and following sham feeding or feeding in dogs with Pavlov pouches or gastric fistulae. Sham feeding caused immediate elevations of plasma gastrin concentrations that rapidly returned to basal levels following the onset of acid secretion although acid was continuously secreted for several hours. Sham feeding with the gastric fistula open produced higher gastrin concentrations and acid output than with the fistula closed. Feeding raised the plasma gastrin concentrations considerably higher than sham feeding in the same dogs although the peak acid output equaled that following sham feeding with gastric fistula open. The delay in onset of acid secretion was more pronounced during feeding than during sham feeding. Atropinization did not significantly influence basal plasma gastrin concentration but virtually abolished the gastrin response to sham feeding. Plasma gastrin responses were observed following feeding despite atropinization.