Does hyperparathyroidism cause hypergastrinemia?
To define the relationship between hyperparathyroidism (HPT) and gastric function, 31 patients with HPT were prospectively studied before and 2 to 25 months after parathyroidectomy. The gastrin response to a standard test meal (STM), the basal acid output (BAO), and the peak acid output (PAO) were determined. Parathormone and calcium were elevated in all patients and returned to normal following parathyroidectomy. The mean fasting gastrin concentration, mean integrated gastrin response (IGR) to feeding, mean basal acid output (BAO), and mean peak acid output (PAO) were not changed by successful parathyroidectomy. There was no significant correlation between gastrin concentration or gastrin response to feeding and gastric acid secretion. Eight of 31 HPT patients had fasting gastrin concentrations above normal preoperatively and remained so postoperatively. Hypergastrinemia in six of these eight patients could be explained by the Zollinger-Ellison (Z-E) syndrome or chronic atrophic gastritis. The hypothesis that peptic ulcer disease seen in some HPT patients is the result of calcium-induced hypergastrinemia causing gastric hypersecretion is not supported by this study.
D000293:Adolescent; D000328:Adult; D000368:Aged; D002118:Calcium / Q000097:blood; D005260:Female; D005502:Food; D005750:Gastric Juice / Q000378:metabolism; D005755:Gastrins / Q000097:blood*; D006801:Humans; D006961:Hyperparathyroidism / Q000150:complications*; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000601:surgery; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D011863:Radioimmunoassay; D015043:Zollinger-Ellison Syndrome / Q000150:complications
D005755:Gastrins; D010281:Parathyroid Hormone; D010758:Phosphorus; D002118:Calcium