Recent reports that cimetidine, a blocker of histamine H2 receptors, lowered serum calcium and/or immunoreactive parathyroid hormone (PTH) concentrations in primary or secondary hyperparathyroidism prompted us to administer the drug (300 mg, orally, every 6 h) to two patients with hyperparathyroidism accompanying familial multiple endocrine neoplasia type 1.
FBH resembles hyperparathyroidism in that the plasma phosphate level is often in the low-normal range and in that parathyroid hormone is often detectable in the plasma.
Consideration of these age-of-onset and G6PD findings suggest that hyperparathyroidism may result from either non-neoplastic or mutational-induced processes even though no histologic distinctions have been observed in the hyperplasia associated with these processes.
Serum calcium, serum phosphate, plasma parathormone and vitamin D metabolites do not distinguish affected members from patients with hyperparathyroidism.
These results indicated the presence of mRNA coding for pre-pro-PTH (PTH mRNA) in an apparently nonfunctioning parathyroid carcinoma, suggesting that PTH synthesis is not always absent in parathyroid carcinomas which are not accompanied by hyperparathyroidism.
Lack of effect of parathyroidectomy or calcium channel blockade on serum gastrin concentration and gastric acid secretion in a patient with hyperparathyroidism and Zollinger-Ellison syndrome.
These data suggest that the recurrence of hyperparathyroidism is not due to enhanced PTH synthetic activity of autotransplant grafts but to the abnormal growth rate of the transplanted gland.