Reports of parathyroid suppression during cimetidine therapy suggest that prolonged therapy with H2 antagonists may, by inducing relative hypoparathyroidism, compromise skeletal homeostasis and that under appropriate circumstances, these drugs may serve as a new modality in treating hyperparathyroidism. Using three different region-specific immunoassays, we have been unable to show an effect of cimetidine (1,800 mg/day) on parathyroid hormone concentration, or on urinary cyclic adenosine monophosphate and renal threshold phosphate concentration in 4 normal subjects. Ranitidine given for 8 weeks to 4 haemodialysed patients likewise failed to decrease parathyroid hormone concentration. H2 antagonists appear not to alter parathyroid status in either normal subjects or in uraemics and therefore are unlikely to influence skeletal metabolism in either instance.