Cunningham J, Segre G V, Slatopolsky E, Avioli L V
Nephron. 1984;38(1):17-21. doi: 10.1159/000183271.
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.
西咪替丁治疗期间甲状旁腺受抑制的报告表明，H2拮抗剂的长期治疗可能通过诱发相对性甲状旁腺功能减退而损害骨骼内环境稳定，并且在适当情况下，这些药物可能成为治疗甲状旁腺功能亢进的一种新方法。我们使用三种不同的区域特异性免疫测定法，未能显示西咪替丁（1800毫克/天）对4名正常受试者的甲状旁腺激素浓度、尿环磷酸腺苷和肾阈磷浓度有影响。给4名接受血液透析的患者服用雷尼替丁8周同样未能降低甲状旁腺激素浓度。H2拮抗剂似乎不会改变正常受试者或尿毒症患者的甲状旁腺状态，因此在这两种情况下都不太可能影响骨骼代谢。
