Neer R M, Tregear G W, Potts J T
J Clin Endocrinol Metab. 1977 Feb;44(2):420-3. doi: 10.1210/jcem-44-2-420.
To gain further insight into the biological significance of parathyroid hormone (PTH) metabolism, native parathyroid hormone and synthetic peptides, similar to PTH metabolites generated in vivo, have been given intravenously to human subjects. The resultant changes in renal excretion of adenosine 6':5' monophosphate (cyclic AMP) and inorganic phosphate have been measured in five pseudohypoparathyroid, four hypoparathyroid, and one pseudopseudohypoparathyroid patient. As anticipated, native PTH promptly increased urinary cyclic AMP and phosphate excretion in the hypoparathyroid and pseudo-pseudohypoparathyroid patients, and had little or no effect on their excretion in the pseudohypoparathyroid patients. Synthetic bovine parathyroid hormone 1-34 and synthetic human parathyroid hormone 1-34 had effects essentially identical to each other and to native PTH. We conclude that the PTH resistance of pseudohypoparathyroidism is probably not caused by a defect in PTH metabolism. We further conclude that synthetic human or bovine parathyroid hormone 1-34 could be used for diagnostic evaluation of patients.
为了进一步深入了解甲状旁腺激素(PTH)代谢的生物学意义,已将天然甲状旁腺激素和与体内产生的PTH代谢产物相似的合成肽静脉注射给人类受试者。在5例假性甲状旁腺功能减退症患者、4例甲状旁腺功能减退症患者和1例假假性甲状旁腺功能减退症患者中,测量了由此导致的尿中腺苷6':5'单磷酸(环磷酸腺苷)和无机磷排泄的变化。正如预期的那样,天然PTH迅速增加了甲状旁腺功能减退症和假假性甲状旁腺功能减退症患者的尿中环磷酸腺苷和磷排泄,而对假性甲状旁腺功能减退症患者的排泄几乎没有影响或没有影响。合成牛甲状旁腺激素1-34和合成人甲状旁腺激素1-34的作用彼此基本相同,且与天然PTH相同。我们得出结论,假性甲状旁腺功能减退症的PTH抵抗可能不是由PTH代谢缺陷引起的。我们进一步得出结论,合成人或牛甲状旁腺激素1-34可用于患者的诊断评估。