Wills M R
J Clin Pathol. 1971 Apr;24(3):219-27. doi: 10.1136/jcp.24.3.219.
A study is reported of the estimation of plasma chloride concentration and acid-base status in the differentiation of primary hyperparathyroidism from all other causes of hypercalcaemia. In the two groups of patients studied, all of whom had hypercalcaemia, there was complete separation between the two groups on the basis of plasma chloride concentration and acid-base status. In 16 patients with primary hyperparathyroidism the increase in plasma chloride concentration and associated metabolic acidosis could have been accounted for by the known renal tubular effects of parathyroid hormone. In 13 patients with hypercalcaemia due to various other causes the decrease in plasma chloride concentration and associated metabolic alkalosis could be accounted for either by the known effects of an excess of calcium-ion on the renal tubules, or perhaps by suppression of endogenous parathyroid hormone secretion. In patients with hypercalcaemia and hypophosphataemia of ;pseudohyperparathyroidism' associated with non-endocrine tumours it is postulated that the low plasma chloride concentrations and metabolic alkalosis found in these patients were due either to a differing biological activity of the parathyroid-hormone-like polypeptide secreted by the tumour cells, or possibly to simultaneous secretion by these cells of an ACTH-like polypeptide.
本文报道了一项关于在鉴别原发性甲状旁腺功能亢进与其他所有高钙血症病因时,血浆氯离子浓度及酸碱状态评估的研究。在研究的两组患者中,所有患者均患有高钙血症,基于血浆氯离子浓度及酸碱状态,两组患者完全区分开来。在16例原发性甲状旁腺功能亢进患者中,血浆氯离子浓度升高及相关代谢性酸中毒可由甲状旁腺激素已知的肾小管效应来解释。在13例因其他各种原因导致高钙血症的患者中,血浆氯离子浓度降低及相关代谢性碱中毒可由钙离子过量对肾小管的已知效应来解释,或者可能是由于内源性甲状旁腺激素分泌受抑制所致。在与非内分泌肿瘤相关的“假性甲状旁腺功能亢进”导致高钙血症和低磷血症的患者中,推测这些患者中发现的低血浆氯离子浓度和代谢性碱中毒,要么是由于肿瘤细胞分泌的甲状旁腺激素样多肽具有不同的生物活性,要么可能是由于这些细胞同时分泌了促肾上腺皮质激素样多肽。