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因骨形成减少所致的制动性高钙血症及对静脉注射硫酸钠的反应

Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate.

作者信息

Evans R A, Lawrence P J, Thanakrishnan G, Hills E, Wong S Y, Dunstan C R

出版信息

Postgrad Med J. 1986 May;62(727):395-8. doi: 10.1136/pgmj.62.727.395.

DOI:10.1136/pgmj.62.727.395
PMID:3763550
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2418697/
Abstract

A young man developed acute renal failure and hypercalcaemia following severe burns. The hypercalcaemia was initially controlled by haemodialysis, but it persisted after return of renal function. Plasma PTH was inappropriately elevated, but the nephrogenous cyclic adenosine monophosphate level was low; thus the PTH was probably not biologically active, and may have been artefactually elevated by the moderate renal impairment. Bone histology, showed a normal resorbing surface, but a zero forming surface, implying that the bone dissolution leading to hypercalcaemia resulted from a failure of bone formation. Because of widespread infection and impaired renal function, the hypercalcaemia could not be treated by corticosteroid drugs, mithramycin or phosphate, and there was no response to salmon calcitonin. He was therefore treated with intravenous sodium sulphate, which increased urinary calcium excretion and reduced the plasma calcium. Sodium sulphate still has a role in the treatment of patients with hypercalcaemia.

摘要

一名年轻男性在严重烧伤后出现急性肾衰竭和高钙血症。高钙血症最初通过血液透析得到控制,但肾功能恢复后仍持续存在。血浆甲状旁腺激素(PTH)不适当升高,但肾源性环磷酸腺苷水平较低;因此,PTH可能没有生物活性,可能因中度肾功能损害而出现假性升高。骨组织学显示吸收表面正常,但形成表面为零,这意味着导致高钙血症的骨质溶解是由于骨形成失败所致。由于广泛感染和肾功能受损,高钙血症无法用皮质类固醇药物、光辉霉素或磷酸盐治疗,对鲑鱼降钙素也无反应。因此,他接受了静脉注射硫酸钠治疗,这增加了尿钙排泄并降低了血浆钙水平。硫酸钠在高钙血症患者的治疗中仍有作用。

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