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[肾功能不全继发甲状旁腺功能亢进。病理生理学、临床放射学表现及治疗]

[Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment].

作者信息

Ben Hamida F, Ghazali A, Boudzernidj M, Amar M, Morinière P, Westeel P, Fournier A

机构信息

Service de Néphrologie-Médecine Interne, Réanimation et Transplantation, CHU d'Amiens, Hôpital Sud, Amiens.

出版信息

Ann Endocrinol (Paris). 1994;55(5):147-58.

PMID:7857079
Abstract

Stimulation of PTH secretion and synthesis in chronic renal failure involves direct and indirect factors. The indirect ones are those contributing to a decrease of plasma ionized calcium concentration which stimulates the release of PTH (1) primarily the negative calcium balance due to the iatrogenic reduction of dietary calcium intake associated with an inadequate synthesis of calcitriol, this latter being explained by a reduction in the nephronic mass, the phosphate retention, the acidosis and the retention of uremic toxins (2) more accessorily, the physicochemical dysequilibrium induced by the late occurring hyperphosphatemia. The factors acting directly on the parathyroid gland stimulating synthesis of prepro PTH at its transcription level: not only hypocalcitriolemia but also hypocalcemia and hyperphosphatemia. The clinicoradiological manifestations appear late, mostly only after the patient has been put on dialysis. The most precocious sign is the subperiosteal resorption assessed on the hand X-rays. Therefore diagnosis of hyperparathyroidism relies mainly on the measurement of plasma concentration of intact PTH. In dialysis patients the optimal range corresponding to the best bone histology is between 1 an 3 times the upper limit of normal. No such data exist for predialysis patients. Medical treatment of hyperparathyroidism should primarily be preventive, probably in predialysis lipin patient as soon as plasma intact PTH is greater than the normal upper limit. This treatment is based primarily on the prevention of phosphate retention, of negative calcium balance and acidosis by the use of oral alkaline salts of calcium given with the meals in association with appropriate dietary protein and phosphate restriction. Native vitamin D depletion should also be prevented but use of 1 alpha OH vitamin D3 metabolites in controversial: it is reasonable to administer them only when plasma intent PTH is above 3-7 the normal upper limit and when plasma phosphate is below 1.2 in predialysis patients below 1.5 mmol/l in dialysis patients and plasma calcium remains below 2.3 mmol/l in spite of CaCO3 administration. This situation is encountered in less than 50% of the dialysis patients and rarely in predialysis patients. In dialysis patients the calcium concentration in the dialysate should be chosen in relation to the dose of oral calcium and the use of 1 alpha OH vitamin D3. The superiority of the intermittent (oral or intravenous) over the daily oral administration is not yet clinically proven. The surgical parathyroidectomy is indicated when hypercalcemia and/or hyperphosphatemia occur under medical treatment, whereas the intact PTH levels remain very high (> 500 pg/ml).(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

慢性肾衰竭时甲状旁腺激素(PTH)分泌和合成的刺激涉及直接和间接因素。间接因素是那些导致血浆离子钙浓度降低从而刺激PTH释放的因素:(1)主要是由于医源性减少饮食钙摄入以及骨化三醇合成不足导致的负钙平衡,而骨化三醇合成不足可由肾单位数量减少、磷酸盐潴留、酸中毒和尿毒症毒素潴留来解释;(2)其次是晚期高磷血症引起的理化失衡。直接作用于甲状旁腺并在转录水平刺激前甲状旁腺素原合成的因素:不仅有低骨化三醇血症,还有低钙血症和高磷血症。临床放射学表现出现较晚,大多在患者开始透析后才出现。最早出现的体征是通过手部X线检查评估的骨膜下吸收。因此,甲状旁腺功能亢进的诊断主要依赖于检测完整PTH的血浆浓度。对于透析患者,与最佳骨组织学相对应的最佳范围是正常上限的1至3倍。对于透析前患者,尚无此类数据。甲状旁腺功能亢进的药物治疗应主要是预防性的,可能在透析前患者中,一旦血浆完整PTH大于正常上限即可开始。这种治疗主要基于通过餐时服用口服钙碱性盐并适当限制饮食蛋白质和磷酸盐摄入来预防磷酸盐潴留、负钙平衡和酸中毒。还应预防天然维生素D缺乏,但使用1α-羟维生素D3代谢产物存在争议:仅在透析前患者血浆完整PTH高于正常上限的3至7倍且血浆磷酸盐低于1.2(透析患者低于1.5 mmol/l)且尽管给予碳酸钙血浆钙仍低于2.3 mmol/l时给予才合理。这种情况在不到50%的透析患者中出现,在透析前患者中很少见。对于透析患者,应根据口服钙的剂量和1α-羟维生素D3的使用情况选择透析液中的钙浓度。间歇性(口服或静脉内)给药优于每日口服给药的优势尚未得到临床证实。当在药物治疗期间出现高钙血症和/或高磷血症而完整PTH水平仍非常高(>500 pg/ml)时,应进行手术甲状旁腺切除术。

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