Dysfunction of polymorphonuclear leukocytes in uremia: Role of parathyroid hormone
Dysfunction of polymorphonuclear leukocytes in uremia: Role of parathyroid hormone
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DOI：
10.1046/j.1523-1755.2001.59780195.x
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发表时间：
2001-02-01
影响因子：
19.6
通讯作者：
Smogorzewski, M
中科院分区：
文献类型：
--
作者：
Massry, SG;Smogorzewski, M
来自尿毒症患者的多形核白细胞（PMNL）具有升高的细胞溶质钙（[Ca2+]i）的基础水平、在Fc γ RIII受体活化后降低的钙信号和受损的吞噬作用。尿毒症患者甲状旁腺激素（PTH）慢性过量通过持续升高PMNL的[Ca 2 +]i介导其对PMNL代谢和功能的影响。由于钙通道阻滞剂干扰PTH对PMNL的这种作用，因此用维拉帕米、硝苯地平或利多卡因治疗血液透析患者与人类FMNL代谢和吞噬作用的改善相关。应继续使用钙通道阻滞剂治疗，以维持其有益效果。
Polymorphonuclear leukocytes (PMNLs) from uremic patients have elevated basal levels of cytosolic calcium ([Ca2+]i), reduced calcium signal after activation of Fc gamma RIII receptor, and impaired phagocytosis. Chronic excess of parathyroid hormone (PTH) in uremia mediates its effect on PMNL's metabolism and function through the sustained elevation of their [Ca2+]i. Because calcium channel blockers interfere with this effect of PTH on PMNLs, treatment of patients on hemodialysis with verapamil, nifedipine, or amlodipine was associated with an improvement in metabolism and phagocytosis of FMNLs in humans. The therapy with calcium channel blockers should be continued in order to maintain its beneficial effects.