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肾衰竭时甲状旁腺的生长与抑制

Parathyroid growth and suppression in renal failure.

作者信息

Lewin Ewa, Huan Jinxing, Olgaard Klaus

机构信息

Nephrological Department P, Rigshospitalet, Copenhagen, Denmark.

出版信息

Semin Dial. 2006 May-Jun;19(3):238-45. doi: 10.1111/j.1525-139X.2006.00161.x.

Abstract

In advanced uremia, parathyroid hormone (PTH) levels should be controlled at a moderately elevated level in order to promote normal bone turnover. As such, a certain degree of parathyroid hyperplasia has to be accepted. Uremia is associated with parathyroid growth. In experimental studies, proliferation of the parathyroid cells is induced by uremia and further promoted by hypocalcemia, phosphorus retention, and vitamin D deficiency. On the other hand, parathyroid cell proliferation might be arrested by treatment with a low-phosphate diet, vitamin D analogs, or calcimimetics. When established, parathyroid hyperplasia is poorly reversible. There exists no convincing evidence of programmed parathyroid cell death or apoptosis in hyperplastic parathyroid tissue or of involution of parathyroid hyperplasia. However, even considerable parathyroid hyperplasia can be controlled when the functional demand for increased PTH levels is removed by normalization of kidney function. Today, secondary hyperparathyroidism can be controlled in patients with long-term uremia in whom considerable parathyroid hyperplasia is to be expected. PTH levels can be suppressed in most uremic patients and this suppression can be maintained by continuous treatment with phosphate binders, vitamin D analogs, or calcimimetics. Thus modern therapy permits controlled development of parathyroid growth. When nonsuppressible secondary hyperparathyroidism is present, nodular hyperplasia with suppressed expression of the calcium-sensing receptor (CaR) and vitamin D receptor (VDR) has been found in most cases. An altered expression of some autocrine/paracrine factors has been demonstrated in the nodules. The altered quality of the parathyroid mass, and not only the increased parathyroid mass per se, might be responsible for uncontrollable hyperparathyroidism in uremia and after kidney transplantation.

摘要

在晚期尿毒症中,甲状旁腺激素(PTH)水平应控制在适度升高的水平,以促进正常的骨转换。因此,必须接受一定程度的甲状旁腺增生。尿毒症与甲状旁腺生长有关。在实验研究中,尿毒症可诱导甲状旁腺细胞增殖,而低钙血症、磷潴留和维生素D缺乏会进一步促进其增殖。另一方面,低磷饮食、维生素D类似物或拟钙剂治疗可能会抑制甲状旁腺细胞增殖。一旦形成,甲状旁腺增生很难逆转。目前尚无令人信服的证据表明增生的甲状旁腺组织中存在程序性甲状旁腺细胞死亡或凋亡,也没有证据表明甲状旁腺增生会 involution(此处原文可能有误,推测为 involution 应为 involution,意为退化)。然而,当通过肾功能正常化消除对升高PTH水平的功能需求时,即使是相当严重的甲状旁腺增生也可以得到控制。如今,对于预期会出现相当程度甲状旁腺增生的长期尿毒症患者,继发性甲状旁腺功能亢进可以得到控制。大多数尿毒症患者的PTH水平可以被抑制,并且通过持续使用磷结合剂、维生素D类似物或拟钙剂治疗可以维持这种抑制状态。因此,现代治疗允许甲状旁腺生长得到控制。当存在不可抑制的继发性甲状旁腺功能亢进时,在大多数情况下会发现结节性增生,伴有钙敏感受体(CaR)和维生素D受体(VDR)表达受抑制。在这些结节中已证实一些自分泌/旁分泌因子的表达发生了改变。甲状旁腺肿块性质的改变,而不仅仅是甲状旁腺肿块本身的增加,可能是导致尿毒症和肾移植后不可控性甲状旁腺功能亢进的原因。

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