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继发性甲状旁腺功能亢进而非β2微球蛋白淀粉样变是慢性血液透析患者自发性肌腱断裂的原因。

Secondary hyperparathyroidism, and not beta 2-microglobulin amyloid, as a cause of spontaneous tendon rupture in patients on chronic hemodialysis.

作者信息

De Franco P, Varghese J, Brown W W, Bastani B

机构信息

Division of Nephrology, St Louis University Health Sciences Center, MO 63110.

出版信息

Am J Kidney Dis. 1994 Dec;24(6):951-5. doi: 10.1016/s0272-6386(12)81067-5.

DOI:10.1016/s0272-6386(12)81067-5
PMID:7985675
Abstract

Spontaneous bilateral rupture of the extensor mechanisms of the knees, without significant history of trauma, has been reported rarely, generally in association with chronic metabolic disorders, such as chronic renal failure and secondary hyperparathyroidism. We report spontaneous tendon rupture in two patients on chronic hemodialysis for 4 and 11 years, with documented severe secondary hyperparathyroidism. One patient had spontaneous bilateral rupture of his quadriceps and partial avulsion of the left triceps tendons. The other patient had spontaneous rupture of his right quadriceps tendon. Both patients had markedly elevated serum intact parathyroid hormone and moderately elevated serum beta 2-microglobulin levels. Pathologic examination revealed diffuse immunohistochemical staining for beta 2-microglobulin but negative Congo-red staining of the ruptured tendon specimens. These cases and the previous reports in the literature suggest that secondary hyperparathyroidism may play a role in the pathogenesis of this clinical entity.

摘要

膝关节伸肌机制自发性双侧断裂,且无明显外伤史的情况鲜有报道,通常与慢性代谢紊乱有关,如慢性肾功能衰竭和继发性甲状旁腺功能亢进。我们报告了两名接受慢性血液透析4年和11年的患者发生自发性肌腱断裂,并有记录显示其患有严重的继发性甲状旁腺功能亢进。一名患者双侧股四头肌自发性断裂,左侧肱三头肌腱部分撕脱。另一名患者右侧股四头肌腱自发性断裂。两名患者血清完整甲状旁腺激素均显著升高,血清β2-微球蛋白水平中度升高。病理检查显示,断裂肌腱标本的β2-微球蛋白免疫组化染色弥漫,但刚果红染色阴性。这些病例以及文献中的既往报道表明,继发性甲状旁腺功能亢进可能在这一临床病症的发病机制中起作用。

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Secondary hyperparathyroidism, and not beta 2-microglobulin amyloid, as a cause of spontaneous tendon rupture in patients on chronic hemodialysis.继发性甲状旁腺功能亢进而非β2微球蛋白淀粉样变是慢性血液透析患者自发性肌腱断裂的原因。
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