MUSCULOSKELETAL COMPLICATIONS AFTER RENAL-TRANSPLANTATION - PATHOGENESIS AND TREATMENT
MUSCULOSKELETAL COMPLICATIONS AFTER RENAL-TRANSPLANTATION - PATHOGENESIS AND TREATMENT
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DOI：
10.1016/s0272-6386(12)70118-x
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发表时间：
1992-02-01
影响因子：
13.2
通讯作者：
NIEMANN, KMW
中科院分区：
文献类型：
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作者：
JULIAN, BA;QUARLES, LD;NIEMANN, KMW
肾移植与肌肉骨骼系统的功能和结构的几种异常有关。这些骨骼问题中的一些是由于移植时存在的骨和矿物质代谢异常的不完全解决而引起的。在这方面，持续性甲状旁腺功能亢进、1型糖尿病和β2-微球蛋白蓄积可能导致残余骨骼效应，尽管同种异体移植物功能良好。持续性甲状旁腺功能亢进可能加速骨质流失，增加骨坏死的风险，并导致高钙血症和低磷血症;一些严重甲状旁腺功能亢进的患者需要进行甲状旁腺手术。骨坏死是移植后最严重的骨骼并发症，通常需要手术治疗。尽管与铝过载相关的骨软化症通常在移植后消退，但由于透析淀粉样变性和1型糖尿病引起的骨并发症通常无法改善。或者，骨骼异常可以在移植后获得。大多数新的骨和矿物质代谢紊乱是由于免疫抑制药物。糖皮质激素对骨的毒性作用有助于骨坏死的发病机制，通过减少松质骨质量和骨基质的合成增加骨折的风险，并抑制儿科接受者的线性生长反应。环孢霉素是否单独对骨代谢产生明显的毒性作用尚不清楚，但使用这种药物会增加痛风和牙齿问题的患病率。骨坏死、骨量减少和身材矮小仍然是肾移植受者重要的骨骼并发症。治疗的努力应针对减轻移植前骨疾病和减少移植后骨丢失。
Renal transplantation is associated with several abnormalities of function and structure of the musculoskeletal system. Some of these skeletal problems result from incomplete resolution of abnormalities of bone and mineral metabolism present at the time of transplantation. In this regard, persistent hyperparathyroidism, diabetes mellitus type 1, and accumulation of β2-microglobulin may lead to residual skeletal effects despite excellent function of the allograft. Persistent hyperparathyroidism may accelerate bone loss and increase the risk for osteonecrosis, as well as cause hypercalcemia and hypophosphatemia; some patients with severe hyperparathyroidism require parathyroid surgery. Osteonecrosis is the most debilitating skeletal complication after transplantation and frequently requires surgical therapy. Although osteomalacia associated with aluminum overload generally resolves after transplantation, bone complications due to dialysis amyloidosis and diabetes mellitus type 1 often fail to improve. Alternatively, skeletal abnormalities can be acquired after transplantation. Most of the new derangements of bone and mineral metabolism are due to the immunosuppressive medications. Toxic effects of glucocorticoids on bone contribute to the pathogenesis of osteonecrosis, increase the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, and dampen the linear growth response in pediatric recipients. Whether cyclosporine independently causes appreciable toxic effects on bone metabolism is not yet clear, but use of this drug increases the prevalence of gout and dental problems. Osteonecrosis, osteopenia, and short stature remain important skeletal complications in recipients of renal allografts. Therapeutic efforts should be directed toward alleviating pretransplant bone disease and attenuating bone loss after transplantation.