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首页> 外文期刊>Clinical kidney journal. >Knuckle cracking: secondary hyperparathyroidism and what your mother did not tell you
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Knuckle cracking: secondary hyperparathyroidism and what your mother did not tell you

机译：指关节裂开：继发性甲状旁腺功能亢进症和母亲没有告诉你的事情

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Introduction Secondary hyperparathyroidism in end-stage renal disease patients has protean musculoskeletal manifestations. Some of our dialysis patients spontaneously vocalized that they had lost the ability to crack their knuckles and then experienced gratifying restoration after surgical parathyroidectomy. We propose that the physiology and mechanical basis of knuckle cracking would be affected by parathyroid-related mineral and bone disorders. Methods and results We surveyed all of our chronic dialysis outpatients who had undergone surgical parathyroidectomy. Thirteen (～12% of the population) individuals were identified: eight males, age 37.7 ± 12.5 years old, dialysis duration of 10.2 ± 7.0 years and peak preoperative intact parathyroid hormone (PTH) levels of 2344 ± 900 pg/mL. Seven patients had no recollection of knuckle cracking issues, with surgery as remote as decades. Six individuals were able to provide adequate histories: four had postoperative restoration of knuckle cracking and expressed great satisfaction from the emotional relief from what appeared to be habitual knuckle cracking. Two of these patients reported rapid return of cracking, occurring in less than ～2 weeks. Conclusions This is the first report of loss of knuckle cracking due to hyperparathyroidism and its cure in 67% of patients, following surgical parathyroidectomy. We propose that parathyroid (e.g. calcific) changes in articular structures (tendons, ligaments) cause reduced elasticity, limited joint surface separation upon flexion, attenuation of cavitation and thus, loss of the audible crack upon vacuum collapse. The psychological ‘release' from habitual knuckle cracking may be a motivator from some patients to adhere to complex parathyroid regimens or to pursue surgical intervention.
机译：引言终末期肾病患者继发性甲状旁腺功能亢进症有蛋白骨骼肌骨骼表现。我们的一些透析患者自发地说，他们丧失了开裂指关节的能力，然后在进行了甲状旁腺切除术后恢复了令人满意的恢复。我们建议，甲状旁腺相关的矿物质和骨骼疾病会影响指关节开裂的生理和机械基础。方法和结果我们调查了所有接受了手术甲状旁腺切除术的慢性透析门诊患者。确定了13个（约占人口的12％）个体：八名男性，年龄37.7±12.5岁，透析时间为10.2±7.0岁，术前完整甲状旁腺激素（PTH）的最高水平为2344±900 pg / mL。七名患者没有回味到关节开裂的问题，手术时间长达数十年。六个人能够提供足够的病史：四个人在术后恢复了指关节裂开，并从似乎是习惯性指关节裂开的情绪缓解中表达了极大的满足感。这些患者中有两个报告称龟裂迅速恢复，发生时间不到2周。结论这是关于甲状旁腺功能亢进引起的指关节开裂损失的首次报道，其在手术甲状旁腺切除术后的治愈率为67％。我们认为，甲状旁腺（例如钙化）在关节结构（肌腱，韧带）中的变化会导致弹性降低，屈曲时关节表面分离受限，气蚀减弱以及真空塌陷时可听见的裂纹消失。习惯性指关节开裂的心理“释放”可能是某些患者坚持复杂的甲状旁腺疗法或进行手术干预的动力。

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