有或无肾功能衰竭患者的甲状旁腺全切除术而非自体移植的长期结果。

H Hampl, T Steinmüller, P Fröhling, C Naoum, K Leder, U Stabell, N Schnoy, P M Jehle
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引用次数: 54

摘要

治疗严重肾性继发性甲状旁腺功能亢进(sHPT)的最佳手术方式仍有争议。全甲状旁腺切除术(PTX)不进行自体移植被放弃,因为担心动态骨状况;然而,在自体移植的情况下,复发性sHPT是频繁的,并促进动脉粥样硬化。我们研究了11例透析18(12-30)年的血液透析患者(年龄59+/-12岁),这些患者由于严重的sHPT而进行了总PTX (I组;完整PTH: 1,240+/-230 pg/ml), 5例(年龄55+/-10岁)无肾功能不全患者在甲状腺手术期间无意中接受了总PTX (II组)。总PTX后(I组,26+/-18[9-59]个月;II组,252+/-188[22 480]月),两组均未显示可测量的完整甲状旁腺激素水平。通过口服钙(I组,钙透析液2.0 mmol/l)、维生素D和骨化三醇(I组和II组血清参数:钙2.4和2.2 mmol/l;磷酸1.8和1.1 mmol/l;25(OH)-维生素D(3) 21和34 ng/ml;1,25(OH)(2)-维生素D(3)分别为32和41 pg/ml)。在第一组,在全PTX治疗后,骨痛得到了快速和持续的改善,体力活动和耐力明显增强。高转化率骨病明显改善,表现为天然骨钙素(90+/-17 vs. 26+/-18 ng/ml)、骨碱性磷酸酶(74+/-12 vs. 12+/-6 ng/ml)和i型胶原羧基末端交联末端肽(65+/-16 vs. 40+/-21 ng/ml)水平下降,但i型前胶原羧基末端前肽水平升高(120+/-36 vs. 148+/-41 ng/ml)。x线及骨组织学证实骨钙化良好。瘙痒血管外钙化沉积和血管及心脏瓣膜钙化在全PTX后立即停止。此外,6例sHPT患者存在严重的动脉粥样硬化病变,如胸主动脉瘤(n = 3)或腹主动脉瘤(n = 3),在每年超声控制下,在总PTX术前出现尺寸进展,而在PTX后没有。在II组,即使在全PTX治疗后很长一段时间,也没有临床、放射学、组织学或生化证据表明存在低周转率骨病。总之,我们的数据表明,在血液透析患者和肾功能正常的患者中,维生素D(3)代谢物和钙的替代可以防止甲状旁腺功能低下对骨骼的有害影响,并可能补偿缺失的甲状旁腺激素作用。在此基础上,由于总PTX对动脉粥样硬化病变进展的有益作用,预计会有更好的生存率。我们建议对不适合肾移植的严重sHPT透析患者重新考虑全PTX而不进行自身移植。
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Long-term results of total parathyroidectomy without autotransplantation in patients with and without renal failure.

The optimal surgical procedure for severe renal secondary hyperparathyroidism (sHPT) is still a point of controversy. Total parathyroidectomy (PTX) without auto-transplantation was abandoned for fear of an adynamic bone condition; however, in the case of autotransplantation recurrent sHPT is frequent and promotes atherosclerosis. We studied 11 hemodialysis patients (age 59+/-12 years) on dialysis for 18 (12-30) years in whom total PTX was performed due to severe sHPT (group I; intact PTH: 1,240+/-230 pg/ml), and 5 patients (age 55+/-10 years) without renal insufficiency who inadvertently received total PTX during thyroid surgery (group II). After total PTX (group I, 26+/-18 [9-59] months; group II, 252+/-188 [22 480] months) both groups showed no measurable intact PTH levels. Calcium homeostasis was maintained by oral substitution with calcium (group I, calcium dialysate of 2.0 mmol/l), vitamin D and calcitriol (serum parameters in groups I and II: calcium 2.4 and 2.2 mmol/l; phosphate 1.8 and 1.1 mmol/l; 25(OH)-vitamin D(3) 21 and 34 ng/ml; 1,25(OH)(2)-vitamin D(3) 32 and 41 pg/ml, respectively). In group I, after total PTX there was a rapid and sustained improvement in bone pain with markedly enhanced physical activity and endurance. High turnover osteopathy markedly improved as indicated by declining levels of native osteocalcin (90+/-17 vs. 26+/-18 ng/ml), bone alkaline phosphatase (74+/-12 vs. 12+/-6 ng/ml), and carboxyterminal cross-linked telopeptide of type-I collagen (65+/-16 vs. 40+/-21 ng/ml) but increasing levels of carboxyterminal propeptide of type-I procollagen (120+/-36 vs. 148+/-41 ng/ml). Recalcification of bone was excellent as demonstrated by X-ray and confirmed by bone histology. Itching extravascular calcific deposits and calcifications of blood vessel and cardiac valves immediately stopped after total PTX. Moreover, 6 sHPT patients suffered from severe atherosclerotic lesions such as thoracic aortic aneurysm (n = 3) or abdominal aortic aneurysm (n = 3) which showed size progression before but not after total PTX when annually controlled by ultrasonography. In group II, even long after total PTX, there was no clinical, radiological, histological or biochemical evidence for low turnover osteopathy. In conclusion, our data indicate that substitution with vitamin D(3) metabolites and calcium can prevent deleterious bone effects of hypoparathyroidism in hemodialysis patients and in patients with normal kidney function and may compensate for the missing PTH action. Over this, a better survival rate is expected as a consequence of the beneficial effect of total PTX on the progression of atherosclerotic lesions. We suggest reconsideration of total PTX without autotransplantation in dialysis patients with severe sHPT who are not eligible for renal transplantation.

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Author Index Vol. 25, 1999 Manuscript Consultants Contents Vol. 25, 1999 Subject Index Vol. 25, 1999 Subject Index Vol. 25, No. 4–6, 1999
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