【摘要】 目的研究甲状旁腺切除联合自体移植(tPTX+AT)对继发性甲状旁腺功能亢进(SHPT)尿毒症患者的疗效及对左心室肥厚、血清胎球蛋白A(Fetuin-A)、炎症因子的影响。方法 74例SHPT尿毒症患者被随机分为两组,每组37例。对照组行常规治疗,观察组在此基础上行t PTX+AT术。术后6个月比较两组患者甲状旁腺激素(i PTH)、血清钙、磷浓度变化,采用超声心动图检测左心室肥厚的指标变化情况,检测治疗前后血清Fetuin-A、超敏C-反应蛋白(hs-CRP)水平及白细胞介素6(IL-6)水平。结果术后6个月随访,观察组的血清钙、血清磷、钙磷乘积以及i PTH均下降(P <0.05),对照组上述指标变化差异无统计学意义(P>0.05)。观察组舒张末期室间隔厚度(IVST)、左心室重量指数(LVMI)、左心室后壁厚度(LVPWT)均下降,左心室射血分数(LVEF)升高(P <0.05);钙化率变化差异无统计学意义(P>0.05)。对照组的IVST、LVMI、LVPWT变化差异无统计学意义(P>0.05);但钙化率升高(P <0.05)。观察组Fetuin-A升高,hs-CRP和IL-6水平下降(P <0.05);对照组变化差异无统计学意义(P>0.05)。结论 tPTX+AT术能有效降低SHPT尿毒症患者的血磷、血钙和i PTH浓度,改善临床症状及患者的左心室肥厚,延缓心脏瓣膜钙化进展,同时上调Fetuin-A浓度,下调IL-6和hs-CRP浓度。更多还原

【Abstract】 Objective To analyze the effect of total parathyroidectomy with autologous transplantation(tPTX + AT) in the treatment of secondary hyperparathyroidism(SHPT) uremia patients and influence on left ventricular hypertrophy and Fetuin-A. Methods Totally 74 SHPT uremia patients were involved in this study, and were randomly divided into control group and observation group(n = 37). All patients were treated with standard therapy while patients in observation group received additional treatment of tPTX+AT. iPTH, serum concentration of calcium and phosphorus, Fetuin-A, IL-6 and hs-CRP were measured. Left ventricle was evaluated by echocardiographic test. Results Levels of iPTH, serum calcium and phosphorus, calcium-phosphorus product, hs-CRP and IL-6 in observation group were decreased and levels of fetuin-A were increased significantly(P < 0.05), while those in control group did not show any obvious change(P > 0.05). The IVST, LVMI and LVPWT in patients of observation group decreased while LVEF was increased dramatically(P < 0.05). However, no alteration in IVST, LVMI, and LVPWT in control group was witnessed(P < 0.05). Calcification rate did not show any change in observation group while that was increased obviously in control group. Conclusions tPTX + AT can improve the clinical symptoms, and delay the progression of cardiac valve calcification in patients with SHPT uremia.更多还原