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目的探讨Graves病(简称GD)患者131I治愈前后尿微量蛋白变化的影响因素。方法选择GD患者20例(GD组),根据131I治愈前后分成治疗前的GD组、治愈3个月R3M组、治愈12个月R12M组,并设正常对照组20例。采用全自动化学免疫发光法检测血清游离甲功3项[包括游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺素(TSH)]、促甲状腺受体抗体(TRAb)、尿微量白蛋白(Alb)、尿免疫球蛋白(IgG)、尿微球蛋白(β2-MG)含量。采用散射比浊法检测血清中超敏C反应蛋白(hs-CRP)。全自动血凝仪测定血清D-二聚体(D-D)。SPECT计算总肾小球滤过率(TRGFR)。结果 GD组游离甲功3项与各组比较差异有统计学意义(P<0.01)。GD组、R3M组的TRAb、Alb、IgG与其余组比较差异有统计学意义(P<0.01)。直线相关分析显示,FT3与Alb、IgG呈显著正相关(r分别为0.64、0.72,P均<0.01),TRAb与Alb、IgG呈显著正相关(r分别为0.66、0.56,P均<0.01)。结论 GD肾损害的部位在肾小球,与免疫紊乱关系密切;GD相关抗体的消失可作为判断GD肾损害的恢复及治疗效果的参考指标。
Objective To investigate the influencing factors of urinary microalbuminuria in patients with Graves disease (GD) before and after 131I treatment. Methods GD patients (GD group) were selected and divided into the GD group before and after treatment according to 131I. The patients in R3 group were cured for 3 months and cured for 12 months in R12M group. Twenty patients in normal control group were also treated. The levels of free thyroxine in serum [including free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH)] and thyroid stimulating hormone receptor antibody (TRAb) were measured by automated chemiluminescence immunoassay , Urinary albumin (Alb), urinary immunoglobulin (IgG), urinary microglobulin (β2-MG) content. Serum hs-CRP was detected by nephelometry. Automatic blood coagulation analyzer serum D-dimer (D-D). SPECT calculated total glomerular filtration rate (TRGFR). Results There were significant differences among the three groups (P <0.01). The levels of TRAb, Alb and IgG in R3M group were significantly different from those in other groups (P <0.01). Linear correlation analysis showed that there was a significant positive correlation between FT3 and Alb and IgG (r = 0.64,0.72, P <0.01), TRAb was positively correlated with Alb and IgG (r = 0.66,0.56, P <0.01) . Conclusion The location of GD renal lesion in the glomerulus is closely related to the immune disorder. The disappearance of GD-related antibodies can be used as a reference index to determine the recovery and therapeutic effect of GD renal damage.