目的 探讨重症肌无力(MG)患者血清补体和乙酰胆碱受体抗体(AChRAb)的浓度变化及其相关性。方法 对22例MG患者进行糖皮质激素规范化治疗,在治疗前、后检测其血清补体、AChRAb的浓度,并与14例非MG对照组(NC组)作对照,分析两组血清补体和AChRAb变化之间的关系。结果 MG组在糖皮质激素治疗前补体C3浓度明显低于NC组(P〈0.01),治疗后MG组补体C3明显增高(P〈0.05),但仍低于NC组;AChRAb浓度在治疗前MG组明显高于NC组(P〈0.01),治疗后MG组AChRAb浓度明显降低(P〈0.05),但仍高于NC组。C3浓度MG组和NC组差异无显著性(P〉0.05)。但补体(C3、C5)浓度和AChRAb浓度在治疗前(r=0.326、r=0.102,均P〉0.05)和治疗后(r=0.114、r=-0.0146,均P〉0.05),以及二者治疗前后变化值之间(r=-0.346、r=0.058,均P〉0.05)相关性不显著。结论 糖皮质激素治疗后MG患者C3浓度增加、AChRAb浓度下降,二者之间无明显相关性,补体和AChRAb在MG发病过程中可能起协同作用。
Objective To analyze the changes and correlation between the concentration of complement and titer of anti-acetylcholine receptor antibody (AChRAb) in the sera of patients with myastheniagravis (MG). Methods 22 MG patients were given standardize treatment with glucocorticoid, The serum concentrations of C3 , C5 and the titer of AChRAb were detected prior and post-treatment and compared with 14 control patients without MG ( NC group). The changes and correlation between concentration of complement and titer of AChRAb was analyzed, Results Prior-treatment, the concentration of C3 was lower in MG group than in NC group ( P 〈 0.01 ), Posttreatment, the concentration of C3 was increased in MG group, but it was still lower than NC group (P 〈 0. 05 ). The titer of AChRAb was higher in MG group than in NC group prior-treatment ( P 〈 0. 01 ) , and it decreased but still higher than NC group post-treatment ( P 〈 0.05 ), The difference of concentration C5 was not significant between MG group and NC group ( P 〉 0. 05 ). The concentration of C3 , C5 was not correlated to the titer of AChRAb prior and post-treatment ( r = 0. 326, r = 0, 102, both P 〉 0. 05 ), There was also no correlation between variation of C3 , C5 concentration and AChRAb titer prior and post-treatment ( r = - 0. 346, r = 0. 058, both P 〉 0. 05 ), Conclusions The serum concentration of C3 rises and the titer of AChRAb decreases in MG patients after treatment with glucocorticoid. There is no correlation between C3 concentration and titer of AChRAb. The complement possibly cooperates with AChRAb in pathogenesis of MG.