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目的 探讨风湿热的发病机制 ,了解心肌细胞促凝血活性与风湿热发病的关系。方法 用风湿性心脏炎患者的外周血淋巴细胞、血清及A组乙型溶血链球菌膜抗原作为刺激物 ,测定体外培养的人胚心肌细胞促凝血活性 (HPCA)。结果 患者的外周血淋巴细胞能使HPCA明显升高 ;静止期风心病、风湿性关节炎、其他疾病对照组及健康对照组患者的外周血淋巴细胞均无此特性 ,迁延活动型风湿性心脏炎患者的血清及A组乙型溶血链球菌膜抗原对HPCA也无直接影响。结论 HPCA升高参与风湿性心脏炎的发病 ,可能是风湿性心脏炎的特征病理改变———阿少夫小体中纤维素样物质沉积的形成原因。
Objective To investigate the pathogenesis of rheumatic fever and to understand the relationship between cardiomyocyte procoagulant activity and rheumatic fever. Methods Peripheral blood lymphocytes and serum of patients with rheumatic carditis and Group A hemolytic streptococcal membrane antigen were used as stimuli to measure the procoagulant activity (HPCA) of cultured human embryonic cardiomyocytes. Results Patients with peripheral blood lymphocytes can make HPCA significantly increased; quiescent rheumatoid arthritis, rheumatoid arthritis, other disease control group and healthy control patients with peripheral blood lymphocytes are not such characteristics, persistent active rheumatic heart disease Patients’ serum and Group A hemolytic streptococcal membrane antigen also had no direct effect on HPCA. Conclusions The increased HPCA is involved in the pathogenesis of rheumatic carditis, which may be the characteristic pathological change of rheumatic carditis - the reason for the deposition of cellulose-like substance in A-Chau small body.