机构地区:[1]丹阳市人民医院感染科,江苏丹阳212300 [2]南京医科大学第一附属医院,江苏南京210029
出 处:《热带医学杂志》2013年第9期1078-1081,1088,共5页Journal of Tropical Medicine
摘 要:目的研究肾综合征出血热(HFRS)患者血浆白细胞介素-6(IL-6)、白细胞介素-17(IL-17)、转化生长因子β1(TGF-β1)与多器官损害的关系,以指导临床治疗。方法将27例HFRS患者按病情分为轻、重两组,轻症组13例,重症组14例。按病期采集血标本,用酶联免疫吸附试验(ELISA)检测IL-6、IL-17和TGF-β1,采用免疫抑制法检测肌酸激酶同工酶(CKMB),采用自动生化仪检测血尿素氮(BUN)、肌酐(Cr)、丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST),采用血球分类仪检测血小板(Pt)参数;另取20名健康者作对照。结果 HFRS急性期血浆IL-6、IL-17、TGF-β1均显著升高,三者之间呈显著正相关(IL-6与IL-17:df=78,r=0.680,P<0.01;IL-6与TGF-β1:df=78,r=0.778,P<0.01;IL-17与TGF-β1:df=78,r=0.616,P<0.01)。IL-6、IL-17的变化曲线与BUN、AST、CKMB的变化曲线极为相似,相关分析表明IL-6、IL-17与BUN、AST、CKMB均呈正相关,而与Pt呈负相关。结论 HFRS病程中血浆IL-6、IL-17水平异常升高是引起全身炎症反应、毛细血管损伤、凝血功能紊乱和多器官损害的重要因素,故应同时抑制病毒复制,减轻病理损害,必要时改善微循环。Objective To investigate the relationship between the expression levels of serum IL-6, IL-17, transforming grouth factor-β1 (TGF-β1) and multiple organ damage in patients with hemorrhagic fever with renal syndrome, so as to direct clinical management based on laboratory findings. Methods 27 cases with HFRS were divided into two groups according to the severity of illness (moderate group, n=13; severe group, n=14), and 20 healthy individuals serve as control group. Blood samples were collected at every stage of the disease. The levels of plasma IL-6, IL-17 and TGF-β1 were measured by enzymelinked immunosorbent assay (ELISA). Creatinine kinase isoenzyme-MB (CKMB) was determined by immunosuppression method. Blood urea nitrogen (BUN), creatinine ( Cr ), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by automatic biochemical analyzer, and platelet parameters was measured by automated hemacytic analyser. Results During the acute phase of HFRS, the levels of plasma IL-6, IL-17 and TGF-β1 were significantly increased while platelet count was decreased considerably as compared to control group. There were positive correlations among these cytokines (IL-6 and IL-17:df=78, r=0.680, P〈0.01 ; IL-6 and TGF-β1 :df=78, r=0.778, P〈0.01 ; IL-17 and TGF-β1 :df=78, r=0.616, P〈0.01). The dynamic curves of IL-6 and IL-17 were similar to BUN, AST and CKMB, but not to the curve for the platelet count. Positive correlations were observed between the production of pro-inflammatory cytokines (IL-6, IL-17) and the expression of biochemical markers in the kidney, liver and myocardium (BUN, AST and CKMB). Conclusion Elevation of serum IL-6 and IL-17 might be the cause leading to systemic inflammatory response, extensive capillary injury, coagulation dysfunction and multiple organ damage in the course of HFRS. Simultaneous suppression of viral replication and improvement of microcircnlafion may help to reduce the pathological damage.
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