类风湿关节炎患者血清中期因子和白细胞介素-17的表达

目的 探讨中期因子和白细胞介素(IL)-17在类风湿关节炎(RA)患者血清中的表达及其临床意义。方法 应用双抗体夹心酶联免疫吸附试验( ELISA)法检测79例RA、37例骨关节炎及70名健康体检者血清中中期因子、IL-17，同时应用ELISA法检测血清抗环瓜氨酸肽(CCP)抗体，免疫散射比浊法检测C反应蛋白(CRP)、类风湿因子(RF)，间接免疫荧光法检测抗角蛋白抗体(AKA)，分析中期因子与IL-17、抗CCP抗体、CRP、RF、红细胞沉降率(ESR)、AKA及RA疾病活动度评分(DAS)之间的相关性。多组间比较采用Kruskal-WallisH检验，2组间比较采用Mann-Whitney U检验，相关分析采用非参数Spearman相关分析。结果 RA组血清中期因子水平(327±167) pg/ml显著高于骨关节炎组(209±130)pg/ml和健康对照组(225±109) pg/ml,差异有统计学意义（H=22.01,P＜0.01），骨关节炎和健康对照组比较差异无统计学意义(D0.05)。RA组IL-17水平(44±15) pg/ml也显著高于骨关节炎组(26±8) pg/ml和健康对照组( 27±8) pg/ml，差异有统计学意义(H=66.89,P＜0.01)，骨关节炎组和健康对照组比较差异无统计学意义（P＞0.05）。血清中期因子水平与IL-17、CRP呈正相关（r=0.398,P＜0.01；r=0.285，P＜0.01），与DAS、RF、ESR、AKA、抗CCP等无相关性。结论 中期因子和IL-17可能在RA疾病的发生、发展中发挥了一定的作用，通过复杂的细胞因子网络相互协同，促进了RA的发生发展。

Expression of midkine and interleukin-17 in rheumatoid arthritis patients and its clinical significance

Objective To study the midkine (MK) and interleukin (IL)-17 levels in the sera of rheumatoid arthritis (RA) patients. Methods MK, IL-17 and anti-CCP levels in the sera were detected by ELISA in 79 patients with rheumatoid arthritis, 70 healthy controls and 37 patients with osteoarthritis (OA).Krusk-Wallis H test, Mann-whitney U test and Spearman's correlation were used for statistical analysis.Results The serum level of MK of RA patients (327±167) pg/ml was significantly higher than healthy controls (225±109) pg/ml and OA patients (209±130) pg/ml (H=22.01, P＜0.01), but there was no significant difference between that of the healthy controls and OA group (P＞0.05). The serum level of IL-17 (44±15) pg/ml from RA patients was increased significantly than healthy controls (27±8) pg/ml and OA patients (26±8) pg/ml (H=66.89, P＜0.01 ), but there was no significant difference between healthy controls and OA group (P＞0.05). Serum MK values were correlated with IL-17 and CRP (r=0.398, P＜0.01; r=0.285, P＜0.01 ), but not with DAS, RF, ESR, AKA and anti-CCP. Conclusion The serum level of MK and IL-17 from RA patients is increased significantly than healthy controls and OA patients, so MK and IL-17 may be involved in the pathogenesis of RA.