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背景:强直性脊柱炎(ankylosingspondylitis,AS)患者中HLA-B27的阳性率在不同报道间有明显差异,这种差别可能由环境因素造成,但也可能受其它HLA或非HLA因素影响,推测另一些分子可能在AS发病中起一定作用。目的:探讨肿瘤坏死因子α(tumornecrosisfactor-α,TNF-α)启动子多态性与AS的相关性。设计:非随机对照实验研究。地点和对象:资料收集地点:同济医学院附属协和医院。对象:选择2000-06/2003-01武汉地区78例AS患者作为研究对象,所有AS患者均符合VanderLinder1984年修改的诊断标准,平均年龄(37.4±12.8)岁,男67例,女11例。对照组为HLA-B27阳性的武汉籍体检健康汉族人52人,平均年龄(39.2±14.4)岁,男44人,女8人。干预:采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)对AS患者和HLA-B27阳性健康人群进行TNF启动子多态性分析,采用酶联免疫吸附法(ELISA)检测了患者和正常人群血清TNF-α水平。主要观察指标:AS患者TNF基因启动子区域-308位点基因型与AS的关系。结果:AS患者中为-308.1.1基因型的有61例(78%,61/78),明显高于HLA-B27阳性的健康人(56%,29/52),差异有显著性意义(χ2=6.8,P<0.05);AS患者的-308.1.2和-308.2.2基因型频率分别为20%和1%,低于对照的38%(χ2=9.3,P<0.05)和5.8%(χ2=11.4,P<0.01),且后两
BACKGROUND: The positive rate of HLA-B27 in patients with ankylosing spondylitis (AS) is significantly different between different reports. This difference may be caused by environmental factors, but may also be affected by other HLA or non-HLA factors. Some molecules may play a role in the pathogenesis of AS. Objective: To investigate the association of tumor necrosis factor α (TNF-α) promoter polymorphism with AS. Design: Non-randomized controlled trial. Location and object: Data collection Location: Union Hospital of Tongji Medical College. PARTICIPANTS: A total of 78 patients with AS in Wuhan district from 2000-06 / 2003-01 were selected as the study subjects. All AS patients were in accordance with the revised standard of VanderLinder in 1984. The average age was 37.4 ± 12.8 years old, including 67 males and 11 females. The control group was HLA-B27-positive Wuhan nationality health check-up of 52 Han people, the average age (39.2 ± 14.4) years old, 44 males and 8 females. Intervention: Polymorphism analysis of TNF promoter in patients with AS and HLA-B27-positive healthy subjects by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed. The polymorphism of TNF promoter was detected by enzyme linked immunosorbent assay (ELISA) Serum TNF-α levels in patients and normal subjects. MAIN OUTCOME MEASURES: The relationship between genotype at -308 in TNF promoter and AS in AS patients. Results: 61 patients (78%, 61/78) with -308.1.1 genotype were significantly higher in AS patients than in HLA-B27-positive healthy people (56%, 29/52), with significant difference ( χ2 = 6.8, P <0.05). The genotype frequencies of -308.1.2 and -308.2.2 in AS patients were 20% and 1% respectively, lower than those in control 38% (χ2 = 9.3, P <0.05) (χ2 = 11.4, P <0.01), and the last two