基因组甲基化与慢性荨麻疹发病机制间的关系的初步探索  

Association of genome DNA methylation with pathogenesis of chronic urticaria

作　　者：宋彪[1] 房思宁[1] 郑利雄[1] 梅忠喜[1] 黄小芳[1] 

机构地区：[1]深圳市人民医院暨南大学第二临床医学院皮肤科,518010

出　　处：《国际医药卫生导报》2013年第15期2267-2271,共5页International Medicine and Health Guidance News

基　　金：深圳市科技计划项目（201003023）

摘　　要：目的通过检测慢性特发性荨麻疹和自身免疫性荨麻疹的基因组甲基化水平，初步探讨基因组甲基化与其发病机制间的关系。方法采用ASST方法将45例慢性荨麻疹患者分为慢性特发性荨麻疹组和自身免疫性荨麻疹组。分离血清，分别检测血清中TgAb、TPOAb、ANA、SAM和SAH水平，并对结果进行统计分析。结果慢性荨麻疹患者ASST阳性率46．7％，对照组ASST全部阴性，两组比较差异有统计学意义（P〈0．01）。自身免疫荨麻疹组自身抗体检出率最高，TGAb、TPOAb和ANA的阳性率分别是23．80％、14．29％、14．29％；与慢性特发性荨麻疹组及对照组比较，自身免疫荨麻疹组TGAb差异均有统计学意义（P〈0．05），TPOAb和ANA的差异均无统计学意义（P〉O．05）；慢性特发性荨麻疹组与对照组比较，三种自身抗体差异均无统计学意义（P〉0．05）。自身免疫性荨麻疹组SAM较其它两组低，而SAH高于其它两组，SAM／SAH也较其它两组小，但差异均无统计学意义（P〉0．05）。慢性特发性荨麻疹组SAM、SAH和SAM／SAH与对照组比较，差异均无统计学意义（P〉0．05）。结论我科门诊慢性荨麻疹患者中，自身免疫性荨麻疹所占比例达46．7％；TGAb在自身免疫性荨麻疹患者中阳性率显著高于慢性特发性荨麻疹，能否作为一种有价值的自身免疫性荨麻疹的临床检测指标有待进一步研究；SAM、SAH及其比值在自身免疫性荨麻疹、慢性特发性荨麻疹及对照组中无统计学差异，似乎甲基化并不参与到自身免疫性荨麻疹的发病机制中，但有待更大的样本量证实。Objective To explore the association of genome methylation with the pathogenesis of chronic urticaria by detecting genome methylation level of chronic idiopathic urticaria and autoimmune urticaria. Methods 45 patients with chronic urticaria were divided into chronic idiopathic urticaria group and autoimmune urticaria group using ASST method. Serum TgAb, TPOAb, ANA, SAM, and SAH were detected. Results The positive rate of ASST was 46.7% in patients with chronic urticaria, as compared with 0% in control group. There was a statistical significance between the two groups. The positive rates of TgAb, TPOAb, and ANA were 23.80%, 14.29%, and 14.29% in autoimmune urticaria group, 4.16%, 4.16%, and 0 in chronic idiopathic urticaria group, and 5%, 0%, and 0% in the control group. TgAb differed significantly between autoimmune urticaria group and the other two groups, but not between chronic idiopathic urticaria group and the control group. TPOAb and ANA did not differ statistically between the two groups. SAM, SAH, and SAM/SAH did not differ significantly. Conclusions Autoimmune urticaria accounts for 46.7% in patients with chronic urticaria. TGAb is significantly higher in autoimmune urticaria patients than in those with chronic idiopathic urticaria. Further research should be done to confirm whether TGAb can be a kind of valuable clinical detection index of autoimmune urticaria. There is no statistical significance in SAM, SAH, and SAM/SAH between the two groups, which is likely to suggest that methylation is not involved in the pathogenesis of autoimmune urticaria. But this conclusion needs to be confirmed by bigger samples.

关 键 词：荨麻疹 DNA甲基化 S-腺苷蛋氨酸 S-腺苷同型半胱氨酸 

分 类 号：R758.24[医药卫生—皮肤病学与性病学]