关节病性银屑病遗传学发病机制和治疗进展  被引量:2

Update on the genetic pathogenesis and treatment of psoriatic arthritis

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作  者:孟丽[1] 王培光[1] 张学军[1] 

机构地区:[1]安徽医科大学皮肤病研究所,合肥230032

出  处:《国际皮肤性病学杂志》2013年第4期238-241,共4页International Journal of Dermatology and Venereology

摘  要:关节病性银屑病是一种慢性炎症性关节病变,与该病发病显著相关的易感基因或易感位点有IL-23R、IL-12B、HLA—Cw6、TRAF3IP2、NO、FBXL19、PSMA6-NFKBIA附近区域,可能相关的易感基因有IL-23A、TNIPl、TNF*-857T、LCE3C—LCE3Bdel变异体、REL基因、IL-13。针对关节病性银屑病发病环节中的一些重要免疫分子或免疫细胞,多种靶向生物制剂包括细胞因子拮抗剂(英夫利西、益赛普、阿达木、戈利木、优斯它单抗)、磷酸二酯酶抑制剂、T细胞抑制剂(阿贝西普)和B淋巴细胞耗竭剂(利妥昔单抗)用于该病的治疗,疗效好,安全性较高。Psoriatic arthritis is a chronic inflammatory disorder mainly affecting joints. Recent studies have revealed that the development of psoriatic arthritis is assock with many susceptible genes or loci, including interleukin-23 receptor (IL-23R), IL-12B, HLA-Cw6, IrAF3IP2, NO, FBXLI9 and PSMA6- NFKBIA nearby, and likely associated with some genes or single nucleotide polymorphisms (SNPs), such as IL-23A, TNIP1, tumor necrosis factor*-857T, LCE3C-LCE3Bdel variant, REL gene and IL-13. Multiple biological agents targeting some key immune molecules or cells in the pathogenesis of psoriatic arthritis have been used to its treatment with a favorable efficacy and safety, including cytokine inhibitors (infliximab, etanercept, adalimumab, golimumab, ustekinumab) , phosphodiesterase inhibitors (apremilast), T-cell inhibitors (abatacept), and B lymphocyte-depleting agent (rituximab).

关 键 词:关节炎 银屑病 遗传 基因 治疗 

分 类 号:R758.63[医药卫生—皮肤病学与性病学]

 

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