Association between mutation of interleukin 36 receptor antagonist and generalized pustular psoriasis: A PRISMA-compliant systematic review and meta-analysis.
Association between mutation of interleukin 36 receptor antagonist and generalized pustular psoriasis: A PRISMA-compliant systematic review and meta-analysis.
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DOI：
10.1097/md.0000000000023068
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发表时间：
2020-11-06
期刊：
影响因子：
1.6
通讯作者：
Jia XS
中科院分区：
文献类型：
--
作者：
Liu ZJ;Tian YT;Shi BY;Zhou Y;Jia XS
泛发性脓疱性银屑病（Generalized pustular psoriasis，GPP）是一种全身性炎症性疾病，预后差，多项研究表明白细胞介素36受体拮抗剂基因（interleukin 36 receptor antagonist gene，IL 36 RN）突变与GPP相关，其中c.115+ 6 T>C多态性是IL 36 RN最常见的突变。本研究旨在探讨IL 36 RN基因多态性与GPP亚型易感性的关系。为了进行全面的文献综述，使用Pubmed、EMBASE、科克伦、中国国家知识基础设施和万方数据库等数据库获得研究。仅纳入截至2019年12月发表的研究。研究的质量使用Newcastle-Ottawa量表进行评估。汇总总比值比（OR）和相应的95%置信区间（95% CI），并使用STATA 14进行分析。通过使用上述软件进行的Egger检验评价发表偏倚。建立了5个常见基因模型，并分析了C.115+ 6 T>C多态性与GPP亚型之间的关联。共纳入10项研究，包括683例GPP患者。Meta分析显示，IL 36 RN突变在GPP伴或不伴寻常型银屑病患者之间（OR = 3.82，95%CI 2.63-5.56）以及成人GPP与儿童GPP之间（OR = 0.42，95%CI 0.23-0.77）存在显著统计学相关性。 欧洲患者与亚洲患者之间无明显差异（OR = 4.03，95%CI 2.23-7.26），基因模型显示c.115+ 6 T>C多态性与GPP呈显性相关（CC+ TC vs TT，OR 2.74，95%CI 2.06-3.64），隐性模型（CC vs CT + TT，OR 4.33，95%CI 2.84-6.60），纯合子模型（CC vs TT，OR 4.37，95%CI 2.88-6.62）、杂合子模型（CT vs TT，OR 2.26，95%CI 1.32-3.85）和等位基因模型（C vs T，OR 3.35，95%CI 2.63-4.27）。IL 36 RN突变与无寻常型银屑病的GPP和GPP的早发密切相关。IL 36 RN基因c.115+ 6 T>C单核苷酸多态性在GPP易感性中起重要作用，尤其是在纯合突变中。GPP可能是一种不同的炎症性疾病，独立于银屑病。
Generalized pustular psoriasis (GPP) is a systemic inflammatory disease with poor outcomes, and several studies have suggested that the mutation of the interleukin 36 receptor antagonist gene (IL36RN) is related to GPP, where the polymorphism c.115+6T>C is reported to be the most common mutation of IL36RN. This study was performed to clarify and comprehensively evaluate the relationship between IL36RN gene polymorphism and the susceptibility of GPP subtypes. To conduct a thorough literature review, studies were obtained using databases such as Pubmed, EMBASE, Cochrane, China National Knowledge Infrastructure, and the Wanfang database. Only studies published up to December 2019 were included. The quality of the research studies was estimated using the Newcastle–Ottawa scale. The total odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were pooled and analysed using STATA 14. The publication bias was evaluated through the Egger test, performed using the aforementioned software. Five common gene models were built and analysed to assess the association between the polymorphism c.115+6T>C and subtypes of GPP. A total of 10 studies were selected, including 683 cases of GPP patients. Meta-analyses showed that there was a significant statistical correlation of IL36RN mutation between GPP with or without psoriasis vulgaris (OR = 3.82, 95%CI 2.63–5.56) and between adult GPP and paediatric GPP (OR = 0.42, 95%CI 0.23–0.77). No obvious discrepancy between European patients (OR = 4.03, 95%CI 2.23–7.26) and Asian patients was found. The gene models showed clear associations between the polymorphism c.115+6T>C and GPP through the dominant model (CC+ TC vs TT, OR 2.74, 95%CI 2.06–3.64), recessive model (CC vs CT + TT, OR 4.33, 95%CI 2.84–6.60), homozygote model (CC vs TT, OR 4.37, 95%CI 2.88–6.62), heterozygote model (CT vs TT, OR 2.26, 95%CI 1.32–3.85) and allelic model (C vs T, OR 3.35, 95%CI 2.63–4.27). The IL36RN mutation is strongly related to GPP without psoriasis vulgaris and the early onset of GPP. Furthermore, the single-nucleotide polymorphism c.115+6T>C of the IL36RN gene plays a significant role in GPP vulnerability, especially in homozygous mutation. GPP could be a different inflammatory disease, independent of psoriasis.