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肿瘤坏死因子抑制剂在银屑病和银屑病关节炎中的应用潜力。

Potential of tumor necrosis factor inhibitors in psoriasis and psoriatic arthritis.

作者信息

Krueger Gerald, Callis Kristina

机构信息

University of Utah School of Medicine, Department of Dermatology, Salt Lake City, UT 84132, USA.

出版信息

Arch Dermatol. 2004 Feb;140(2):218-25. doi: 10.1001/archderm.140.2.218.

DOI:10.1001/archderm.140.2.218
PMID:14967799
Abstract

OBJECTIVES

To summarize the role of tumor necrosis factor (TNF) in the pathogenesis of psoriasis and psoriatic arthritis (PsA) and to present the latest data on the efficacy of TNF inhibitors in these diseases.

DATA SOURCES

PubMed was used with the following indexing terms: TNF, TNF inhibitor, psoriasis, psoriatic arthritis, etanercept, infliximab, and/or T cell. Abstract booklets and manufacturer's package inserts were also used. When possible, only sources published after the year 2000 were incorporated.

STUDY SELECTION

Sources that described a role for TNF in the pathogenesis of psoriasis and PsA were selected based on relevance. Clinical trials that examined the efficacy of the TNF inhibitors etanercept and infliximab in psoriasis and PsA were selected.

DATA EXTRACTION

Data were extracted if they represented safety information, the American College of Rheumatology criteria for improvement, the Health Assessment Questionnaire, or the PsA response criteria. These data were abstracted independently by the authors.

DATA SYNTHESIS

Aberrant regulation of TNF is involved in the development of psoriasis and PsA. Therefore, recent intervention strategies for psoriasis and PsA have incorporated biologic agents that specifically target TNF. Etanercept and infliximab are effective at reducing disease activity and are generally well tolerated in the treatment of psoriasis and PsA.

CONCLUSION

Tumor necrosis factor plays a major role in the pathogenesis of psoriasis and PsA, and TNF antagonists provide clinicians with a worthy alternative to traditional therapies, which are associated with toxic effects and poor compliance.

摘要

目的

总结肿瘤坏死因子(TNF)在银屑病和银屑病关节炎(PsA)发病机制中的作用,并展示TNF抑制剂治疗这些疾病疗效的最新数据。

数据来源

使用PubMed检索,检索词如下:TNF、TNF抑制剂、银屑病、银屑病关节炎、依那西普、英夫利昔单抗和/或T细胞。也使用了摘要手册和药品制造商的包装说明书。尽可能仅纳入2000年后发表的资料。

研究选择

根据相关性选择描述TNF在银屑病和PsA发病机制中作用的资料。选择检验TNF抑制剂依那西普和英夫利昔单抗治疗银屑病和PsA疗效的临床试验。

数据提取

若数据代表安全性信息、美国风湿病学会改善标准、健康评估问卷或PsA反应标准,则进行提取。这些数据由作者独立提取。

数据综合

TNF的异常调节参与了银屑病和PsA的发生发展。因此,银屑病和PsA的近期干预策略纳入了特异性靶向TNF的生物制剂。依那西普和英夫利昔单抗在降低疾病活动度方面有效,且在银屑病和PsA治疗中总体耐受性良好。

结论

肿瘤坏死因子在银屑病和PsA发病机制中起主要作用,TNF拮抗剂为临床医生提供了一种有价值的替代传统疗法的选择,传统疗法存在毒副作用且依从性差。

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