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严重的皮肤损伤会导致炎症性肠病患者停止使用抗肿瘤坏死因子治疗。

Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy.

机构信息

Department of Gastroenterology, Cliniques Universitaires UCL Mont Godinne, Yvoir, Belgium.

出版信息

Clin Gastroenterol Hepatol. 2010 Dec;8(12):1048-55. doi: 10.1016/j.cgh.2010.07.022. Epub 2010 Aug 20.

DOI:10.1016/j.cgh.2010.07.022
PMID:20728573
Abstract

BACKGROUND & AIMS: Psoriasiform and eczematiform lesions are associated with anti-tumor necrosis factor (TNF)-α therapies. We assessed clinical characteristics, risk factors, and outcomes of skin disease in patients with inflammatory bowel diseases that presented with psoriasiform and eczematiform lesions induced by anti-TNF-α agents.

METHODS

We studied 85 patients (69 with Crohn's disease, 15 with ulcerative colitis, and 1 with indeterminate colitis; 62 women) with inflammatory skin lesions (62 psoriasiform and 23 eczematiform lesions).

RESULTS

Twenty-four patients had a history of inflammatory skin lesions and 15 had a familial history of inflammatory skin disease. Locations of eczematiform lesions varied whereas scalp and flexural varieties were mostly psoriasiform. Skin lesions emerged but inflammatory bowel disease was quiescent in 69 patients following treatment with any type of anti-TNF-α agent (60 with infliximab, 20 with adalimumab, and 5 with certolizumab). Topical therapy resulted in partial or total remission in 41 patients. Patients with psoriasiform lesions that were resistant to topical therapy and that changed anti-TNF-α therapies once or twice developed recurring lesions. Overall, uncontrolled skin lesions caused 29 patients to stop taking TNF-α inhibitors.

CONCLUSIONS

Inflammatory skin lesions following therapy with TNF-α inhibitors occurred most frequently among women and patients with a personal or familial history of inflammatory skin disease; lesions did not correlate with intestinal disease activity. Recurring and intense skin lesions caused 34% of patients in this study to discontinue use of anti-TNF-α agents.

摘要

背景与目的

抗肿瘤坏死因子(TNF)-α 治疗可引起银屑病样和湿疹样病变。我们评估了伴有 TNF-α 拮抗剂诱导的银屑病样和湿疹样病变的炎症性肠病患者的皮肤疾病的临床特征、危险因素和结局。

方法

我们研究了 85 例(69 例克罗恩病,15 例溃疡性结肠炎,1 例未定型结肠炎;62 例女性)有炎症性皮肤病变的患者(62 例银屑病样病变,23 例湿疹样病变)。

结果

24 例患者有炎症性皮肤病变病史,15 例有炎症性皮肤疾病家族史。湿疹样病变的位置不同,而头皮和屈侧病变大多为银屑病样。69 例患者在接受任何类型的 TNF-α 拮抗剂(60 例英夫利昔单抗,20 例阿达木单抗,5 例 Certolizumab)治疗后,炎症性肠病处于静止状态,但出现了皮肤病变。41 例患者接受局部治疗后获得部分或完全缓解。对局部治疗耐药且曾改变 TNF-α 治疗方案 1 或 2 次的银屑病样病变患者出现复发性病变。总的来说,无法控制的皮肤病变导致 29 例患者停止使用 TNF-α 抑制剂。

结论

TNF-α 抑制剂治疗后发生的炎症性皮肤病变最常见于女性和有个人或家族炎症性皮肤疾病史的患者;病变与肠道疾病活动度无关。复发性和强烈的皮肤病变导致本研究中 34%的患者停止使用抗 TNF-α 药物。

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