Department of Pharmacology and Therapeutics, Faculty of Medicine of the University of Porto, Porto, Portugal.
Dermatology and Venereology Service, São João Hospital Center, EPE, Porto, Portugal.
Int J Dermatol. 2018 Dec;57(12):1521-1532. doi: 10.1111/ijd.14072. Epub 2018 Jul 20.
Tumor necrosis factor alpha inhibitors (anti-TNF-α) completely revolutionized the treatment of inflammatory bowel disease (IBD). However, anti-TNF-α-induced cutaneous side effects have been increasingly reported in the literature. Particularly, psoriasis and the recently recognized psoriasiform lesions are of particular concern, as anti-TNF-α agents are also used in the treatment of psoriasis, seemingly reflecting an immunological paradox. The clinical management of these cutaneous lesions is particularly challenging, owing to the potential need of anti-TNF-α discontinuation and scarcity of other therapeutic options. Therefore, optimization of current topical and systemic therapies and incorporation of new therapeutic agents is of great interest. Our aim is to review data in the literature regarding the clinical management of these cutaneous lesions and provide a therapeutic algorithm, supported by our experience as a tertiary referral center for IBD. Although in older reports no distinction was made, anti-TNF-α-induced psoriasiform lesions are not only more prevalent but also bear notable differences from classical psoriasis, possibly reflecting a different nosological entity. Onset of lesions has been related to periods of IBD remission, as supported by low levels of fecal calprotectin. Psoriasiform lesions can be adequately managed either by topical (glucocorticoids, calcineurin inhibitors, and antibiotics) or systemic (phototherapy, acitretin, glucocorticoids, and antibiotics) therapies and/or switch to other anti-TNF-α agents. Data referring to patients who were able to continue on the same IBD therapy ranged from 30.7 to 100%, reinforcing the importance of an adequate control of these lesions. The recently approved ustekinumab offers another step in the management of anti-TNF-α-intolerant patients.
肿瘤坏死因子-α 抑制剂(抗 TNF-α)彻底改变了炎症性肠病(IBD)的治疗方法。然而,抗 TNF-α 诱导的皮肤副作用在文献中越来越多地被报道。特别是银屑病和最近被认识到的银屑病样病变特别令人关注,因为抗 TNF-α 药物也被用于银屑病的治疗,这似乎反映了一种免疫悖论。这些皮肤病变的临床管理具有特别大的挑战性,因为可能需要停止使用抗 TNF-α,并且其他治疗选择稀缺。因此,优化当前的局部和全身治疗方法并引入新的治疗药物非常重要。我们的目的是回顾文献中关于这些皮肤病变的临床管理的数据,并提供一个治疗算法,该算法由我们作为 IBD 三级转诊中心的经验支持。尽管在早期的报告中没有区别,但抗 TNF-α 诱导的银屑病样病变不仅更为普遍,而且与经典银屑病有显著差异,这可能反映了一种不同的分类实体。病变的发生与 IBD 缓解期有关,这得到粪便钙卫蛋白水平低的支持。银屑病样病变可以通过局部(糖皮质激素、钙调神经磷酸酶抑制剂和抗生素)或全身(光疗、阿维 A、糖皮质激素和抗生素)治疗以及/或改用其他抗 TNF-α 药物来进行充分管理。关于能够继续接受相同 IBD 治疗的患者的数据范围为 30.7%至 100%,这强调了充分控制这些病变的重要性。最近批准的乌司奴单抗为治疗抗 TNF-α不耐受患者提供了另一种方法。