Cavailhes A, Ingen-Housz-Oro S, Djennane S, Rafaa M, Fiszenson-Albala F, Weber N, Sigal-Grinberg M
Service de Dermatologie, Centre hospitalier Victor Dupouy, Argenteuil.
Ann Dermatol Venereol. 2007 Apr;134(4 Pt 1):363-7. doi: 10.1016/s0151-9638(07)89192-7.
Anti-TNFalpha drugs are used in certain rheumatologic and gastrointestinal inflammatory diseases and are also effective in cutaneous psoriasis. Several case reports have recently been published concerning induction of paradoxical psoriasis during the course of anti-TNF therapy. We report a new case involving infliximab used to treat Shulman fasciitis.
A 39-year-old woman was treated with infliximab for corticoid-dependent Shulman fasciitis. No personal or familial cutaneous psoriasis was noted in her history. Two months after the third infusion, she developed psoriasis vulgaris and pustular palmoplantar psoriasis which improved under topical corticosteroids. Her psoriatic lesions worsened one month after the first maintenance infusion. Since the Shulman fasciitis was not under control, infliximab was withdrawn and replaced with azathioprine. Six months later, her psoriasis was in remission and the Shulman fasciitis was under control.
TNFalpha plays an important role in the physiopathology of psoriasis through its action on inflammatory infiltrate, angiogenesis and keratinocyte proliferation. Several studies have reported the efficiency of TNFalpha inhibitors in moderate to severe cutaneous psoriasis. However, fourteen cases of induction or worsening of psoriasis have been reported with these drugs, suggesting a class effect. We report a new case of cutaneous psoriasis induced by infliximab in a patient presenting corticoid-dependent Shulman fasciitis, and we discuss the possible immunological mechanisms responsible for this paradoxical side effect. Other cutaneous lesions have been reported during treatment with TNFalpha inhibitors. The benefits of this treatment on the underlying inflammatory disease must be balanced against the potential cutaneous side effects when deciding whether to continue with anti-TNFalpha treatment.
抗TNFα药物用于某些风湿性和胃肠道炎性疾病，对皮肤银屑病也有效。最近有几篇病例报告发表，涉及抗TNF治疗过程中诱发矛盾性银屑病。我们报告1例使用英夫利昔单抗治疗舒尔曼筋膜炎引发的新病例。
一名39岁女性因皮质激素依赖型舒尔曼筋膜炎接受英夫利昔单抗治疗。其病史中无个人或家族性皮肤银屑病记录。第三次输注后两个月，她出现寻常型银屑病和掌跖脓疱型银屑病，局部使用皮质类固醇后病情改善。首次维持输注后1个月，她的银屑病皮损加重。由于舒尔曼筋膜炎未得到控制，停用英夫利昔单抗，换用硫唑嘌呤。6个月后，她的银屑病缓解，舒尔曼筋膜炎得到控制。
TNFα通过对炎症浸润、血管生成和角质形成细胞增殖的作用，在银屑病的病理生理过程中发挥重要作用。几项研究报告了TNFα抑制剂对中度至重度皮肤银屑病的疗效。然而，已有14例使用这些药物后诱发或加重银屑病的报告，提示存在类效应。我们报告1例由英夫利昔单抗诱发皮肤银屑病的新病例，该患者患有皮质激素依赖型舒尔曼筋膜炎，并讨论了导致这种矛盾性副作用的可能免疫机制。TNFα抑制剂治疗期间还报告了其他皮肤损害。在决定是否继续抗TNFα治疗时，必须权衡这种治疗对潜在炎性疾病的益处与潜在的皮肤副作用。
