Le Bidre E, Chaby G, Martin L, Perrussel M, Sassolas B, Sigal M-L, Kaassis C, Lespessailles E, Nseir A, Estève E
Service de dermatologie, hôpital Porte-Madeleine, CHR d'Orléans, France.
Ann Dermatol Venereol. 2011;138(4):285-93. doi: 10.1016/j.annder.2011.01.047. Epub 2011 Mar 27.
In recent years, a growing number of biological agents have been introduced for the treatment of various diseases, and their principal adverse events are known. We present nine cases of alopecia areata (AA) developed in patients treated with TNF-α blocking agents.
Nine cases are described: five men and four women of mean age 39.2 years (range: 29-54 years). Two patients had a past history of alopecia areata. The anti-TNF given was adalimumab (Humira(®)) in eight cases and etanercept (Enbrel(®)) in one case. The time lapse to development of AA following introduction of the anti-TNF alpha agent was between six weeks and eight months (mean: 4.2 months). There were five cases of patchy AA and four of AA universalis. Anti-TNF alpha treatment was stopped in all patients. Complete regrowth was seen in five patients. Two patients showed no improvement. In two patients, partial hair regrowth (<50%) was seen after systemic corticosteroid therapy and methotrexate.
Our nine cases of alopecia areata developed in patients treated with TNF-α blockers constitute the largest series reported to our knowledge. 17 cases of AA during anti-TNF-alpha therapy have previously been described in the literature. AA may be a side effect of anti-TNF-alpha drugs. In our patients, no conclusive triggers could be associated with the development of AA, except a context of stress in four patients. Complete regrowth in three patients after discontinuation of the anti-TNF-alpha (without other therapy) is an additional argument in favour of the implication of biotherapies. However, a random coincidence of AA with anti-TNF-alpha cannot be completely ruled out. The role of anti-TNF-alpha therapy in the pathogenesis of AA is poorly understood. Activation of self-reactive T cells by anti-TNF-alpha could lead to the development of AA.
近年来,越来越多的生物制剂被用于治疗各种疾病,其主要不良事件已为人所知。我们报告了9例在用肿瘤坏死因子-α(TNF-α)阻断剂治疗的患者中发生斑秃(AA)的病例。
描述了9例病例:5名男性和4名女性,平均年龄39.2岁(范围:29 - 54岁)。2例患者有斑秃既往史。使用的抗TNF药物中,8例为阿达木单抗(修美乐(®)),1例为依那西普(恩利(®))。在引入抗TNF-α药物后出现AA的时间间隔为6周至8个月(平均:4.2个月)。有5例为斑秃,4例为全秃。所有患者均停用抗TNF-α治疗。5例患者毛发完全再生。2例患者无改善。2例患者在接受全身皮质类固醇治疗和甲氨蝶呤后出现部分毛发再生(<50%)。
据我们所知,我们报告的这9例在用TNF-α阻断剂治疗的患者中发生斑秃的病例是最大的系列病例。此前文献中曾描述过17例在抗TNF-α治疗期间发生AA的病例。AA可能是抗TNF-α药物的一种副作用。在我们的患者中,除了4例患者存在应激情况外,没有确凿的触发因素与AA的发生相关。3例患者在停用抗TNF-α(无其他治疗)后毛发完全再生,这进一步支持了生物疗法与之有关的观点。然而,不能完全排除AA与抗TNF-α治疗随机巧合的可能性。抗TNF-α治疗在AA发病机制中的作用尚不清楚。抗TNF-α激活自身反应性T细胞可能导致AA的发生。