Allergy/Dermatology Unit, Department of Internal Medicine, Kantonsspital Winterthur, Winterthur, Switzerland.
Department of Dermatology, Bellinzona Regional Hospital, Bellinzona, Switzerland.
Clin Rev Allergy Immunol. 2018 Feb;54(1):177-184. doi: 10.1007/s12016-017-8667-7.
Recognition and timely adequate treatment of erythema multiforme remain a major challenge. In this review, current diagnostic guidelines, potential pitfalls, and modern/novel treatment options are summarized with the aim to help clinicians with diagnostic and therapeutic decision-making. The diagnosis of erythema multiforme, that has an acute, self-limiting course, is based on its typical clinical picture of targetoid erythematous lesions with predominant acral localization as well as histological findings. Clinically, erythema multiforme can be differentiated into isolated cutaneous and combined mucocutaneous forms. Atypical erythema multiforme manifestations include lichenoid or granulomatous lesions as well as lesional infiltrates of T cell lymphoma and histiocytes. Herpes simplex virus infection being the most common cause, other infectious agents like-especially in children-Mycoplasma pneumoniae, hepatitis C virus, Coxsackie virus, and Epstein Barr virus may also trigger erythema multiforme. The second most frequently identified cause of erythema multiforme is drugs. In different studies, e.g., allopurinol, phenobarbital, phenytoin, valproic acid, antibacterial sulfonamides, penicillins, erythromycin, nitrofurantoin, tetracyclines, chlormezanone, acetylsalicylic acid, statins, as well as different TNF-α inhibitors such as adalimumab, infliximab, and etanercept were reported as possible implicated drugs. Recently, cases of erythema multiforme associated with vaccination, immunotherapy for melanoma, and even with topical drugs like imiquimod have been described. In patients with recurrent herpes simplex virus-associated erythema multiforme, the topical prophylactic treatment with acyclovir does not seem to prevent further episodes of erythema multiforme. In case of resistance to one virostatic drug, the switch to an alternative drug, and in patients non-responsive to virostatic agents, the use of dapsone as well as new treatment options, e.g., JAK-inhibitors or apremilast, might be considered.
识别和及时充分的治疗多形红斑仍然是一个主要挑战。在这篇综述中，总结了当前的诊断指南、潜在的陷阱以及现代/新型治疗选择，旨在帮助临床医生进行诊断和治疗决策。具有急性、自限性病程的多形红斑的诊断基于其典型的临床表现，即靶形红斑性病变，主要位于四肢，以及组织学发现。临床上，多形红斑可分为孤立性皮肤和联合黏膜形式。不典型多形红斑表现包括苔藓样或肉芽肿样病变以及 T 细胞淋巴瘤和组织细胞的病变浸润。单纯疱疹病毒感染是最常见的原因，其他感染因子，如支原体肺炎、丙型肝炎病毒、柯萨奇病毒和爱泼斯坦-巴尔病毒，也可能引发多形红斑。多形红斑的第二大常见原因是药物。在不同的研究中，例如别嘌醇、苯巴比妥、苯妥英、丙戊酸、抗菌磺胺类药物、青霉素类、红霉素、呋喃妥因、四环素类、氯美扎酮、乙酰水杨酸、他汀类药物以及不同的 TNF-α 抑制剂，如阿达木单抗、英夫利昔单抗和依那西普等，都被报道为可能的相关药物。最近，多形红斑与疫苗接种、黑色素瘤免疫治疗，甚至与咪喹莫特等局部药物相关的病例已有描述。在复发性单纯疱疹病毒相关多形红斑患者中，阿昔洛韦的局部预防性治疗似乎并不能预防多形红斑的进一步发作。对于一种抗病毒药物耐药的患者，可以换用另一种药物，对于抗病毒药物无反应的患者，可以使用氨苯砜以及新的治疗选择，如 JAK 抑制剂或阿普米司特。
