Bodmer Michael, Egger Sabin S, Hohenstein Elisabeth, Beltraminelli Helmut, Krähenbühl Stephan
Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland.
Ann Pharmacother. 2006 Sep;40(9):1688-90. doi: 10.1345/aph.1H094. Epub 2006 Aug 8.
To report a case of lichenoid drug eruption (LDE) after starting antihypertensive treatment with nebivolol, a cardioselective beta-blocker.
Five weeks after starting treatment with nebivolol, a 62-year-old woman presented with erythematous papules on both extremities and skin lesions spreading over the back. She was not being treated with any other drugs. Because the administration of levocetirizine, topical methylprednisolone, and systemic prednisone was unsuccessful, the treatment was stopped and the lesions were biopsied. The histopathological features of the lesions were consistent with LDE. After withdrawal of nebivolol and subsequent readministration of topical methylprednisolone and systemic prednisone, the skin lesions resolved within 12 days. Assessment of the causality revealed a probable relationship between nebivolol and the lichenoid eruptions.
Although beta-blockers can be associated with LDE, as of July 7, 2006, this has not been previously reported with nebivolol. T cells invading the dermis are considered to be responsible for epidermal destruction associated with LDE, as has been described for lichenoid forms of chronic graft versus host disease and idiopathic lichen ruber planus.
Nebivolol can cause LDE, as has been reported with other beta-blockers. The underlying mechanism appears to be T cell-mediated. Cross-reactivity with other beta-blockers cannot be excluded; therefore, the risk of recurrent LDE should be weighed carefully against the clinical benefit before switching to another beta-blocker.
报告一例在开始使用心脏选择性β受体阻滞剂奈必洛尔进行抗高血压治疗后发生苔藓样药疹（LDE）的病例。
一名62岁女性在开始使用奈必洛尔治疗五周后，双下肢出现红斑丘疹，背部皮肤损害蔓延。她未使用任何其他药物。由于给予左西替利嗪、外用甲基泼尼松龙和全身性泼尼松治疗均未成功，遂停止治疗并对皮损进行活检。皮损的组织病理学特征与LDE一致。停用奈必洛尔并随后重新给予外用甲基泼尼松龙和全身性泼尼松后，皮肤损害在12天内消退。因果关系评估显示奈必洛尔与苔藓样皮疹之间可能存在关联。
尽管β受体阻滞剂可与LDE相关，但截至2006年7月7日，此前尚未有奈必洛尔相关的报道。侵入真皮的T细胞被认为是与LDE相关的表皮破坏的原因，这在慢性移植物抗宿主病和特发性扁平苔藓的苔藓样形式中已有描述。
奈必洛尔可导致LDE，其他β受体阻滞剂也有相关报道。潜在机制似乎是T细胞介导的。不能排除与其他β受体阻滞剂的交叉反应；因此，在换用另一种β受体阻滞剂之前，应仔细权衡复发性LDE的风险与临床益处。
