Development of psoriasis after B cell depletion with rituximab
Development of psoriasis after B cell depletion with rituximab
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DOI：
10.1002/art.22811
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发表时间：
2007-08-01
影响因子：
--
通讯作者：
Emery, Paul
中科院分区：
文献类型：
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作者：
Dass, Shouvik;Vital, Edward M.;Emery, Paul
去除B细胞的单克隆抗体利妥昔单抗（rituximab）是一种治疗风湿性疾病的新型药物，其安全性和有效性的证据越来越多。然而，其在自身抗体阴性疾病中的潜在用途和影响存在不确定性。我们描述了3例患者，没有已知的银屑病危险因素，谁开发银屑病（和我谁也开发银屑病关节炎的功能）后，接受利妥昔单抗的各种适应症，即血清阳性和血清阴性类风湿性关节炎和系统性红斑狼疮。在所有病例中，基础疾病对利妥昔单抗反应良好。利妥昔单抗的这种可能的副作用的解释仍然不清楚，但B细胞耗尽的环境可能诱导异常的T细胞应答，可能由亚临床感染或由B细胞调节T细胞的机制的去除引起。这些病例表明银屑病的发病机制可能不需要正常数量的B细胞，并且建议用利妥昔单抗治疗银屑病和银屑病关节炎可能导致不可预测的反应。
The B cell-depleting monoclonal antibody rituximab is a novel therapy for the rheumatic diseases, with an increasing body of evidence regarding its safety and efficacy in an expanding range of indications. However, there is uncertainty over its potential use in, and impact on, autoantibody-negative diseases. We describe 3 patients, with no known risk factor for psoriasis, who developed psoriasis (and I who also developed features of psoriatic arthritis) after receiving rituximab for a variety of indications, namely, seropositive and seronegative rheumatoid arthritis and systemic lupus erythematosus. In all cases, the underlying disease responded well to rituximab. The interpretation of this possible side effect of rituximab remains unclear, but a B cell-depleted environment may induce abnormal T cell responses, possibly provoked either by subclinical infection or by the removal of mechanisms whereby B cells regulate T cells. These cases suggest that the pathogenesis of psoriasis may not require normal numbers of B cells and that proposed treatment of psoriasis and psoriatic arthritis with rituximab may result in unpredictable responses.