Clinical images: Hydroxychloroquine-associated mucocutaneous hyperpigmentation.
Clinical images: Hydroxychloroquine-associated mucocutaneous hyperpigmentation.
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临床图像：羟氯喹相关的皮肤粘膜色素沉着过度。
DOI：
10.1002/art.10278
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发表时间：
2002
影响因子：
--
通讯作者：
Richard A. Bernert
中科院分区：
文献类型：
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作者：
David G. True;L. Bryant;Mark D. Harris;Richard A. Bernert
我们饶有兴趣地阅读了Charles等人关于肿瘤坏死因子（TNF）阻断与抗双链DNA（抗dsDNA）和系统性红斑狼疮（SLE）样综合征诱导之间可能的关系的文章（1）。本文描述了一位抗肿瘤坏死因子α治疗后出现肾病综合征的患者，该患者在1982年被诊断为类风湿因子阳性、抗核抗体（ANA）阴性的糜烂性类风湿关节炎（RA），但没有抗dsDNA抗体或SLE体征。诊断后不久，患者接受D-青霉胺治疗，然后接受肠外金硫葡萄糖治疗。1984年因蛋白尿（至1.5 gm/l）而停止。停止这种治疗后，蛋白尿完全消失。继续使用缓解病情的抗风湿药物（DMARD）治疗，这次使用甲氨蝶呤，随后再次使用金硫葡萄糖。蛋白尿在第二次金疗法中没有发生，在接下来的几年中也没有发生。此后，他接受了一系列DMARD治疗，没有临床疗效。
We read with interest the article by Charles et al concerning the possible relationship between tumor necrosis factor (TNF) blockade and the induction of anti–doublestranded DNA (anti-dsDNA) and systemic lupus erythematosus (SLE)–like syndromes (1). Herein we describe a patient who developed a nephrotic syndrome as an adverse effect of treatment with anti-TNFα, without the presence of antidsDNA or signs of SLE.The patient was diagnosed in 1982 as having rheumatoid factor–positive, antinuclear antibody (ANA)–negative erosive rheumatoid arthritis (RA). Shortly after diagnosis he was treated with D-penicillamine and then with parenteral aurothioglucose. This was stopped in 1984 because of proteinuria (to 1.5 gm/liter). After cessation of this therapy, the proteinuria completely disappeared. Disease-modifying antirheumatic drug (DMARD) therapy was continued, this time with methotrexate, followed again by aurothioglucose. Proteinuria did not develop during this second episode of gold therapy, nor did it occur during the next several years. Thereafter he was treated with a succession of DMARDs, without clinical efficacy.