【多发性肌炎后并发类风湿关节炎2例】。

Ryumachi. [Rheumatism] Pub Date : 2003-06-01
Tomoko Miyoshi, Yasuhiko Yoshinaga, Yusuke Ota
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引用次数: 0

摘要

我们报告两例风湿性关节炎(RA)谁后来发展后多发性肌炎(PM)。第一位患者为男性,64岁,10年前四肢近端肌肉无力。由于血清CK升高和肌电图的肌源性模式,他被诊断为PM,并通过皮质类固醇治疗改善了他的症状。2年前开始主诉多关节痛,随后出现间质性肺炎、胸膜炎和皮肤溃疡。患者因多发关节痛加重、多发皮下结节、皮肤出疹及发热而入院。血清CK在正常范围内,CRP升高,ch50降低。实验室检查冷球蛋白阳性,类风湿因子高滴度,抗jo 1抗体阴性。手部x线片显示双侧腕关节骨侵蚀。皮肤活检显示白细胞破裂性血管炎。根据这些发现,他被诊断为恶性类风湿性关节炎。经甲泼尼龙脉冲疗法、环磷酰胺和前列腺素e1治疗成功。第二例患者为77岁男性尘肺患者,4年前出现近四肢肌肉无力。根据他的临床和实验室检查结果,他被诊断为PM,并接受了暂时性皮质类固醇治疗。他从去年开始出现多发性关节痛,在接受肺结核治疗后,因关节痛加重而入院。血清CK因甲状腺功能减退轻微升高,CRP高升高。类风湿因子、冷球蛋白阳性,抗jo 1抗体阴性。手部x线片显示双侧腕关节骨侵蚀。膝关节内可见焦磷酸钙结晶。诊断为类风湿关节炎伴假性眩晕。经皮质类固醇、萨拉唑磺胺吡啶和抗结核治疗,症状得到缓解。这两个病例的临床特征从PM转变为明确的RA,并且都有肺部并发症。以前的报道描述了RA后PM的病例,大多数是由d -青霉胺等药物引起的,但PM后来发展为RA的病例极为罕见。RA和PM重叠的病例往往与肺部病变高度相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Two cases of rheumatoid arthritis developed after polymyositis].

We report two cases of rheumatoid arthritis (RA) who later had developed after polymyositis (PM). The first patient was 64-year old male who experienced muscular weakness of the four limbs in proximity 10 years ago. He was diagnosed as PM because of the elevated serum CK and the myogenic pattern of EMG, and his symptoms were improved by treatment with corticosteroid. He started to complain polyarthralgia 2 years ago, followed by interstitial pneumonia, pleuritis and skin ulcer. He was admitted because of exacerbated polyarthralgia, multiple subcutaneous nodules, skin eruption and fever. The level of serum CK was within normal range but CRP was elevated and CH 50 was decreased. The laboratory examination showed positive cryoglobulin and high titer of rheumatoid factor, but anti-Jo 1 antibody was negative. The hand X-ray showed bone erosions in bilateral wrist joints. Skin biopsy revealed leukocytoclastic vasculitis. Based on these findings, he was diagnosed as malignant RA. He was successfully treated with methylprednisolone pulse therapy, cyclophosphamide and prostaglandin E 1. The second patient was 77-year old male with pneumoconiosis who experienced muscular weakness of the four limbs in proximity 4 years ago. He was diagnosed as PM based on his clinical and laboratory findings and was treated with temporary corticosteroid. He started to have polyarthralgia last year, and he was admitted because of increasing arthralgia after the treatment of pulmonary tuberculosis. The level of serum CK was slightly elevated due to hypothyroidism, and CRP was highly elevated. Rheumatoid factor and cryoglobulin were positive, but anti-Jo 1 antibody was negative. The hand X-ray showed bone erosions in bilateral wrist joints. Crystals of pyrophosphate calcium was observed in knee joints. He was diagnosed as RA associate with pseudogout. His symptoms were relieved with corticosteroid, salazosulfapyridine and anti-tuberculous therapy. These two cases had altered their clinical features from PM to definite RA, and both had pulmonary complications. Previous reports described the cases of RA followed by PM, most of which were induced by such drugs as D-penicillamine, but the cases of PM who later had developed RA are extremely unusual. The overlapped cases of RA and PM tend to highly associate with pulmonary lesions.

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