著者

吉田 秀 遠藤 平仁 西 正大 飯塚 進子 木村 美保 田中 住明 石川 章 近藤 啓文

出版者

一般社団法人 日本臨床リウマチ学会

雑誌

臨床リウマチ (ISSN:09148760)

巻号頁・発行日

vol.18, no.3, pp.225-231, 2006-09-30 (Released:2016-12-30)

参考文献数

16

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Tattoo sarcoidosis is a rare clinical entity that shows a sarcoidosis like granuloma developing from tattoo skin and clinical symptoms of systemic sarcoidosis after long term courses of tattoos. Hypersensitivity reaction for metal included in a pigment of tattoo pigment may assume to be the cause of tattoo sarcoidosis. A man aged 20s developed symptoms similar to those of systemic sarcoidosis after receiving a multicolored tattoo covering the skin of his entire body. He put a tattoo (red, green, black, gray, yellow and gray) over his entire body 10 years ago. There were severely painful subcutaneous masses about 1 cm in size on a brown and green tattoo on back and lower extremities. A biopsy of the part of the nodule showed a foreign body granuloma containing multinuclear giant cells. Photophobia and decreased visual acuity developed afterwards, and he was diagnosed with bilateral iritis. In addition, hilar lymphadenopathy was founded in a chest X-ray and CT, persistent fever also showed. We diagnosed it as sarcoid reaction by the tattoo because of skin epithelioid granuloma, iritis, and bilateral hilar lympadenopathy in CT. After hospitalization, his eyes were injected with dexamethazone and he took oral prednisolone 40 mg/day for iritis. Severe iritis was not improved by administration of only steroids and improved in combinating azathioprine. We report this as the interesting case that showed a sarcoidosis like reaction to the pigment of a tattoo.

著者

吉田 秀 遠藤 平仁 田中 淳一 飯塚 進子 木村 美保 橋本 篤 田中 住明 石川 章 廣畑 俊成 近藤 啓文

出版者

一般社団法人 日本臨床リウマチ学会

雑誌

臨床リウマチ (ISSN:09148760)

巻号頁・発行日

vol.20, no.4, pp.302-309, 2008-12-30 (Released:2016-11-30)

参考文献数

26

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A woman of 50 years of age who had a 13-year history of hypothyroidism was diagnosed with systemic lupus erythematosus (SLE) with butterfly rash, leukopenia, positivity of antinuclear antibody, anti-DNA antibody and anti-Sm antibody. Two years later, she developed nephritis (WHO type IV) and remitted with corticosteroid pulse and intermittent intravenous cyclophosphamide pulse therapy (IVCY). Four years after the onset of SLE, she relapsed with proteinuria and leukopenia when she was taking 9 mg/day of prednisolone (PSL) but she stopped all the medication of her own accord. Four months passed without any therapy, she was admitted to our hospital with disturbance of consciousness and anasarca. Laboratory findings showed pancytopenia (WBC 1300/μl, RBC 233×10⁴/μl, Hb6.9g/dl, Plt3.6×10⁴/μl), aggravation of lupus nephritis and hypothyroidism. Chest X-ray and ultrasonography demonstrated pleural and pericardial effusion and the absence of hepatosplenomegaly. She was also diagnosed with myelofibrosis upon bone marrow inspection. Three instances of corticosteroid pulse therapy, oral corticosteroid (PSL was tapered from 50 mg/day) and supplement therapy of levothyroxine improved every symptom and pancytopenia. The second bone marrow biopsy showed reduced fibrosis and recovery of bone marrow cells. These findings implied the secondary myelofibrosis caused by SLE because the myelofibrosis came along with aggravation of SLE and corticosteroid therapy was effective. This is a rare case of SLE in which myelofibrosis improved by high-dose corticosteroid therapy, which was confirmed by bone marrow biopsy and suggests the pathogenic mechanisms for myelofibrosis.