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丙硫氧嘧啶诱发的抗中性粒细胞胞浆抗体及粒细胞缺乏症与粒细胞集落刺激因子共同导致了1例格雷夫斯病患者出现Sweet综合征。

Propylthiouracil-induced anti-neutrophil cytoplasmic antibodies and agranulocytosis together with granulocyte colony-stimulating factor induced Sweet's syndrome in a patient with Graves' disease.

作者信息

Ozlem Celik, Deram Buyuktas, Mustafa Sevinc, Koray Tascilar, Cuyan Demirkesen, Ertugrul Tasan

机构信息

Division of Endocrinology and Metabolism, Department of Internal Medicine, Cerrahpasa Medical School, University of Istanbul, Turkey.

出版信息

Intern Med. 2011;50(18):1973-6. doi: 10.2169/internalmedicine.50.4483. Epub 2011 Sep 15.

Abstract

Propylthiouracil (PTU) is an antithyroid drug which is known to cause drug-induced vasculitis. PTU is implicated in 80-90% of cases of anti-neutrophil cytoplasm circulating antibody (ANCA)-associated vasculitis caused by anti-thyroid drugs which induce ANCA production. Sweet's syndrome is characterized by fever, leucocytosis, neutrophilia and the sudden onset of painful skin lesions. The pathology of the disease is still unclear. Cytokine dysregulation including interleukin-6 and endogenous granulocyte colony-stimulating factor (G-CSF) are thought to play a role in the pathogenesis of Sweet's syndrome. PTU and G-CSF are known to cause Sweet's syndrome and other neutrophilic dermatosis. The presence of ANCA can have a diagnostic value in Sweet's syndrome. Systemic corticosteroids are the first-line therapy for both diseases. Here we report a female patient with Graves' disease who developed ANCA and Sweet's syndrome after using PTU and G-CSF.

摘要

丙硫氧嘧啶(PTU)是一种抗甲状腺药物,已知可引起药物性血管炎。在由诱导抗中性粒细胞胞浆循环抗体(ANCA)产生的抗甲状腺药物引起的ANCA相关性血管炎病例中,80%-90%与PTU有关。Sweet综合征的特征为发热、白细胞增多、中性粒细胞增多以及疼痛性皮肤病变的突然发作。该病的病理仍不清楚。包括白细胞介素-6和内源性粒细胞集落刺激因子(G-CSF)在内的细胞因子失调被认为在Sweet综合征的发病机制中起作用。已知PTU和G-CSF可引起Sweet综合征和其他嗜中性皮病。ANCA的存在对Sweet综合征具有诊断价值。全身用皮质类固醇是这两种疾病的一线治疗方法。在此,我们报告一名患有格雷夫斯病的女性患者,在使用PTU和G-CSF后出现了ANCA和Sweet综合征。

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