Silicon exposure and vasculitis
Silicon exposure and vasculitis
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DOI：
10.1097/00002281-199801000-00003
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发表时间：
1998-01-01
影响因子：
5.1
通讯作者：
Kallenberg, Coes G. M.
中科院分区：
文献类型：
--
作者：
Tervaert, Jan Willem Cohen;Stegeman, Coen A.;Kallenberg, Coes G. M.
多种危险因素共同影响着原发性或继发性血管炎的易感性。大多数形式的血管炎可能是由基因引起的，但由环境引发。这篇综述讨论了目前可用的证据，一个可能的环境触发，二氧化硅的病理生理作用。自1960年以来，一些肺矽肺患者被描述为缺乏免疫坏死性新月形肾小球肾炎，即免疫荧光结果完全阴性或沿毛细血管壁有非特异性颗粒状IgM或C3沉积。最近有报道称，这些患者有抗中性粒细胞胞浆抗体（ANCAs），在大多数情况下针对髓过氧化物酶。此外，肺矽肺患者可能出现显微镜下的多血管炎、肺出血和肾炎综合征或韦格纳肉芽肿病。为了进一步证实硅暴露与肾衰竭或血管炎之间的关系，已经报道了几项病例对照研究。研究发现，接触含硅化合物与慢性肾衰竭（比值比为1.7:2.5）或血管炎（比值比为6.5:14.0）有关。二氧化硅诱导anca相关肾小球肾炎或血管炎的机制尚不清楚。含硅化合物对免疫应答有明显的辅助作用，二氧化硅颗粒是淋巴细胞、单核细胞或巨噬细胞的有效刺激物。此外，二氧化硅可能诱导单核细胞或巨噬细胞以及可能的中性粒细胞凋亡。总之，目前有充分的证据表明，职业暴露于含硅化合物与anca相关的肾小球肾炎和血管炎的发展有关，而二氧化硅是这些疾病的第一个充分记录的环境触发因素之一。
A combination of risk factors are involved in susceptibility to a primary or secondary form of vasculitis. Most forms of vasculitis are probably genetically based but environmentally triggered. This review discusses currently available evidence for a pathophysiologic role of one possible environmental trigger, silica. Since 1960, several patients with pulmonary silicosis have been described that developed pauci-immune necrotizing crescentic glomerulonephritis, ie, with either completely negative immunofluorescence findings or nonspecific granular IgM or C3 deposits along the capillary wall. Recently it was reported that these patients have antineutrophil cytoplasmic antibodies (ANCAs) that are in most cases directed to myeloperoxidase. Further, patients with pulmonary silicosis may develop microscopic polyangiitis, the syndrome of lung hemorrhage and nephritis, or Wegener's granulomatosis. To further substantiate the relation between silicon exposure and renal failure or vasculitis, several case-control studies have been reported. Exposure to silicon-containing compounds was found to be related to chronic renal failure (odds ratio, 1.7: 2.5) or vasculitis (odds ratio, 6.5: 14.0). The mechanisms by which silica may induce ANCA-associated glomerulonephritis or vasculitis are not well known. Silicon-containing compounds have a pronounced adjuvant effect on immune responses, and silica particles are potent stimulators of lymphocytes and monocytes or macrophages. Further, silica may induce apoptosis of monocytes or macrophages and possibly neutrophils. In conclusion, at present there is ample evidence that occupational exposure to silicon-containing compounds is related to the development of ANCA-associated glomerulonephritis and vasculitis, and silica is one of the first well-documented environmental triggers in these diseases.