Christopher-Stine Lisa, Plotz Paul H
Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Curr Opin Rheumatol. 2004 Nov;16(6):700-6. doi: 10.1097/01.bor.0000141925.21941.d8.
The etiology and much about the pathogenesis of the inflammatory myopathies remain a mystery. In this review, we investigate recent research efforts to understand the pathogenesis of the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM), diseases that result from interactions between environmental risk factors and genetic susceptibility.
Over the past year, there has been considerable progress toward better understanding of IBM, with relatively few developments toward understanding PM and DM. Although these diseases may share some common clinical phenotypic and serologic components, they differ on a molecular and cellular level.
The need for definitive, safer therapies in these diseases makes vital the search for defining detailed pathogenesis of inflammation and muscle fiber damage at the molecular level.
炎性肌病的病因及许多发病机制仍不明晰。在本综述中，我们探讨了近期为理解多发性肌炎（PM）、皮肌炎（DM）和包涵体肌炎（IBM）等不同类型疾病的发病机制所做的研究工作，这些疾病是环境危险因素与遗传易感性相互作用的结果。
在过去一年里，对IBM的理解取得了显著进展，而对PM和DM的认识进展相对较少。尽管这些疾病可能有一些共同的临床表型和血清学特征，但它们在分子和细胞水平上存在差异。
这些疾病需要明确、更安全的治疗方法，因此在分子水平上探寻炎症和肌纤维损伤的确切发病机制至关重要。
