首页> 外文期刊>Forensic science international >Alcoholic cardiomyopathy versus chronic myocarditis-immunohistological investigations with LCA, CD3, CD68 and tenascin.
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Alcoholic cardiomyopathy versus chronic myocarditis-immunohistological investigations with LCA, CD3, CD68 and tenascin.

机译:酒精性心肌病与慢性心肌炎的免疫组织学研究,使用LCA,CD3,CD68和腱生蛋白。

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摘要

Dilated cardiomyopathy (DCM) is a disorder of unknown aetiology characterized by the left ventricular cavity enlargement and wall thinning associated with reduced left ventricular wall motion. DCM in chronic alcoholics is supposed to be caused by alcohol induced myocardial damage (alcoholic cardiomyopathy). Nevertheless, cardiotropic viruses, such as enteroviruses have long been suspected as causative agents for at least some forms of DCM. In the present study, 13 cases of DCM in chronic alcoholics were investigated with qualification and quantification of infiltrating leucocytes using immunohistological antibodies against leucocyte common antigen (LCA), T-lymphocytes (CD3) and macrophages (CD68). In addition, the expression of tenascin, playing a role in the initiation of fibrotic changes, was examined. All antigens were known to be possibly enhanced in cases of chronic myocarditis. Using these immunohistological techniques, 2 out of 13 cases had evidence for chronic inflammatory myocardial alterations in the sense of lymphocytic infiltrates (>2.0 CD3 T-lymphocytes/visual field at 400x (HPF); >7 CD3 T-lymphocytes per mm(2)). These cases were diagnosed as having inflammatory cardiomyopathy. The other cases without myocardial inflammation were diagnosed as idiopathic/alcoholic DCM.
机译:扩张型心肌病(DCM)是一种病因不明的疾病,其特征在于左心室扩大和壁变薄与左心室壁运动减少有关。慢性酒精中毒患者中的DCM可能是由酒精引起的心肌损害(酒精性心肌病)引起的。然而,长期以来人们一直怀疑向心性病毒,例如肠病毒是至少某些形式的DCM的病原体。在本研究中,使用针对白细胞共同抗原(LCA),T淋巴细胞(CD3)和巨噬细胞(CD68)的免疫组织学抗体,对13例慢性酒精中毒患者的DCM进行了浸润白细胞的鉴定和定量研究。此外,检查了肌腱蛋白的表达,其在纤维化变化的启动中起作用。已知在慢性心肌炎的情况下所有抗原都可能增强。使用这些免疫组织学技术,在13例患者中有2例有证据表明存在淋巴细胞浸润的慢性炎症性心肌改变(400 x(HPF)时大于2.0 CD3 T淋巴细胞/视野;每mm> 7 CD3 T淋巴细胞(2) )。这些病例被诊断为患有炎症性心肌病。其他无心肌炎症的病例被诊断为特发性/酒精性DCM。

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