HEMOSIDERIN DEPOSITION IN INTRAHEPATIC SMALL VESSELS IN CHRONIC HEPATITIS C : PATHOLOGICAL SIGNIFICANCE AND ITS PREDICTING ROLE IN RESPONSE TO INTERFERON

我们在慢性丙型肝炎患者中发现了一种特殊的肝内小血管含铁血黄素沉着症，这种病变与慢性丙型肝炎的进展(纤维化)密切相关，但与肝炎的活动性无关。罕见的是，这种病变也见于其他形式的慢性肝病和晚期肝病，如原发性胆汁性肝硬变和自身免疫性肝炎。患有这种病变的患者有抵抗干扰素治疗的倾向，这表明这种病变是一种组织学标志，代表了对这种治疗的不良反应。病理上，这种损害可能是由于肝炎病毒感染引起的肝髓损伤过程中肝门周围区肝细胞溶解的含铁物质(S)渗漏所致。这种损害可能会影响内皮细胞的抗原提呈能力和其他固有的免疫功能，因为这种损害伴随着HLAI类和HLAII类分子以及其他黏附分子的表达，如ICAM-1和VCAM-1。然而，这可能有利于慢性丙型肝炎的病毒增殖，因为铁被认为是丙型肝炎病毒增殖的关键元素。肝脏小血管内皮细胞的功能，特别是它们在晚期肝病中的功能尚不清楚。这项研究将为了解该内皮细胞节段的病理生理功能提供线索。

We found out a peculiar hemosiderosis involving intrahepatic small vessels in portal tracts in chronic hepatitis C.This lesion is closely related to the advancement (fibrosis) of chronic hepatitis C,but not to hepatitis activity. Infrequently, this lesion was also encountered in other forms of chronic liver diseases with advanced liver diseases such as primary biliary cirrhosis and autoimmune hepatitis. The patients with this lesion have a tendency to resist interferon therapy, suggesting that this lesion is a histologic marker representing poor response to this therapy. Pathogenetically, this lesion might have been caused by leakage of iron-containing substance (s) from the hepatocytolysis of periportal regions during hepatocullelar damages due to hepatitis viral infeciton. This lesion may influence the capacity of antigen presentation and other immunological functions inherent to endothelial cells, because this lesions accompany with expression of HLA-class I and HLA-class II and also other adhesion molecules such as ICAM-1 and VCAM-1. However, this could be beneficial for viral proliferation in chronic hepatitis C,because iron is said to an essential element in proliferation of HCV.The fuction of endothelial cells of small vessels in the liver, particularly their functions in advancedliver diseases, remains unclear. This study will geve a clue to understanding of the pathophysiologic fuction of this endothelial segement.