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

慢性丙型肝炎肝内小血管中含铁血黄素沉积：病理学意义及其对干扰素反应的预测作用

• 批准号: 08670198
• 负责人: NAKANUMA Yasuni
• 金额: $ 1.34万
• 依托单位: KANAZAWA UNIVERSITY SCHOOL OF MEDICINE
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08670198/
• 关键词: chronic hepatitis C; hemosiderin; cell injury; HCV; interferon; HBV; intrahepatic small vessels; inflammatory cells; 細胞接着因子; 肝細胞

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.

我们发现了一种特殊的含铁血黄素沉着症，涉及肝内小血管在门脉束在慢性丙型肝炎。这种病变是密切相关的进展（纤维化）的慢性丙型肝炎，但没有肝炎活动。很少，这种病变也遇到了其他形式的慢性肝病与先进的肝脏疾病，如原发性胆汁性肝硬化和自身免疫性肝炎。有此病变的患者有抵抗干扰素治疗的倾向，这表明此病变是一个组织学标志，代表对这种治疗的反应差。从病理学上讲，这种病变可能是由于肝炎病毒感染引起肝细胞损伤时，门脉周围肝细胞溶解，导致含铁物质渗漏所致。这种病变可能影响抗原呈递的能力和内皮细胞固有的其他免疫功能，因为这种病变伴随着HLA-I类和HLA-II类以及其他粘附分子如ICAM-1和VCAM-1的表达。然而，这可能有利于慢性丙型肝炎病毒的增殖，因为铁被认为是HCV增殖的必需元素。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。本研究为进一步了解这一内皮段的病理生理功能提供了线索。

项目成果

M.Hoso,Y.Nakanuma: "Granulomafous cholangitis in chronic hepatitis C : A new dragnostic problem in liver pathology" Pathology International. 46・3. 301-305 (1996)

M.Hoso，Y.Nakanuma：“慢性丙型肝炎中的肉芽肿性胆管炎：肝脏病理学中的一个新的严重问题”《病理学国际》46·3（1996）。

K.Kaji, Y.Nakanuma: "Hemosiderin deposition in portal endothelial cells is a histologic markar predicting poor response to interferon-α therapy in chronic hepatitis C" Pathology Fnternational. 47(6). 347-352 (1997)

K.Kaji，Y.Nakanuma：“门脉内皮细胞中的含铁血黄素沉积是预测慢性丙型肝炎对干扰素-α 治疗反应不佳的组织学标志”，病理学国际杂志 47(6) (1997)。

Y.Nakanuma,et al: "Histopathology of the liver in non-cirrhotic portal hypertension of unknour etiology" Histopathology. 28・1. 195-204 (1996)

Y. Nakanuma 等人：“未知病因的非肝硬化门静脉高压症的肝脏组织病理学”组织病理学 28・1（1996）。

Kaji K,Nakanuma Y.: "Dendtritic cells in portal tracts in chronic hepatitis C with relevance to bile duct damage" Hepatology Res. 8 (1). 1-12 (1997)

Kaji K，Nakanuma Y.：“慢性丙型肝炎门静脉中的树突状细胞与胆管损伤相关”肝病学研究。

M.Sasaki,Y.Nakanuma: "Characterization of apomacin expresion in intrahepatic cholangrocarcinowas and their preursor lesious" Hepafology. 24・5. (1996)

M.Sasaki，Y.Nakanuma：“肝内胆管癌及其前体病变中阿朴霉素表达的特征”Hepafology (1996)。