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慢性肝脏疾病的病因学与病理生理学

Aetiology and pathophysiology of chronic liver disorders.

作者信息

Schölmerich J, Holstege A

机构信息

Department of Internal Medicine, University of Freiburg, Federal Republic of Germany.

出版信息

Drugs. 1990;40 Suppl 3:3-22. doi: 10.2165/00003495-199000403-00003.

DOI:10.2165/00003495-199000403-00003
PMID:2081479
Abstract

The aetiology of chronic liver disease covers a wide range of congenital or acquired abnormalities of the hepatocellular biochemical network. Although our knowledge has considerably increased in recent years, the aetiology of chronic liver disease often remains obscure. Acquired irreversible disturbances of normal liver function can be mediated by hepatotrophic viruses, chemicals, chronic oxygen depletion, or interference with the immune system. Considerable progress has been made in the detection and characterisation of hepatitis B, C, and D viruses as causative agents of chronic active hepatitis. Alcohol abuse remains the predominant cause of chronic liver disease in the Western world. The targets of autoantibodies used to diagnose autoimmune diseases of the liver and primary biliary cirrhosis continue to be biochemically defined. Their significance for the aetiology of the disease, however, remains to be established. Nonparenchymal cells play an important role in the sequence of events following hepatocellular injury and ultimately leading to liver cirrhosis. They release vasoactive compounds, cytokines, and other important mediators, and participate in the modulation of the extracellular matrix that is characteristic of liver fibrosis and cirrhosis. The biochemical basis of liver cell necrosis remains poorly defined. In spite of recent progress, and the detection of some new pathogenic principles that help in the understanding of the complications of chronic liver disease such as portal hypertension, oesophagogastric variceal bleeding, portosystemic encephalopathy, ascites, and other metabolic disturbances, many questions concerning the aetiology and pathophysiology of chronic liver disease and its complications remain to be answered.

摘要

慢性肝病的病因涵盖肝细胞生化网络的一系列先天性或后天性异常。尽管近年来我们的认识有了显著提高,但慢性肝病的病因往往仍不明确。正常肝功能的后天性不可逆紊乱可由嗜肝病毒、化学物质、慢性缺氧或免疫系统干扰介导。在检测和鉴定作为慢性活动性肝炎病原体的乙型、丙型和丁型肝炎病毒方面已取得了相当大的进展。酗酒仍然是西方世界慢性肝病的主要原因。用于诊断肝脏自身免疫性疾病和原发性胆汁性肝硬化的自身抗体的靶标在生化方面仍有待明确。然而,它们在疾病病因中的意义仍有待确定。非实质细胞在肝细胞损伤后最终导致肝硬化的一系列事件中起重要作用。它们释放血管活性化合物、细胞因子和其他重要介质,并参与肝纤维化和肝硬化所特有的细胞外基质的调节。肝细胞坏死的生化基础仍不清楚。尽管最近取得了进展,并且发现了一些有助于理解慢性肝病并发症(如门静脉高压、食管胃静脉曲张出血、门体性脑病、腹水和其他代谢紊乱)的新致病机制,但关于慢性肝病及其并发症的病因和病理生理学仍有许多问题有待解答。

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2
Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats.门静脉高压大鼠海马和额叶皮质中谷氨酰胺合成酶活性及谷氨酸摄取情况
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本文引用的文献

1
Studies of chronic idiopathic jaundice (Dubin-Johnson syndrome). I. Demonstration of hepatic excretory defect.慢性特发性黄疸(杜宾-约翰逊综合征)的研究。I. 肝排泄缺陷的证明。
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Hepatogastroenterology. 1981 Jun;28(3):139-42.
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[Liver damage caused by drugs].药物引起的肝损伤
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The in vivo metabolism of C3 in hepatobiliary disease associated with ulcerative colitis.C3在与溃疡性结肠炎相关的肝胆疾病中的体内代谢。
Scand J Gastroenterol. 1982 Jun;17(4):523-7. doi: 10.3109/00365528209182243.
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Normal fasting-state levels of serum cholyl-conjugated bile acids in Gilbert's syndrome: an aid to the diagnosis.吉尔伯特综合征患者空腹状态下血清胆酰共轭胆汁酸的正常水平:对诊断的辅助作用
Hepatology. 1982 May-Jun;2(3):340-3. doi: 10.1002/hep.1840020309.
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Drug-induced liver disease: an overview.药物性肝病:概述
Semin Liver Dis. 1981 May;1(2):93-103. doi: 10.1055/s-2008-1040722.