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肝肉芽肿:发病机制与鉴别诊断。

Hepatic granulomas: pathogenesis and differential diagnosis.

机构信息

Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA.

出版信息

Clin Liver Dis. 2010 Nov;14(4):605-17. doi: 10.1016/j.cld.2010.07.005.

DOI:10.1016/j.cld.2010.07.005
PMID:21055685
Abstract

Granulomatous liver disease constitutes a category of hepatic disorders and is at present diagnosed in approximately 4% of liver biopsies. Hepatic granulomas develop through the interactions of T lymphocytes and macrophages, with the integral involvement of T-helper (T(H)) 1 or T(H)2 pathways or both, depending on the specific granulomatous disease. Hepatic granulomas may be manifested clinically by elevated levels of serum alkaline phosphatase and g-glutamyltransferase enzymes, damage to specific structures (eg, intrahepatic bile ducts in primary biliary cirrhosis), or infrequently, progressive liver disease with portal hypertension and cirrhosis (eg, sarcoidosis). Systemic immunologic disorders, infectious diseases, drug hepatotoxicity, and reaction to neoplastic disease are the major causative factors responsible for granulomas in the liver. These causes and recent epidemiologic trends are covered in this discussion.

摘要

肉芽肿性肝病构成了一类肝脏疾病,目前约占肝活检的 4%。肝肉芽肿是通过 T 淋巴细胞和巨噬细胞的相互作用发展而来的,其整体涉及 T 辅助 (T(H))1 或 T(H)2 途径或两者兼有,具体取决于特定的肉芽肿性疾病。肝肉芽肿可能在临床上表现为血清碱性磷酸酶和 g-谷氨酰转移酶水平升高、特定结构损伤(例如原发性胆汁性肝硬化中的肝内胆管),或者很少见的进展性肝疾病伴门静脉高压和肝硬化(例如结节病)。全身性免疫性疾病、传染病、药物肝毒性和对肿瘤性疾病的反应是导致肝脏肉芽肿的主要原因。本讨论涵盖了这些原因和最近的流行病学趋势。

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Hepatic granulomas: pathogenesis and differential diagnosis.肝肉芽肿:发病机制与鉴别诊断。
Clin Liver Dis. 2010 Nov;14(4):605-17. doi: 10.1016/j.cld.2010.07.005.
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