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Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2002; 8(6): 961-965
Published online Dec 15, 2002. doi: 10.3748/wjg.v8.i6.961
Intestinal endotoxemia as a pathogenetic mechanism in liver failure
De-Wu Han
De-Wu Han, Institute of Hepatology, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: De-Wu Han,M.D., Professor of Pathophysiology, Director of Institute of Hepatology, Shanxi Medical University, 86 Xin Jian Nan Road, Taiyuan 030001, Shanxi Province, China. smuhan@public.ty.sx.cn
Telephone: +86-351-4690082 Fax: +86-351-4690865
Received: July 17, 2002
Revised: August 12, 2002
Accepted: August 20, 2002
Published online: December 15, 2002
Abstract

Liver injury induced by various pathogenic factors (such as hepatitis virus, ethanol, drugs and hepatotoxicants, etc.) through their respective special pathogenesis is referred to as “primary liver injury” (PLI). Liver injury resulted from endotoxin (lipopolysaccharide, LPS) and the activation of Kupffer cells by LPS while intestinal endotoxemia (IETM) occurred during the occurrence and development of hepatitis is named the “secondary liver injury” (SLI).The latter which has lost their own specificities of primary pathogenic factors is ascribed to IETM. The “secondary liver injury” is of important action and impact on development and prognosis of hepatitis. More severe IETM commonly results in excessive inflammatory responses, with serious hepatic necrosis, further severe hepatitis and even induces acute liver failure. The milder IETM successively precipitates a cascade, including repeated and persistent hepatocytic impairment accompanied by infiltration of inflammatory cells, hepatic fibrosis, cirrhosis and hepatocarcinoma. Generally, the milder IETM ends with chronic hepatic failure. If PLI caused by various pathogenic factors through their independent specific mechanismis regarded as “the first hit” on liver, then SLI mediated by different chemical mediators from KCs activated by IETM in the course of hepatitis is “the second hit” on liver. Thus, fusing and overlapping of the primary and scondary liver injuries determine and influeuce the complexity of the illness and outcome of the patient with hepatitis. For this reason, the viewpoint of “SLI” induced by the “second hit” on liver inflicted by IETM suggests that medical professionals should attach great importance to both “PLI” and “SLI” caused by IETM. That is, try to adjust the function of KSs and eliminate endotoxemia of the patient.

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