Liver injury induced by various pathogenic factors(such ashepatitis virus,ethanol,drugs and hepatotoxicants,etc.)through their respective special pathogenesis is referred toas“primary liver injury”(PLI).Liver injury resulted fromendotoxin(lipopolysaccharide,LPS)and the activation ofKupffer cells by LPS while intestinal endotoxemia(IETM)occurred during the occurrence and development of hepatitisis named the“secondary liver injury”(SLI).The latter whichhas lost their own specificities of primary pathogenic factorsis ascribed to IETM.The“secondary liver injury”is ofimportant action and impact on development and prognosisof hepatitis.More severe IETM commonly results in excessiveinflammatory 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 impairmentaccompanied by infiltration of inflammatory cells,hepaticfibrosis,cirrhosis and hepatocarcinoma.Generally,the milderIETM ends with chronic hepatic failure.If PLI caused byvarious pathogenic factors through their independent specificmechanismis regarded as“the first hit”on liver,then SLImediated by different chemical mediators from KCs activatedby IETM in the course of hepatitis is“the second hit”onliver.Thus,fusing and overlapping of the primary andscondary liver injuries determine and influeuce the complexityof the illness and outcome of the patient with hepatitis.Forthis reason,the viewpoint of“SLI”induced by the“secondhit”on liver inflicted by IETM suggests that medicalprofessionals should attach great importance to both“PLI”and“SIT”caused by IETM.That is,try to adjust the functionof KSs and eliminate endotoxemia of the patient. Liver injury induced by various pathogenic factors (such as hepatitis virus, ethanol, drugs and hepatotoxicants, etc.) Through their respective special pathogenesis is referred toas “primary liver injury” (PLI) .Liverization of fromendotoxin (lipopolysaccharide, LPS) and the activation of Kupffer cells by LPS while intestinal endotoxemia (IETM) occurred during the occurrence and development of hepatitisis named “secondary liver injury ” (SLI) .the latter whichhas lost their own specificities of primary pathogenic factorsis ascribed to IETM.The “secondary liver injury” is of atmportant 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. milder IETM successively precipitates a cascade, including repeated and persistent hepatocytic impairmentaccompanied by infiltration of inflammatory cells, hepaticfibrosis, cirrhosis and hepatoc arcinoma.Generally, the millerIETM ends with chronic hepatic failure .If PLI caused byvarious pathogenic factors through their independent specificmechanismis regarded as “the first hit ” on liver, then SLImediated by different chemical mediators from KCs activatedby IETM in the course of hepatitis is “the second hit ” onliver.Thus, fusing and overlapping of the primary and second liver injuries determine and influeuce the complexity of the illness and outcome of the patient with hepatitis. Forthis reason, the viewpoint of “SLI ” induced by the “secondhit ” on liver inflicted by IETM suggests that medicalprofessionals should attach great importance to both “PLI ” and “SIT ” caused by IETM.That is, try to adjust the functionof KSs and eliminate endotoxemia of the patient.