Intestinal XXXX as a pathogenetic mechanism in @entity1578 .

@entity1 @entity558 @entity5694 @entity82 @entity1956 @entity879 @entity73 @entity1578 @entity99 @entity1068
@entity99 induced by various pathogenic factors (such as @entity1956 , @entity1068 , drugs and hepatotoxicants, etc.) through their respective special pathogenesis is referred to as primary @entity99 (PLI). @entity99 resulted from endotoxin (lipopolysaccharide, @entity558 ) and the activation of Kupffer cells by @entity558 while intestinal @entity5694 (IETM) occurred during the occurrence and development of @entity99 is named the @entity99 ( @entity99 ). The latter which has lost their own specificities of primary pathogenic factors is ascribed to IETM. The @entity99 is of important action and impact on development and prognosis of @entity99 . More severe IETM commonly results in excessive inflammatory responses, with serious @entity99 , further severe @entity99 and even induces @entity879 . The milder IETM successively precipitates a cascade, including repeated and persistent @entity73 accompanied by infiltration of inflammatory cells, hepatic @entity82 , @entity82 and hepatocarcinoma. Generally, the milder IETM ends with @entity1578 . If PLI caused by various pathogenic factors through their independent specific mechanismis regarded as the first hit on liver, then @entity99 mediated by different chemical mediators from KCs activated by IETM in the course of @entity99 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 @entity1 with @entity99 . For this reason, the viewpoint of @entity99 induced by the second hit on liver inflicted by IETM suggests that medical professionals should attach great importance to both PLI and @entity99 caused by IETM. That is, try to adjust the function of KS(s) and eliminate @entity5694 of the @entity1 .
