non disponibileIn cirrhotic patients there is an increased susceptibility to bacterial infection, related to the
degree of liver dysfunction leading to several abnormalities of defense mechanisms, all
of which increase the susceptibility to infection, including deficiency of bactericidal and
opsonic activities, impaired monocyte function, depressed phagocytic activity of the
reticuloendothelial system (RES), defective chemotaxis, and low levels of
complement in serum.
A particularly important role is played by the reduced RES activity, which is due to the
presence of extrahepatic shunts and intrahepatic shunts through sinusoids without Kupffer
cells, a reduced number of Kupffer cells, and impaired Kupffer cell function. Thus
cirrhotics with impaired RES phagocytic activity (as assessed by the elimination of 99m
technetium-sulfur colloid) develop acute bacterial infections more frequently than cirrhotics
with normal RES phagocytic activity.
Both community and hospital acquired bacterial infections are frequently diagnosed
in cirrhotics, the most frequent being spontaneous bacterial peritonitis (SBP), urinary
tract infections, pneumonia and skin infections, their incidence increasing with the
severity of liver dysfunction. Importantly, half of these episodes may be
asymptomatic.
Recently bacterial infections and/or endotoxaemia have been associated with failure to control
variceal bleeding, more early variceal rebleeding, abnormalities in coagulation, vasodilatation of the systemic vasculature and worsening of liver function.
There is an increased recognition that bacterial infections are involved in several
pathophysiological abnormalities in cirrhosis, so that in this introduction we aim to evaluate
the potential mechanisms and the clinical evidence illustrating the pivotal role of bacterial
infection. This could lead to new treatment strategies
