作者: Christian J. Steib , Julia Schewe , Alexander L. Gerbes
DOI: 10.1159/000375352
关键词: Hepatic stellate cell 、 Rifaximin 、 Gastroenterology 、 Medicine 、 Cirrhosis 、 Immune system 、 Portal venous pressure 、 Portal hypertension 、 Kupffer cell 、 Internal medicine 、 Spontaneous bacterial peritonitis
摘要: BACKGROUND Microbial infections are a relevant problem for patients with liver cirrhosis. Different types of bacteria responsible different kinds infections: Escherichia coli and Klebsiella pneumoniae frequently observed in spontaneous bacterial peritonitis or urinary tract infections, Streptococcus Mycoplasma pulmonary infections. Mortality is up to 4-fold higher infected cirrhosis than without Key Messages: Infections due three major reasons: translocation, immune deficiency an increased incidence systemic Nonparenchymal cells like Kupffer cells, sinusoidal endothelial hepatic stellate the first come into contact microbial products when infection translocation occurs. cell (KC) activation by Toll-like receptor (TLR) agonists dysfunction have been shown be important mechanisms increasing portal pressure following intraperitoneal lipopolysaccharide pretreatment cirrhotic rat livers. Reduced intrahepatic vasodilation vasoconstriction pathophysiological pathways. Thromboxane A2 leukotriene (LT) C4/D4 identified as vasoconstrictors. Accordingly, treatment montelukast inhibit cysteinyl-LT1 reduced Clinical studies demonstrated that KCs, estimated amount soluble CD163 blood, correlates risk variceal bleeding. Additionally, intestinal decontamination rifaximin alcohol-associated CONCLUSIONS TLR nonparenchymal pathogens results hypertension. This might explain pathophysiologic correlation between hypertension These findings basis both better stratifying new options, such specific inhibition