title: Gut microflora in the pathogenesis of the complications of cirrhosis.
abstract: The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Cirrhotic patients are prone to develop bacterial infections, mainly the 'spontaneous' infection of ascites or spontaneous bacterial peritonitis. Other complications of cirrhosis, such as variceal haemorrhage and ascites, occur mostly or solely as a consequence of portal hypertension. Portal pressure increases initially as a consequence of an increased intrahepatic resistance but, once collaterals have formed, high portal pressure is maintained by an increased splanchnic blood inflow secondary to vasodilatation. Splanchnic vasodilatation is the initiating event in the hyperdynamic circulatory state that aggravates the complications of cirrhosis. The gut flora plays a role in both the development of infections and in the hyperdynamic circulatory state of cirrhosis and, although less prominently, it also plays a role in the pathogenesis of hepatic encephalopathy. This chapter presents evidence regarding gut flora and its modification in the pathogenesis and management of these complications of cirrhosis.
authors.affiliation: Gastroenterology Service, VA Connecticut Healthcare System and Section of Digestive Diseases, Yale University School of Medicine, 333 Cedar Street-1080 LMP, P.O. Box 3333, New Haven, CT 06520-8019, USA. guadalupe.garcia-tsao@yale.edu
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Garcia-Tsao
authors.forename: Reiner
authors.initials: R
authors.lastname: Wiest
mesh_terms: D001201:Ascites / Q000209:etiology / Q000382:microbiology; D001424:Bacterial Infections / Q000209:etiology / Q000382:microbiology*; D018988:Bacterial Translocation / Q000502:physiology; D004755:Enterobacteriaceae / Q000472:pathogenicity* / Q000502:physiology; D006501:Hepatic Encephalopathy / Q000209:etiology / Q000382:microbiology; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications / Q000382:microbiology*; D010538:Peritonitis / Q000209:etiology / Q000382:microbiology; D013152:Splanchnic Circulation / Q000502:physiology; D014664:Vasodilation / Q000502:physiology