Therefore, patients with a history of both ascites and variceal bleeding should be considered for liver transplantation, as should patients with hepatic encephalopathy. There have been attempts to describe the clinical course of cirrhosis as a progression

through successive stages defined by the presence of particular complications. Our study shows that such a staging system cannot be based on ascites, variceal bleeding, and hepatic encephalopathy because these complications do not develop chronologically. The same conclusion applies to nonbleeding varices, bleeding varices, and ascites, which have been studied by D’Amico et al.28 Hepatocellular carcinoma, alcoholic hepatitis, and bacterial infection also may occur at any time during the clinical course of cirrhosis, and so it appears that STI571 supplier cirrhosis

complications develop in a random sequence. Therefore, a staging system may need to be based on factors that determine the development of complications, such as metabolic liver function and portal pressure,28 but alcohol consumption could Fulvestrant also be important, as indicated by its strong association with mortality.3 However, this study was not designed to examine whether particular patient characteristics accelerate the clinical course or predispose patients to developing one particular complication instead of another, and we could not reach a firm conclusion on the prognostic click here role of alcohol consumption without also considering the possibly confounding

effects of factors such as gender, age, comorbidity, treatment, and compliance. Such an analysis was not possible within the framework of the present study. In conclusion, we systematically examined the clinical course of alcoholic cirrhosis among patients treated in a Danish geographic region. Our findings demonstrate that patients with alcoholic cirrhosis have a high prevalence of complications at the time of diagnosis, and that these complications are strong predictors of 1-year mortality, but not of the risk of developing more complications. In addition, because complications develop in a seemingly random sequence, the clinical course of alcoholic cirrhosis cannot be determined based on the presence or absence of particular cirrhosis complications. “
“Toll-like receptor 7 (TLR7) signaling predominantly regulates production of type I interferons (IFNs), which has been suggested in clinical studies to be antifibrotic. However, the mechanistic role of the TLR7-type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver fibrosis was induced in wild-type (WT), TLR7-deficient, and IFN-α/β receptor-1 (IFNAR1)-deficient mice and TLR7-mediated signaling was assessed in liver cells isolated from these mice.