[Clinical characteristics of non-alcoholic steatohepatitis (NASH) patients who progressed from F3 stage fibrosis to cirrhotic NASH].

The present study investigated the clinical characteristics of non-alcoholic steatohepatitis (NASH) patients who progressed from stage 3, zone 3 bridging fibrosis (F3 stage NASH) to cirrhosis. Of 95 NASH patients with repeated liver biopsies during a period of 4.6 years, 6 patients progressed to cirrhosis. The initial liver biopsies of these 6 patients were diagnosed as F3 stage NASH. Simple clinical variables and non-invasive biological tests were evaluated in 33 cases of F3 stage NASH. Increases in body mass index and fluctuations in transaminase levels, as well as the evaluation of homeostatic model assessment-insulin resistance, ferritin, and hyaluronic acid in F3 stage NASH patients may prove useful in identifying individuals at risk of progression to cirrhosis.

Comparison of outcomes between patients with alcoholic cirrhosis and those with hepatitis C virus-related cirrhosis.

BACKGROUND AND AIM: The natural history of alcoholic cirrhosis, especially in Asian countries, has not been completely understood thus far. METHODS: We retrospectively compared the outcomes of compensated cirrhosis between Japanese alcoholic and hepatitis C virus (HCV)-infected patients. RESULTS: A total of 227 patients (75 alcoholic and 152 HCV-infected patients) with compensated cirrhosis were enrolled. The median follow-up period was 4.9 years. The cumulative rates of hepatocellular carcinoma (HCC) development were significantly lower in the alcoholic patients than in the HCV-infected patients (6.8% vs 50.3% at 10 years, P = 0.0003), while the cumulative rates of hepatic decompensation (37.4% vs 51.7% at 10 years) and survival (53.8% vs 47.4% at 10 years) did not significantly differ between the two groups (Kaplan-Meir analysis). The main causes of death were hepatic failure and non-hepatic diseases in the alcoholic patients and HCC and hepatic failure in the HCV-infected patients. Multivariate analyses using the Cox proportional hazard model revealed that the risk of HCC was lower in alcoholic cirrhosis than in HCV-related cirrhosis (hazard ratio (HR), 0.46), while the risk of hepatic decompensation and mortality was the same. Predictors of decreased survival were non-abstinence (HR, 2.53) in the alcoholic patients and low serum albumin level (1.58) in the HCV-infected patients. CONCLUSIONS: Survival of patients with alcoholic cirrhosis was similar to that of patients with HCV-related cirrhosis. The risk of HCC development was lower in alcoholic cirrhosis than in HCV-related cirrhosis. Abstinence from alcohol was important for improving the survival of patients with alcoholic cirrhosis.

Association of primary biliary cirrhosis with idiopathic thrombocytopenic purpura.

Although both primary biliary cirrhosis (PBC) and idiopathic thrombocytopenic purpura (ITP) are autoimmune diseases, the association of the 2 diseases is rare. Here, we report a case of ITP that developed during the follow-up of PBC in a 74-year-old man. The patient had been diagnosed with PBC 12 years previously, and had received treatment with ursodeoxycholic acid. The platelet count decreased from approximately 60 x 10(9)/L to 8 x 10(9)/L, and the association of decompensated liver cirrhosis (PBC) with ITP was diagnosed. Steroid and immune gamma globulin therapy were successful in increasing the platelet count. Interestingly, human leukocyte antigen genotyping detected the alleles DQB1*0601 and DRB1*0803, which are related to both PBC and ITP in Japanese patients. This case suggests common immunogenetic factors might be involved in the development of PBC and ITP.