The aim of this study was to assess the incidence of decompensation (ascites, jaundice, variceal bleeding, and encephalopathy), hepatocellular carcinoma (HCC) and death or liver transplantation in patients with compensated hepatitis C virus (HCV)-related cirrhosis, taking into account the viral genotype and interferon (IFN) therapy. Between 1989 and 1994, 668 patients with no clinical evidence of decompensation were referred to our department for liver biopsy because of positivity for anti-HCV antibodies and elevated aminotransferase activity; 103 of these patients had cirrhosis. The median follow-up was 40 months. Fifty-nine patients were treated with IFN for a mean duration of 11 ؎ 6 months; 3 (5%) had a prolonged biochemical and virological response. Baseline characteristics of IFN-treated and untreated patients were not significantly different. HCV genotypes (InnoLiPa) were predominantly 1b (48%) and 3a (20%). During follow-up, complications of cirrhosis occurred in 26 patients, HCC in 11 patients, and decompensation not related to HCC in 19 patients. Sixteen patients died, 94% of liver disease. Three patients were transplanted for liver failure. The 4-year risk of HCC was 11.5% (annual incidence 3.3%) and that of decompensation was 20%. Survival probability was 96% and 84% at 2 and 4 years, respectively. In multivariate analysis, the absence of IFN therapy was the only independent factor predictive both for HCC and decompensation. A low albumin level at entry and the absence of IFN therapy were the two independent factors predictive of death or liver transplantation. Probability of survival at 2 and 4 years was significantly different between IFN-treated and untreated patients (respectively 97% and 92% vs 95% and 63%, P F .0001). In conclusion, in patients with compensated HCV-related cirrhosis: 1) complications of cirrhosis are frequent, whatever the viral genotype; and 2) the severity of cirrhosis and the absence of IFN therapy are independently predictive of bad outcome. (HEPATOLOGY 1998;27:1435-1440.)Hepatitis C virus (HCV) infection is one of the main causes of death related to cirrhosis and liver transplantation in France. 1 The incidence of hepatocellular carcinoma (HCC) and decompensation is not precisely known, particularly in Europe and the United States. Indeed, study populations are often heterogeneous in terms of the severity of liver disease, as well as interferon (IFN) treatment. [2][3][4][5][6][7][8][9][10][11] The long-term mortality rate among patients with chronic hepatitis C is controversial. 2,8 Prognostic factors for complications of HCVrelated cirrhosis are not clearly defined, particularly the role of the HCV genotype. 12-15 Recent studies have suggested that IFN therapy reduces the risk of HCC in HCV-related cirrhosis. 16,17 The aim of this study was to assess in a cohort of patients with compensated HCV-related cirrhosis the following: 1) the incidence of decompensation (ascites, jaundice, variceal bleeding, and encephalopathy), HCC, and death or liver transplantation; and 2) facto...
Long-term ursodiol therapy slows the progression of primary biliary cirrhosis and reduces the need for liver transplantation.
Ursodeoxycholic acid (UDCA) is the only approved treatment for primary biliary cirrhosis (PBC). However, the benefit from UDCA therapy on the progression of PBC from its early stage towards extensive fibrosis and cirrhosis has not been clearly shown. The aim of this study was to assess the effect of UDCA therapy on liver fibrosis progression in PBC. A Markov model was used to analyze the progression rates between early and late histologic stages in 103 patients with PBC enrolled in a randomized, double-blind, placebo-controlled trial of UDCA. Early stage was defined by the presence of portal and periportal lesions without extensive fibrosis, whereas late stage was defined by the presence of numerous septa, bridging fibrosis, or cirrhosis. A total of 162 pairs of liver biopsy specimens were studied. The model accurately described the observed data. UDCA therapy was associated with a 5-fold lower progression rate from early stage disease to extensive fibrosis or cirrhosis (7% per year under UDCA vs. 34% per year under placebo, P <.002), but was not associated with a significant difference in regression rates (3% per year under both UDCA and placebo). At 4 years, the probability of UDCA-treated patients to remain in early stage disease is 76% (95% confidence interval: 58%-88%), as compared with 29% (15%-52%) in placebo-treated patients. In conclusion, UDCA therapy significantly delays the progression of liver fibrosis in PBC. Markov modeling should prove useful in assessing the efficacy of future medical treatments in clinical trials involving histologic endpoints.
Ursodeoxycholic acid (UDCA) treatment has been shown to increase survival without orthotopic liver transplantation (OLT) in patients with primary biliary cirrhosis (PBC) at 4 years. Whether this beneficial effect was maintained over the long term remained to be established. In a large cohort of UDCA-treated patients with PBC, we aimed to determine the 10-year outcome of these patients using two endpoints: (1) survival without OLT, and (2) survival. The cohort was comprised of 225 patients with PBC treated with UDCA (13-15 mg/kg/d) monitored from the beginning of treatment until time of last follow-up, OLT, or death. Because of the absence of a control group, survival without OLT was compared with survival predicted by the Mayo model (first 7 years), and observed 10-year survival with an estimation of survival of a standardized control cohort of the French population. Observed survival without OLT of UDCAtreated patients was significantly higher (P F .04) than survival predicted by the Mayo model. Observed survival was significantly lower (P F .01) than survival predicted from the French population. Observed survival of noncirrhotic patients was not different (P G .9) from that of the French control population but survival of cirrhotic patients was significantly lower (P F .0001). Twenty-two patients died; 13 patients died of hepatic causes and 4 patients died after OLT. In conclusion, survival without OLT among patients treated with UDCA for PBC is higher than that of untreated patients, as predicted by the Mayo model. Tenyear survival among UDCA-treated patients is slightly lower than that of an age-and sex-matched general population, the difference mainly being explained by mortality among cirrhotic patients. (HEPATOLOGY 1999; 29:1668-1671.)
The impact of primary biliary cirrhosis (PBC) on health-related quality of life (HRQOL) is poorly documented. We assessed quality of life in a group of 276 unselected patients with PBC using the Nottingham Health Profile (NHP). This is a generic scale that assesses six major areas commonly associated with HRQOL. Data were compared with those of a sex-and age-matched control group. The associations between NHP scores and the severity of PBC were tested. Patients (86% women) had a median age of 62 years (range 33-87). Most patients were treated with UDCA. PBC patients showed a strong statistically significant difference in energy compared to controls (respectively, 40.6 vs. 22.9, P < .0001) and had worse scores for emotional reactions (22.2 vs. 16.1, P < .005). No other differences were observed. No associations of the dimension subscores were found with biochemical liver tests, histological stages, or duration of the disease. Among the signs or symptoms, fatigue was the finding most often associated with the dimension subscores. In conclusion, patients with PBC feel that their overall quality of life is worse than that of the control population. This difference is mainly due to the decrease in the subscores of energy and emotional reactions, both associated with fatigue. These effects must be taken into account by clinicians when treating these patients, as they constitute the clinical outcomes that have the most impact on patients' lifestyle and adherence to treatment. (HEPATOLOGY 2004;40:489 -494.)
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