Liver fibrosis in hepatitis C patients of Pakistani versus Scandinavian origin.

OBJECTIVE: The aim of this study was to examine the significance of native country for the stage of liver fibrosis in a population of HCV patients of Pakistani or Scandinavian origin living in Oslo. PATIENTS AND METHODS: We included 122 consecutive HCV patients at two hepatitis clinics in Oslo, 73 of Scandinavian and 49 of Pakistani origin. Inclusion criteria were being HCV RNA positive, treatment naïve and having an adequate liver biopsy. The biopsies were scored according to the Metavir index, which scores fibrosis on a scale from 0 to 4 and necroinflammatory activity on a scale from 0 to 3. Steatosis was scored according to the percentage of hepatocytes having lipid droplets in their cytoplasm. Demographical, clinical, virological and biochemical data for the two groups were registered from the patient files. RESULTS: The median age was 43 and 42 years and 53% and 51% were male among the Scandinavian and Pakistani patients, respectively. Among the patients of Pakistani origin 18/49 (37%) had bridging fibrosis (F3) or cirrhosis (F4) compared to 11/73 (15%) Scandinavian patients (p=0.006). The mean fibrosis score was 1.78 in the Pakistani and 0.82 in the Scandinavian group (p<0.001). The mean necroinflammatory activity score was 1.22 and 0.78 in the Pakistanis and Scandinavians, respectively (p<0.001). In the Pakistani group more patients had ≥5% steatosis (59% vs. 33%; p=0.004), diabetes mellitus (24% vs. 0%; p<0.001), overweight (46% vs. 34%; p=0.232), genotype 3 (84% vs. 42%; p<0.001) and ALT and AST levels above the reference range (84% vs. 64%; p=0.020 and 88% vs. 68%; p=0.014) compared to the Scandinavian. Multivariate regression analyses identified age ≥40 years (OR 10.13; 95% CI 2.65-39.12) and genotype 3 (OR 5.02; 95% CI 1.19-21.17) as independent predictors of bridging fibrosis/cirrhosis. CONCLUSIONS: In HCV patients of similar age, those of Pakistani origin had more advanced liver disease than those of Scandinavian origin. Possible explanations are longer duration of the infection and higher occurrence of diabetes mellitus, liver steatosis and genotype 3 in the Pakistani group.

ASAT/ALAT ratio provides prognostic information independently of Child-Pugh class, gender and age in non-alcoholic cirrhosis.

OBJECTIVE: The aspartate amino transferase/alanine amino transferase (ASAT/ALAT) ratio is increased in cirrhosis. Some studies indicate that the ratio may provide prognostic information as well. The purpose of this study was to further elucidate the role of the ASAT/ALAT ratio as a predictor of survival by assessing it together with classical risk factors such as age, gender and Child-Pugh (CP) class in a mixed cohort of patients with cirrhosis. MATERIAL AND METHODS: Eighty-nine patients with alcoholic cirrhosis and 81 patients with non-alcoholic cirrhosis treated at Aker University Hospital between 1999 and 2004 were identified retrospectively. Survival data from these patients per August 2006 were retrieved from the Norwegian Death Registry. Clinical and biochemical data at time of diagnosis were assessed as predictors of survival using the Kaplan-Meier method and Cox regression models. RESULTS: Median ASAT/ALAT ratio was significantly higher in alcoholic cirrhosis (2.42) as compared with non-alcoholic cirrhosis (1.42). In both groups, a ratio above the median was predictive of poor outcome, p=0.024 and p=0.032, respectively. Other significant predictors of death were CP class (p<0.001), clinical decompensation (p<0.001) and age (p=0.001). Cox regression analyses showed that the ASAT/ALAT ratio was a predictor of death independently of CP class, gender and age in non-alcoholic, but not in alcoholic cirrhosis. The estimated increased hazard (risk of dying) in non-alcoholic cirrhosis was 5% (CI: 1-8%) per 0.10 increase in ASAT/ALAT ratio. CONCLUSIONS: A high ASAT/ALAT ratio is associated with increased mortality in cirrhosis. In non-alcoholic patients the ratio may provide prognostic information independently of classical risk factors.

Incidence rates and causes of cirrhosis in a Norwegian population.

OBJECTIVE: To investigate the incidence rate and causes of cirrhosis in a Norwegian population. We also sought to assess the degree of underreporting of cirrhosis to the Norwegian Death Registry. MATERIAL AND METHODS: All 1264 patients treated at Aker University Hospital in the period January 1999 to March 2004 who were given a diagnosis indicating cirrhosis, chronic liver disease or symptoms possibly attributable to cirrhosis were screened retrospectively. A search in the registry of histological diagnoses at Department of Pathology was also carried out. Based on the results of histological examinations and non-histological criteria, cirrhosis was confirmed in 194 patients. Calculations of the incidence rate of cirrhosis and frequencies of the various etiologies were based on 93 patients living in the catchment area of the hospital. Causes of death were retrieved from the Norwegian Death Registry. RESULTS: The incidence rate of cirrhosis was 134 per million per year. The majority of cases were due to alcoholic liver disease (53%), followed by viral liver disease (12%), various autoimmune liver diseases (12%), hemochromatosis (4%) and non-alcoholic steatohepatitis (NASH) (3%). No etiology was established in 16%, a group with a high prevalence of diabetes mellitus, indicating that some of these cases were possibly caused by NASH. Among 105 deaths in this cohort of 194 cirrhotic patients, the diagnosis of cirrhosis was absent in the Norwegian Death Registry in 30% of cases. CONCLUSIONS: The incidence of cirrhosis in Norway is relatively low, with alcohol as the most important etiologic factor. Significant underreporting to the Norwegian Death Registry was observed.

Treatment with pegylated interferon and ribavarin in HCV infection with genotype 2 or 3 for 14 weeks: a pilot study.

The aim of this study was to determine the efficacy of 14 weeks of treatment in patients infected with hepatitis C virus (HCV) genotype 2 or 3 who achieve early virological response (EVR). In a noncontrolled multicenter trial, 122 treatment-naive patients received 1.5 mug/kg pegylated interferon alfa-2b subcutaneously once weekly and 800 to 1,400 mg/d ribavirin based on body weight. Treatment was stopped at week 14 in patients with EVR, defined as undetectable HCV RNA at weeks 4 and 8. Patients without EVR were assigned to 24 weeks of treatment. The primary end point was sustained virological response (SVR), defined as undetectable HCV RNA 24 weeks after end of treatment. Among the 122 patients, 95 (78%) had EVR and received 14 weeks of treatment. The remaining 27 (22%) were treated for 24 weeks. SVR was obtained in 85 (90%) of 95 patients in the 14-week treatment group and 15 of (56%) 27 in the 24-week treatment group. Altogether, SVR was obtained in 100 of 122 patients (82%; 95% CI, 75%-89%). SVR after 14 weeks of treatment was achieved more frequently among genotype 3a patients with low viral load compared with high viral load (98% vs. 79%; P = .019). Logistic regression analysis showed that absence of bridging fibrosis/cirrhosis was the only independent predictor of SVR. In conclusion, patients with genotype 2 or 3 and EVR obtained a high SVR after 14 weeks of treatment. The results need to be confirmed in a randomized, controlled study before this treatment approach can be recommended, particularly for patients with genotype 3 and high viral load or severe fibrosis.