Abstract

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.

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