Autores: Reggiardo María Virginia, Fay Fabián, Tanno Mario, García Camacho Gabriela, Bottasso Oscar, Ferretti Sebastián, Godoy Alicia, et al
Background & aims: Studies about the natural history of hepatitis C virus (HCV) infection report variable progression to cirrhosis depending on study design. Retrospective cross-sectional liver clinic studies overestimate the rate of fibrosis progression due to inclusion of patients with more severe disease leaving mild and asymptomatic patients underrepresented. We evaluated fibrosis progression in a group of “healthy” asymptomatic subjects, attending to a voluntary campaign for the detection of HCV infection. Material and methods: A detection campaign was launched on subjects transfused before 1993. Of 1699 volunteers, 61(3.6%) had HCV infection. A liver biopsy was performed in 40 (65%). Assessed risk factors for liver fibrosis were: sex, body mass index, alcohol consumption (> 20 g/dmujeres - > 40g/hombres), genotype, HLA-DRB1 alleles, present age, age at infection and duration of infection. Results: 25 (62.5%) were women with a median age of 52.5 years. The median duration of infection was 21.5 years with a median age at infection of 27 years. As regards fibrosis, 25 (62.5%) had a Low Stage (F0-F1), 8 patients, 20%, had severe fibrosis, one patient (2.5%) had cirrhosis. Alcohol consumption was the only risk factor associated with fibrosis progression. Conclusions: The low progression to cirrhosis may be explained by the clinical characteristics of our population: asymptomatic middle-aged “healthy” subjects infected at young age. The progression to severe fibrosis was noticeable; hence a longer follow-up might demonstrate changes in this outcome. Significant alcohol consumption clearly worsens the natural history of HCV infection; this is no so evident for occasional or mild alcohol consumers.
Palabras clave: Alcohol consumption fibrosis progression fibrosis risks factors.
2012-08-21 | 556 visitas | Evalua este artículo 0 valoraciones
Vol. 11 Núm.5. Septiembre-Octubre 2012 Pags. 658-666 Ann Hepatol 2012; 11(5)