**2. Methods**

We performed a descriptive, prospective, and longitudinal study in 194 patients with liver cirrhosis. All were referred to the consultation of hepatology and liver transplantation at CIMEQ hospital between January 2004 and April 2011. The sample was composed of 144 patients who met the following inclusion criteria: diagnosis of liver cirrhosis (confirmed by laparoscopy, liver biopsy or ultrasound) and rolling up at least 36 months (three years). Patients who underwent liver transplantation during the study period, those who were lost to follow-up, died of causes unrelated to liver disease, and those who at the time of assessment presented hepatocellular carcinoma, cholangiocarcinoma or other malignancies were excluded. Were also excluded four patients with spontaneous bacterial peritonitis and hepatorenal syndrome. The frequency of evaluations was determined by clinical assessment of patients at least twice a year.

The confirmation of alcoholic and viral etiology was performed. The surface antigen for hepatitis B virus (HBsAg) by UMELISA HBsAg and antibody for HCV by HCV–UMELISA, both produced by the National Center for Immunoassay in Havana, Cuba were investigated. HCV infection was confirmed by qualitative PCR (UMELOSA) produced by the National Center for Immunoassay in Havana, Cuba. The criterion for toxic alcohol intake was: 60 g daily intake for men and 40 g for women over 10 years. (Cavalry J, 2002) Patients with HBV or HCV and alcohol were included in the viral etiology, because liver damage is increased more by the virus than by alcohol. (Safdar K, 2004)
