Int. J. Environ. Res. Public Health 2010, 7 1881 although has disadvantages such as cost, invasiveness, sampling errors, pain, and bleeding risk, provides an accurate staging of liver fibrosis, grade of necroinflammation, steatosis, iron overload, and comorbidities (i.e., autoimmunity) [36]. Recently FibroTest and FibroScan have been used as alternative diagnostic tools. Different studies have demonstrated their efficacy in clinical practice. Nonetheless, liver biopsy is still the gold standard to assess liver fibrosis. 6. Complications High amount of chronic consumption pattern of ethanol increases the risk to develop other health problems. This pattern has a wide variety of adverse effects. It has been already described that ALD involves significant crosstalk among intracellular signaling events in the liver. Overall, inflammatory and innate immune responses in Kupffer cells are activated by elevated gut-derived plasma endotoxin levels [6]. It increases ROS which induces damage and metabolites production, such as acetaldehyde or lipid peroxidation products, that contribute to activation of HSC (the key cell type involved in liver fibrosis) [21]. Complications start when these events diminish the functional hepatocytes. Considering all patients with ALD as a single group, the average 1- and 5-year survival rates are approximately 80 and 50%, respectively [28]. Liver cirrhosis is the most severe form of ALD. Scar tissue replaces normal hepatocytes, disrupting blood flow. When the liver becomes fibrotic and cirrhotic, the number of functional hepatocytes decreases, and the liver loses its capacity to remove toxic substances from the blood [32]. Patients with cirrhosis and superimposed alcoholic hepatitis had a 4-year mortality greater than 60%. The prognosis of individual patients with ALD depends on the degree of pathological injury, the patient's nutritional status, the presence of complications of advanced disease, other comorbid conditions, such as HCV infection, and the patient’s inability to eliminate destructive drinking patterns. Alcoholic cirrhosis also appears to be an independent risk factor for hepatocellular carcinoma [34]. One month mortality in patients with spontaneous hepatic encephalopathy is approximately 50% and 75% in those with hepatorenal syndrome; the median survival of patients with hepatorenal syndrome is less than two weeks. Comparing alcoholic cirrhosis to other etiologies, it is known that alcohol in Japanese society accounts for 13.6 percent of all cases of cirrhosis [11] while Hepatitis B virus (HBV) and HCV infection account for 13.9% and 60.9% of cases respectively. Other causes were primary biliary cirrhosis with 2.4% and autoimmune hepatitis with 1.9% [37]. Alcoholic hepatitis is perhaps the most overwhelming manifestation of alcoholic liver disease. Up to 40% of patients with severe alcoholic hepatitis die within the first 6 months after the onset of the clinical syndrome. It is well known that more severe forms of alcoholic hepatitis are associated with higher mortality rates [38]. Among alcoholic hepatitis signs jaundice and fever may resolve in alcoholic hepatitis within several weeks after discontinuation of alcohol intake, but ascites and hepatic encephalopathy might persist for months to years. Mortality rate in alcoholic hepatitis is about 50% in severe cases. If the heavy drinking pattern continues, 40 percent will develop cirrhosis. When clinical symptoms of encephalopathy appear, ammonia levels in the brain may increase more than twenty fold, this happens in patients with advanced stages of encephalopathy, resulting from chronic liver failure.