1879 Int. J. Environ. Res. Public Health 2010, 7 4.1. Clinical Presentation of Alcoholic Liver Disease There is a wide variety of clinical presentations of ALD. Symptoms depend on the severity and stage of liver injury. Liver steatosis is the first structural change in liver secondary to chronic ethanol consumption. There are no clinical symptoms except for hepatomegaly. At the onset of the disease, steatosis is a typical finding, constituting the mildest form of ALD. It is a benign entity and the only clinical symptom in abdominal examination is the finding of an enlarged and tender liver. As damage progresses, the architecture of liver parenchyma changes inducing hepatic fibrosis due to increased collagen deposit. At this stage, patients might suffer decompensated ALD presenting alcoholic hepatitis (AH). AH is an acute liver inflammation in response to constant injury. The cardinal sign of the disease is the rapid onset of jaundice. Other common signs include fever, ascities and proximal muscle loss. The most common symptoms and clinical signs in alcoholic hepatitis include swollen liver, nausea, vomiting and abdominal pain [31]. The diagnosis is based on a history of heavy alcohol use, jaundice, and the absence of other possible causes of hepatitis [6]. It is usually diagnosed when the liver biopsy indicates inflammatory changes, hepatic degeneration, fibrosis, and other cellular changes. The combination of elevated aspartate aminotransferase level (but <300 IU per milliliter) and a ratio of the aspartate aminotransferase level to the alanine aminotransferase level greater than 2, a total serum bilirubin level above 5 mg per deciliter (86 μmol per liter), an elevated INR, and neutrophilia in a patient with ascites and a history of heavy alcohol use, is indicative of alcoholic hepatitis until proven otherwise. Patients with liver failure resulting from alcoholic liver disease who do not recover within the first 3 months of abstinence are unlikely to survive [6]. When cirrhosis has developed, clinical signs include palmar erythema, contractures in the finger muscles caused by toxic effects of fibrous changes, white nails, ―drummer‖ fingers, liver enlargement or inflammation and fatty infiltration [32]. The clinical presentation is florid and it appears in advanced stages so it is advisable to perform routine liver function tests to patients with a history of ingesting quantities of alcohol capable of increasing health vulnerability, according to WHO recommendations on intake grams of alcohol. Cirrhosis might be manifested by encephalopathy, which is a clinical manifestation of a severe form of liver disease, as well as malnutrition status and altered liver function tests such as marked prolongation of prothrombin time values, elevation in serum bilirubin above 25 mg/dL, depressed serum albumin, and elevated serum creatinine. Portal hypertension, hepatorenal syndrome, and esophageal varices are the major causes of clinical complications and mortality in ALD [32]. 5. Diagnostic Tests 5.1. Steatosis and Steatohepatitis Steatosis can be determined with a good level of accuracy by using noninvasive imaging techniques. Currently, there is no available noninvasive diagnostic test to distinguish between steatosis from steatohepatitis or to fibrosis stage [33]. Therefore, liver biopsy remains a useful tool to establish the diagnosis and to exclude other liver disease remaining the only instrument capable to provide prognostic information by staging and grading these diseases. Alcoholic steatohepatitis is a progressive