Clinically, the patient is usually asymptomatic, and the examination reveals a firm, smooth, enlarged liver. Occasionally the fatty liver may be so severe that the patient is anorexic and nauseated, and has right upper quadrant pain or discomfort. This usually follows a prolonged heavy alcoholic binge. Liver function tests including bilirubin, albumin and INR are usually normal, although the g-glutamyl transpeptidase (GGT) is invariably elevated while the aminotransferases and alkaline phosphatase may be slightly increased. A fatty liver is usually detected by ultrasound. Liver biopsy is required to make a definitive diagnosis. When fatty liver is not associated with alcoholic hepatitis, its prognosis is excellent. Complete abstinence from alcohol and a nutritious diet will lead to disappearance of the fat over four to six weeks.

Alcoholic hepatitis may occur separately or in combination with cirrhosis. There are all grades of severity. It is a condition characterized by liver cell necrosis and inflammatory reaction. Histologically, hepatocytes are swollen as a result of an increase in intracellular water secondary to increase in cytosolic proteins. Steatosis, often of the macrovesicular type, is present. Alcoholic hyaline (Mallory's) bodies are purplish red intracytoplasmic inclusions consisting of clumped organelles and intermediate microfilaments. Polymorphs are seen surrounding Mallory-containing cells and also within damaged hepatocytes. Collagen deposition is usually present. It is maximal in the zone 3 and extends in a perisinusoidal pattern to enclose hepatocytes, giving it a "chicken wiring" effect. Changes in the portal triad are inconspicuous. Marked portal inflammation suggests an associated viral hepatitis such as hepatitis C, whereas fibrosis suggests complicating chronic hepatitis. When the acute inflammation settles, a varying degree of fibrosis is seen, which may eventually lead to cirrhosis.

Clinically, mild cases of alcoholic hepatitis are recognized on liver biopsy only in patients who present with a history of alcohol abuse and abnormal liver enzymes. In the moderately severe case, the patient is usually malnourished and presents with a two-to three-week prodrome of fatigue, anorexia, nausea and weight loss. Clinical signs include a fever of <40ºC, jaundice and tender hepatomegaly. In the most severe case, which usually follows a period of heavy drinking without eating, the patient is gravely ill with fever, marked jaundice, ascites, and evidence of a hyperdynamic circulation such as systemic hypotension and tachycardia. Florid palmar erythema and spider nevi are present, with or without gynecomastia. Hepatic decompensation can be precipitated by vomiting, diarrhea or intercurrent infection leading to encephalopathy. Hypoglycemia occurs often and can precipitate coma. Gastrointestinal bleeding is common, usually from a local gastric or duodenal lesion, resulting from the combination of a bleeding tendency and portal hypertension. Signs of malnutrition and vitamin deficiencies are common. Intake of moderate doses of acetaminophen in an alcoholic may precipitate florid alcoholic hepatitis.

Laboratory abnormalities include elevations of the aminotransferases, bilirubin, alkaline phosphatase and GGT. The aminotransferase levels rarely exceed 300 IU/L, except in association with acetaminophen ingestion; the AST/ALT ratio is usually >2. Hyperbilirubinemia can be quite marked, with levels reaching 300 to 500 µmol/L, and is a reflection of the severity of the illness. The increase in GGT is proportionally greater than that of alkaline phosphatase. There is also leukocytosis of up to 20-25 x 10⁹/L and increased INR/prothrombin time, which does not respond to vitamin K. The serum albumin falls. Serum IgA is markedly increased, with IgG and IgM raised to a lesser extent.

Patients with acute alcoholic hepatitis often deteriorate during the first few weeks in hospital, with a mortality rate of 20-50%. Bad prognostic indicators include spontaneous encephalopathy, markedly increased INR/PT unresponsive to vitamin K and severe hyperbilirubinemia of greater than 350 µmol/L. The condition may take one to six months to resolve, even with complete abstinence. Alcoholic hepatitis progresses to cirrhosis in 25-30% of clinical episodes.

Established cirrhosis is usually a disease of middle age after the patient has had many years of drinking. Although there may be a history of alcoholic hepatitis, cirrhosis can develop in apparently well-nourished, asymptomatic patients. Occasionally the patient may present with end-stage liver disease with malnutrition, ascites, encephalopathy and a bleeding tendency. A history of alcohol abuse usually points to the etiology. Clinically, the patient is wasted. There may be bilateral parotid enlargement and Dupuytren's contracture in alcohol abuse. The patient may have palmar erythema and multiple spider nevi of chronic liver disease. Males develop gynecomastia and small testes. Hepatomegaly is often present, affecting predominantly the left lobe as a result of marked hypertrophy. There may be signs of portal hypertension, which include splenomegaly, ascites and distended abdominal wall veins. At the late stage, the liver may become shrunken and impalpable. There may be signs of alcohol damage in other organ systems, such as peripheral neuropathy and memory loss from cerebral atrophy. Alcoholic cirrhosis is also associated with renal problems, including IgA nephropathy, renal tubular acidosis and the development of hepatorenal syndrome. There is an association between hepatitis B and C and alcoholic cirrhosis.

Histologically, the cirrhosis is micronodular. The degree of steatosis is variable and alcoholic hepatitis may or may not be present. Pericellular fibrosis around hepatocytes is widespread. Portal fibrosis contributes to the development of portal hypertension. There may be increased parenchymal iron deposition. When parenchymal iron deposition is marked, genetic hemochromatosis has to be excluded. With continued cell necrosis and regeneration, the cirrhosis may progress to a macronodular pattern.

Biochemical abnormalities include a low serum albumin, and elevated bilirubin and aminotransferases. AST and ALT levels rarely exceed 300 IU/L and the AST/ALT ratio usually exceeds 2. GGT is disproportionately raised with recent alcohol ingestion and is a widely used screening test for alcohol abuse. With severe disease, the INR/PT may be increased. Portal hypertension results in hypersplenism leading to thrombocytopenia, anemia and leukopenia. Other nonspecific serum changes in acute and chronic alcoholics include elevations in uric acid, lactate and triglyceride, and reductions in glucose and magnesium.

The prognosis of alcoholic cirrhosis depends on whether the patient can abstain from alcohol; this in turn is related to family support, financial resources and socioeconomic state. Patients who abstain have a five-year survival rate of 60-70%, which falls to 40% in those who continue to drink. Women have a shorter survival rate than men. Bad prognostic indicators include a low serum albumin, increased INR/PT, low hemoglobin, encephalopathy, persistent jaundice and azotemia. Zone 3 fibrosis and perivenular sclerosis are also unfavorable features. Complete abstinence may not improve prognosis when portal hypertension is severe. Hepatocellular carcinoma occurs in 10% of stable cirrhotics. This usually develops after a period of abstinence when macronodular cirrhosis is present. It is usually fatal in six months.

Early recognition of alcoholism is important. Physicians should have a high index of suspicion when a patient presents with anorexia, nausea, diarrhea, right upper quadrant tenderness and an elevated GGT. The most important therapeutic measure is total abstinence from alcohol. Support groups and regular follow-up can reinforce the need for abstinence. Withdrawal symptoms should be treated with chlordiazepoxide or diazepam. A nutritious, well-balanced diet with vitamin supplements should be instituted.

Alcoholic fatty liver responds to alcohol withdrawal and a nutritious diet. Patients with severe alcoholic hepatitis should be admitted to hospital and complications of liver failure treated appropriately. These patients usually have significant metabolic abnormalities that have to be corrected. Hyperglycemia is a common manifestation of chronic liver disease because of insulin resistance, whereas hypoglycemia is a manifestation of (especially fulminant) hepatic failure because of failure of gluconeogenesis and depletion of glycogen stores. Hypomagnesemia and hypokalemia are common as a result of reduced dietary intake and increased urinary excretion. Metabolic acidosis may be present, which may relate to the failure to convert lactic acid to pyruvate as well as possible underlying ketoacidosis. Specific treatments for alcoholic hepatitis include the use of corticosteroids. A recent meta-analysis of 11 controlled trials showed a significant benefit of steroids for patients with severe alcoholic hepatitis complicated by encephalopathy. Propylthiouracil has been used to dampen the hepatic hypermetabolic state in alcoholic hepatitis, and may reduce the two-year mortality rate. Testosterone and anabolic androgenic steroids have been tried with conflicting results. Intravenous amino acid supplements have been given to the severely protein malnourished with varying degrees of success. Oral supplementation is the preferred route if the patient can tolerate a diet.