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Alcoholic hepatitis

Hepatitis is a gastroenterological disease, featuring inflammation of the liver. The clinical signs and prognosis, as well as the therapy, depend on the cause. more...

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Signs and symptoms

Hepatitis is characterised by fatigue, malaise, joint aches, abdominal pain, vomiting 2-3 times per day for the first 5 days, loss of appetite, dark urine, fever, hepatomegaly (enlarged liver) and jaundice (icterus). Some chronic forms of hepatitis show very few of these signs and only present when the longstanding inflammation has led to the replacement of liver cells by connective tissue; the result is cirrhosis. Certain liver function tests can also indicate hepatitis.

Types of hepatitis


Most cases of acute hepatitis are due to viral infections:

  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • D-agent (requires presence of the hepatitis B virus)
  • Hepatitis E
  • Hepatitis F (discredited)
  • Hepatitis G
Please see the respective articles for more detailed information.
See also infectious canine hepatitis.

Hepatitis A

Hepatitis A is an enterovirus transmitted by the orofecal route, such as contaminated food. It causes an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against hepatitis A that confer immunity against future infection. People with hepatitis A are usually advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent infection from hepatitis A for life. It can be spread through personal contact,consumption of raw sea food or drinking contaminated water.

Hepatitis B

Hepatitis B causes both acute and chronic hepatitis in some patients who are unable to eliminate the virus. Identified methods of transmission include blood (blood transfusion, now rare), tattoos (both amateur and professionally done), horizontally (sexually or through contact with blood or bodily fluids), or vertically (from mother to her unborn child). However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention. In the United States, 95% of patients clear their infection and develop antibodies against hepatitis B virus. 5% of patients do not clear the infection and develop chronic infection; only these people are at risk of long term complications of hepatitis B.

Patients with chronic hepatitis B have antibodies against hepatitis B, but these antibodies are not enough to clear the infection that establishes itself in the DNA of the affected liver cells. The continued production of virus combined with antibodies is a likely cause of immune complex disease seen in these patients. A vaccine is available that will prevent infection from hepatitis B for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are three, FDA-approved treatment options available for persons with a chronic hepatitis B infection: alpha-interferon, adefovir and lamivudine. In about 45% of persons on treatment achieve a sustained response.


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Alcoholic hepatitis
From American Family Physician, 4/1/93 by Scott E. Woods

Although the abuse of illicit substances generates much publicity, alcohol remains the most commonly consumed mood-altering drug in the United States. One reason for alcohol's popularity is its initial effectiveness in relieving the symptoms of depression, anxiety and stress. In addition, alcohol is easily available and socially acceptable. However, alcohol use costs more than $116 billion each year in direct medical care expenditures and lost productivity.[1] The incidence of alcoholism in the United States is approximately 7 percent.[1]

Alcohol is responsible for an estimated 350 disease processes (Table 1),[2] with hepatic disorders being the major medical consequence of alcohol abuse. The pathologic spectrum of alcoholic liver injury includes hepatic steatosis, perivenular fibrosis, alcoholic hepatitis and cirrhosis. All of these microscopically identified lesions may coexist in a patient. Alcoholic hepatitis is an acute, toxic degeneration and inflammatory process of the liver characterized by necrosis, inflammation and Mallory bodies.

Although Lainnec described cirrhosis during the 18th century, alcoholic hepatitis was not chronicled until more recently. In 1892, Osler recognized that alcohol consumption leads to acute necrosis of the liver. However, in 1961 Beckett defined the entity and employed the term "alcoholic hepatitis." This article reviews the clinical presentation, diagnosis, prognosis and treatment of alcoholic hepatitis.



Although the hepatotoxic nature of ethanol has been inferred for some time, most of the evidence has been epidemiologic. How ethanol exerts its toxic effect on the liver is not completely understood. One definition of an alcoholic is an individual who consumes enough alcohol to produce organic pathology. However, not all alcoholics develop significant liver disease. Why some persons are more susceptible to the ravages of ethanol than others is still a mystery. A retrospective study comparing ethanol consumption to histologic evidence of liver disease found that the amount of alcohol ingested and the duration of intake were important factors in the development of pathologic changes.[3]

While no threshold level of ethanol intake at which disease occurs abruptly has been found, the incidence of liver disease increases with an increasing amount of alcohol or duration of consumption. Although susceptibility to ethanol injury varies markedly, for most people an excess of 80 g per day is required - i.e., more than eight 12-oz beers (96 g), one liter of 12 percent wine (80 g) or one-half pint of 80-proof whiskey (64 g) each day. In the Veterans Affairs Cooperative Study[4] on alcoholic hepatitis, the mean consumption for persons with mild disease was 234 g each day.

Alcohol consumption correlates with morbidity and mortality. During Prohibition, mortality from cirrhosis fell precipitously and remained low until the Prohibition Amendment was repealed, after which mortality rates from cirrhosis climbed progressively.[1] Internationally, there is a significant correlation between alcohol consumption and death from cirrhosis. However, mortality comparisons across countries show a variation that suggests interaction with other factors, including genetic predisposition, malnutrition or concomitant hepatitis B infection.

Approximately 90 percent of the ethanol absorbed by the body is oxidized by the liver; the rest is eliminated by the kidneys and lungs. Ethanol oxidation produces striking metabolic imbalances in the liver. When present, ethanol is the preferred fuel for the liver, completely overtaking its intermediary metabolism.

There are two simultaneous pathways for the metabolism of alcohol, one utilizing alcohol dehydrogenase, the other involving the microsomal ethanol oxidizing system. The alcohol dehydrogenase pathway results in the production of acetaldehyde and hydrogen. The microsomal ethanol oxidizing system pathway generates acetaldehyde and free radicals. These products are responsible for a variety of metabolic alterations that play a role in the development of liver injury. Alcohol and other hepatotoxins are interrelated in a complex fashion. Alcohol can enhance the toxic effects of other substances. For example, therapeutic doses of acetaminophen can be hepatotoxic in alcoholics.[5]

Clinical Presentation

The spectrum of presenting signs and symptoms ranges from those symptoms associated with very mild hepatic injury to those symptoms accompanying life-threatening liver decompensation. In mild cases, the only finding may be hepatomegaly in a patient with a definite or suspected history of ethanol consumption. In the Veterans Affairs Cooperative Study,[6] the symptoms of mild forms of the disease (group 1) were nonspecific (Table 2). Hepatomegaly, anorexia, weight loss, fatigue and symptoms of alcohol withdrawal pre-dominated. In more severe cases (groups 2 and 3), the dominant features were liver decompensation and its complications - jaundice, ascites, portal hypertension and hepatic encephalopathy.

A significant subset of patients presents with severe right upper quadrant pain, fever, jaundice and leukocytosis. This combination of symptoms may be confused with obstructive cholangitis or cholecystitis, a misdiagnosis that could be disastrous because surgery is associated with high morbidity and mortality in patients with alcoholic hepatitis.[7]

Although jaundice, ascites and encephalopathy may subside with abstinence, continued ethanol use and malnutrition usually lead to recurrent exacerbations. Some patients die during acute events. Clinical recovery may be protracted, requiring six months or longer. Even with complete abstinence, recovery is not guaranteed.


Laboratory Findings

The wide spectrum of laboratory abnormalities associated with alcoholic hepatitis reflects its multisystem effects (Table 3). In the Veterans Affairs Cooperative Study,[6] 41 percent of the patients exhibited leukocytosis, with the frequency increasing with severity of disease. It has been hypothesized that leukemoid reactions represent a poor prognostic sign in alcoholic hepatitis.[8] Although leukocytosis was common, leukopenia was also observed in 8 percent of patients, presumably as a direct result of bone marrow suppression by ethanol. Anemia occurred in 82 percent of patients. Typically, anemia in this group of patients is macrocytic, resulting from ethanol-induced red blood cell membrane alterations, vitamin [B.sup.12] deficiency or, most commonly, folate deficiency. However, microcytic iron deficiency anemia can occur if the alcoholic patient also has gastrointestinal blood loss.


Typically, alcoholic liver disease causes only modest elevation in the liver enzymes. The AST level is less than five times the upper limits of normal. Values higher than this should spur an investigation into causes of hepatitis other than ethanol (Table 4).[9] The serum ALT level is typically less than half of the AST level. It has been suggested that an AST-to-ALT ratio greater than 2 is diagnostic for alcoholic hepatitis. In the Veterans Affairs study,[6] 93 percent of the patients had an AST level greater than the ALT level, but the ratio exceeded two in 58 percent of cases. This percentage suggests that a ratio greater than two is not necessary for the diagnosis of alcoholic hepatitis but is highly specific for the disease. Equally important is the finding that 20 percent of the patients in the Veterans Affairs study had normal AST levels, and 44 percent had normal ALT levels. Thus, normal enzyme levels do not rule out alcoholic hepatitis.

It is not known why hepatocellular enzyme levels can be low despite necrosis and cellular injury. Concomitant pyridoxine deficiency has been hypothesized as a cause, but this remains unproved.

Biochemically, alcoholic hepatitis may be considered a cholestatic form of liver disease, commonly causing hepatocanalicular enzymes to be elevated out of proportion to the aminotransaminase levels. Serum alkaline phosphatase and bilirubin levels tend to parallel each other and were observed to be abnormal in 82 percent and 78 percent, respectively.[6] The gamma-glutamyltransferase level is frequently elevated in patients with liver disease, but because of its low specificity, this abnormality isnot useful in the diagnosis of alcoholic hepatitis.


Histologic diagnosis of alcoholic hepatitis requires three essential features: liver cell damage, an inflammatory infiltrate and fibrosis. Hepatocyte injury, typically described as ballooning degeneration, begins in the centrilobular area. It is characterized by swollen hepatocytes, with pale granular cytoplasm. Mallory bodies are frequently present within these cells. Mallory bodies are intracellular eosinophilic aggregates of dense proteinaceous material, perinuclear in location (Figure 1). They are thought to result from derangement of the intermediate filament component of the hepatocyte cytoskeleton. Mallory bodies possess strong chemotaxic properties. Neutrophils migrate into liver cells containing Mallory bodies, contributing to ethanol-induced hepatocellular damage.[10] Mallory bodies are highly suggestive but not specific for alcoholic hepatitis, since they also occur in other hepatic disorders. They disappear following six to 12 weeks of alcohol abstinence.[11]

Although Mallory bodies are common in the centrilobular area, the mechanism causing early hepatic injury is not understood. The centrilobular location of hepatic injury may be induced by hypoxia. This part of the lobule has the lowest oxygen tension. Also, ethanol withdrawal causes an increase in hepatocyte oxygen consumption, with a simultaneous decrease in hepatic venous oxygen content. Thus, the centrilobular area becomes more hypoxic, with increased susceptibility to injury and necrosis. Loss of hepatocytes in the centrilobular area is replaced by an acellular confluent sclerotic area, termed "sclerosing hyaline necrosis."

The inflammatory infiltrate in alcoholic hepatitis is predominantly polymorphonuclear. The heaviest penetration of neutrophils is in locations of necrosis and Mallory bodies, usually in the centrilobular area. Although less numerous, cytotoxic Tlymphocytes also invade the liver, typically in portal areas. These cells bind to hepatocytes, causing cell death. It has been theorized that this process is a contributing factor in chronic alcoholic hepatitis.

Although deposition of fibrous tissue in the liver lobule can occur almost anywhere, early fibrosis typically surrounds central veins. This perivenular (pericentral) fibrosis (Figure 2) is often associated with sclerosing hyaline necrosis. Central vein obliteration can occur with severe fibrosis, leading to postsinusoidal portal hypertension and ascites prior to the development of cirrhosis. Perivenular fibrosis, however, can be seen in the absence of inflammation and necrosis.[12] Perivenular fibrosis is commonly associated with fibrosis encircling hepatocytes (pericellular). Some investigators[13] believe that pericellular fibrosis (Figure 3) is of greater prognostic significance for the development of cirrhosis than perivenular fibrosis.

In time, pericellular fibrosis causes progressive lobular distortion (Figure 4). This process mimics micronodular cirrhosis, since lobules are converted into smaller aggregates of hepatocytes surrounded by fibrosis (Figure 5). Micronodular cirrhosis is distinguished from pericellular fibrosis by the presence of regeneration nodules. Cirrhosis is a pathologically defined entity in which the parenchyma is characterized by extensive fibrosis and regeneration nodules.


Sometimes alcoholic hepatitis is an apparent diagnosis. The presence of fever, leukocytosis, jaundice and tender hepatomegaly in an alcoholic patient can clinically be diagnostic of alcoholic hepatitis. However, frequently the disease is less obvious, requiring an index of suspicion. The clinician may not elicit a history or even suspect ethanol abuse. Hepatomegaly may be the only physical sign. Liver enzyme levels could be normal. Because of the spectrum of clinical presentations, liver biopsy is frequently required for diagnosis. Biopsy could also uncover other alcohol-induced liver disease, such as cirrhosis, which could affect prognosis and treatment.


The prognosis for patients with acute alcoholic hepatitis is variable and depends on the severity of the acute lesion and the prx-sence or absence of cirrhosis. Although several prognostic indicators have been investigated, a formula derived by Maddrey and colleages[14] has shown consistent reliability. These investigators found that serum bilirubin and prothrombin time offer the best correlation with morbidity and mortality: (total bilirubin + [prothrombin time - control]) x 4.6.

According to the authors'discriminant functions, patients with a score of 32 or higher have a 50 percent mortality rate in the first 30 days of hospitalization, even if they abstain from ethanol. Long-term complete recovery depends on the achievement of abstinence. However, cirrhosis can develop even if a patient remains sober.

Women are at higher risk of developing cirrhosis, because of higher blood alcohol levels at equivalent consumption. A lower quantity of gastric alcohol dehydrogenase, an enzyme responsible for the first-pass metabolism of ethanol, causes the higher levels in women.[15]

Recently published prognostic data from the Veterans Affairs Cooperative Study[16] reveal the gravity of the disease. The study subjects were stratified into four categories according to liver biopsy results: (1) hepatic steatosis, (2) acute alcoholic hepatitis, (3) cirrhosis and (4) cirrhosis with alcoholic hepatitis. After four years of follow-up, group 1 had a 30 percent mortality rate; the deaths, however, were not due to liver disease. Groups 2, 3 and 4 had 42 percent, 51 percent and 65 percent mortality rates, respectively. Most of the deaths in groups 2, 3 and 4 were related to liver disease. In group 4, the most significant predictors of survival were age, grams of ethanol consumed and histologic severity of disease. Alcoholic liver disease has a worse prognosis than most cancers.


Medical therapy is directed at reducing the severity of alcoholic hepatitis and trying to prevent fibrosis. It is clear that ethanol is essential for the initiation and progression of alcoholic liver disease. Thus, abstinence should be the mainstay of all treatment plans. The Twelve Step program of Alcoholics Anonymous is one of the most successful in achieving abstinence.

Nutritional therapy is the next most important treatment modality. Correction of malnutrition is essential for improvement of liver disease.[17] Even with abstinence, only minimal improvement will occur if nutritional deficiency persists. In the absence of hepatic encephalopathy, a high-calorie, high-protein diet is required to obtain the desired positive nitrogen balance. Since vitamin and mineral deficiencies are common, these patients should also take a high-potency multivitamin every day. If nutritional status improves (e.g., increased albumin and transferrin levels, total lymphocyte count and creatinine-height index) during hospitalization, the patient's one-year survival is better.[18]

Because alcoholic hepatitis is characterized by inflammation, corticosteroids could theoretically be of benefit. Despite several clinical trials, their utilization in this instance remains controversial. Several studies have demonstrated reduced mortality in selected patients; however, other studies have not confirmed this finding. Even in studies in which steroids appeared to be beneficial, they had no effect on progression to fibrosis. A meta-analysis of the multiple studies suggests that corticosteroids are of benefit in patients with hepatic encephalopathy only.[19] A recently published randomized double-blind study[20] comparing 28 days of prednisolone treatment with placebo in patients with biopsy-proven alcoholic hepatitis and either hepatic encephalopathy or a discriminant function greater than 32 showed that prednisolone resulted in significant improvement in short-term survival of patients with severe alcoholic hepatitis. The primary end point was death. The results suggest that corticosteroid therapy is useful in severe alcoholic hepatitis.

Anabolic steroids have been investigated as a method of reversing the catabolic state of alcoholic liver disease. Although several studies have shown benefit, the only double-blind placebo-controlled study employing anabolic steroids found no effect on either short- or long-term mortality.[21]

Colchicine (Colbenemid) interferes with microtubule assembly and the transcellular movement of collagen. This drug has been found to reduce fibrosis in rats and has been used with some benefit in the treatment of human primary biliary cirrhosis. In one randomized placebo-controlled trial,[22] colchicine had no effect on short-term morbidity and mortality. One long-term study,[23] however, showed significant improvement with colchicine. Although the results are promising, this trial had a small treatment population. Thus, further investigation will be required to accurately assess the efficacy of colchicine.

Other investigational therapies include insulin and glucagon infusions, penicillamine and liver transplantation.

REFERENCES 1. Zakim D, Boyer TD, Montgomery C. Alcoholic liver disease. In: Zakim D, Boyer TD, eds. 2d ed. Hepatology: a textbook of liver disease. Philadelphia: Saunders, 1990:821. 2. West LJ, Maxwell DS, Noble EP, Solomon DH. Alcoholism. Ann Intem Med 1984;l00: 405-16. 3. Lelbach W. Epidemiology of alcoholic liver disease: continental Europe. In: Hall P, ed. Alcoholic liver disease: pathobiology, epidemiology, and clinical aspects. London: Arnold, 1985:130. 4. Goldberg S, Mendenhall C, Anderson S, et al. VA Cooperative Study on Alcoholic Hepatitis. IV. The significance of clinically mild alcoholic hepatitis - describing the population with minimal hyperbilirubinemia. Am J Gastroenterol 1986;81:1029-34. 5. Maddrey WC. Hepatic effects of acetaminophen. Enhanced toxicity in alcoholics. J Clin Gastroenterol 1987;9:180-5. 6. Mendenhall CL. Alcoholic hepatitis. Clin Gastroenterol 1981;10:417-41. 7. Mendenhall CL. Alcoholic hepatitis. In: Schiff L, Schiff ER, eds. Diseases of the liver. 6th ed. Philadelphia: Lippincott, 1987:669. 8. Mitchell RG, Michael M 3d, Sandidge D. High mortality among patients with the leukemoid reaction and alcoholic hepatitis. South Med J 1991;84:281-2. 9. Woods S, Colon VF. Wilson's disease. Am Fam Physician 1989;40(l):171-8. 10. Takahashi T, Kamimura T, Ichida F. Ultrastructural findings on polymorphonuclear leukocyte infiltration and acute hepatoceullar damage in alcoholic hepatitis. Liver 1987; 7:347-58. 11. Tsutsumi M, Lasker JM, Shimizu M, Rosman AS, Lieber CS. The intralobular distribution of ethanol-inducible P450IIE1 in rat and human liver. Hepatology 1989; 10:437-46. 12. Nakano M, Worner TM, Lieber CS. Perivenular fibrosis in alcoholic liver injury: ultrastructure and histologic progression. Gastroenterology 1982;83:777-85. 13. Caulet S, Fabre M, Schoevaert D, Lesty C, Meduri G, Martin E. Quantitative study of centrolobular hepatic fibrosis in alcoholic disease before cirrhosis. Virchows Arch A Pathol Anat Histopathol 1989;416:11-7. 14. Maddrey W, Carithers R, Herlong H, et al. Prednisolone therapy in patients with severe alcoholic hepatitis: results of a multicenter trial. Hepatology 1986;6:1202. 15. Frezza M, di Padova C, Pozzato G, Terpin M, Baraona E, Lieber CS. High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. N Engl J Med 1990;322:95-9 [Published erratum appears in N Engl J Med 1990;322:1540 and 1990;323:553]. 16. Chedid A, Mendenhall CL, Gartside P, French SW, Chen T, Rabin L. Prognostic factors in alcoholic liver disease. VA Cooperative Study Group. Am J Gastroenterol 1991;86:210-6. 17. Phillips GB. Acute hepatic insufficiency of the chronic alcoholic - revisited. Am J Med 1983; 75:1-3. 18. Mendenhall CL, Tosch T, Weesner RE, et al. VA cooperative study on alcoholic hepatitis. II. Prognostic significance of protein-calorie malnutrition. Am J Clin Nutr 1986;43:213-8. 19. Imperiale TF, McCullough AJ. Do corticosteroids reduce mortality from alcoholic hepatitis? A meta-analysis of the randomized trials. Ann Intern Med 1990;113:299-307. 20. Ramond MJ, Poynard T, Rueff B, et al. A randomized trial of prednisolone in patients with severe alcoholic hepatitis. N Engl J Med 1992; 326:507-12. 21. Mendenhall CL, Anderson S, Garcia-Pont P, et al. Short-term and long-term survival in patients with alcoholic hepatitis treated with oxandrolone and prednisolone. N Engi J Med 1984;311:1464-70. 22. Akiriviadis EA, Steindel H, Pinto PC, et al. Failure of colchicine to improve short-term survival in patients with alcoholic hepatitis. Gastroenterology 1990;99:811-8. 23. Kershenobich D, Vargas F, Garcia-Tsao G, Perez Tamayo R, Gent M, Rojkind M. Colchicine in the treatment of cirrhosis of the liver. N Engl J Med 1988;318:1709-13.

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