PATHOPHYSIOLOGY
Alcoholic hepatitis is a precursor of cirrhosis characterized by inflammation. The inflammation within the liver can lead to degeneration and necrosis of hepatocytes, infiltration of neutrophils, macrophages, and lymphocytes, and oxidative stress leading to lipid peroxidation. The injured hepatocytes contain Mallory Bodies, which is indicative of the onset of fibrosis. Neutrophils infiltrate and surround degenerating hepatocytes. The mechanisms of hepatocyte injury are not well understood, but inflammatory mediators, acetaldehyde, reactive oxygen and nitrogen species, and genetic factors are involved. Alcohol also increases gut permeability, and translocation of bacteria-derived lipopolysaccharide contributes to information, oxidative stress, and the severity of the alcoholic liver disease. Serum IgA level is often elevated in individuals with alcoholic hepatitis, and liver antigens and antibodies have been identified in persons with progressive alcoholic liver disease. The inflammation and necrosis caused by alcoholic hepatitis stimulate the fibrosis characteristics of the cirrhotic stage of the disease. Treatment includes corticosteroids and/or pentoxifylline and alcohol abstinence supported by Baclofen (McCance & Huether, 2019).
CLINICAL MANIFESTATIONS
The clinical manifestations of alcoholic hepatitis can be mild or severe. Nonspecific symptoms include fatigue, weight loss, and anorexia. Manifestations of acute illness include nausea, anorexia, fever, abdominal pain, and jaundice. Toxic effects of alcohol also can be gynecomastia, testicular atrophy, reduced libido, azoospermia, and decrease testosterone levels in men (McCance & Huether, 2019).
EVALUATION & TREATMENT
The diagnosis of alcoholic hepatitis is based on the individual’s history and clinical manifestations. Results of liver function tests are abnormal, and serological studies show elevated levels of serum enzymes and bilirubin and decreased serum albumin levels. Prolonged prothrombin time cannot easily be corrected without vitamin K therapy (McCance & Huether, 2019).
There is no specific treatment for alcoholic liver disease, but many of the complications are treatable. Rest, nutritious diet, corticosteroids, antioxidants, drugs that slow fibrosis, and management of complications such as ascites, gastrointestinal bleeding, anemia, infection, and encephalopathy slow disease progression. Cessation of alcohol consumption slows the progression of liver damage, improves clinical symptoms, and prolongs life. Although the liver damage is irreversible, measures that halt the inflammation and destruction of liver cells and fibrosis prolong life. Guidelines are available to guide treatment and predict clinical outcomes. Liver transplant is the treatment for liver failure, and artificial liver support systems are being developed (McCance & Huether, 2019).