Most cases of acute hepatitis are caused by infection with one of five viruses: hepatitis A. B. C, D, or E. They can produce virtually indistinguishable clinical syndromes, although it is unusual to observe acute hepatitis C. Affected individuals often complain of a prodrome of nonspecific constitutional symptoms, including fever, nausea, fatigue, arthralgias, myalgias, headache, and sometimes pharyngitis and coryza. This is followed by the onset of visible jaundice caused by hyperbilirubinemia, with tenderness and enlargement of the liver, and dark urine caused by bilirubinuria. The clinical course, and prognosis then vary based on the type of virus causing the hepatitis.
Hepatitis A and E both are very contagious and transmitted by fecal-oral route, usually by contaminated food or water where sanitation is poor, and in daycare by children. Hepatitis A is found worldwide and is the most common cause of acute viral hepatitis in the United States. Hepatitis E is much less common and is found in Asia. Africa. Central America, and the Caribbean. Both hepatitis A and E infections usually lead to self-limited illnesses and generally resolve within weeks. Almost all patients with hepatitis A recover completely and have no long-term complications. A few may have fulminant disease resulting in liver failure. Most patients with hepatitis E also have uncomplicated courses, but some patients, particularly pregnant women, have been reported to develop severe hepatic necrosis and fatal liver failure.
Hepatitis B is the second most common type of viral hepatitis in the United States, and it is usually sexually transmitted. It also may be acquired par-enlerally. such as by intravenous drug use. and during birth from chronically infected mothers. The outcome depends on the age at which the infection was acquired. Up to 90% of infected newborns develop chronic hepatitis B infection. which places the affected infant at significant risk of hepatocellular carcinoma later in adulthood. For individuals infected later in life, approximately 95% of patients will recover completely without sequelae. Between 5% and 10% of patients will develop chronic hepatitis, which may progress to cirrhosis. A chronic carrier state may be seen in which the virus continues to replicate, but it does not cause irreversible hepatic damage in the host.
Hepatitis C is transmitted parenterally by blood transfusions or intravenous drug use. and rarely by sexual contact. The mode of transmission is unknown in approximately 40% of cases. It is uncommonly diagnosed as a cause of acute hepatitis, often producing subclinical infection, but is frequently diagnosed later as a cause of chronic hepatitis.
Hepatitis I) is a defective RNA virus that requires the presence of the hepatitis B virus to replicate. It can be acquired as a coinfection simultaneously with acute hepatitis B or as a later superinfection in a person with a chronic hepatitis B infection. Patients afflicted with chronic hepatitis B virus who then become infected with hepatitis D may suffer clinical deterioration; in 10-20% of these cases, individuals develop severe fatal hepatic failure.
Fortunately, in most cases of acute viral hepatitis, patients recover completely, so the treatment is generally supportive. However, fulminant hepatic failure as a result of massive hepatic necrosis may progress over a period of weeks. This usually is caused by infection by the hepatitis B and D viruses, or is drug-induced. This syndrome is characterized by rapid progression of encephalopathy from confusion or somnolence to coma. Patients also have worsening coagulopathy as measured by increasing prothrombin times, rising bilirubin levels, ascites and peripheral edema, hypoglycemia, hyperammonemia, and lactic acidosis. Fulminant hepatitis carries a poor prognosis (the mortality for comatose patients is 80%) and often is fatal without an emergency liver transplant.
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