Michael R. Narkewicz, M.D.
Hewit-Andrews Chair in Pediatric Liver Disease
Associate Professor of Pediatrics, Medical Director,
The Pediatric Liver Center
University of Colorado School of Medicine and The Children's Hospital
The term "hepatitis" is used to describe inflammation, swelling, or soreness of the liver. Hepatitis can have many different causes, including the hepatitis A, B, and C viruses; the delta and hepatitis E viruses; the Epstein-Barr virus (the mono virus); the cytomegalovirus (CMV); the herpes simplex virus; and varicella (chicken pox).
Other causes of hepatitis include toxins, such as drugs or alcohol. More rarely, autoimmune diseases, bacterial infections, fungal infections, and parasitic infections can cause hepatitis. The three most common causes of hepatitis are the hepatitis A, B, and C viruses.
The hepatitis A virus (an RNA virus) causes hepatitis A. This virus infects the liver and causes liver injury. Hepatitis A is the most common cause of acute viral hepatitis in the world.
Hepatitis A commonly is spread from person-to-person by contact with a stool from an infected person, or from water or food that has been contaminated by infected stool. Hepatitis A also can be found in shellfish from certain waters where raw sewage may drain. It often can pass from caregivers to children or adults in settings where there is close contact.
Most commonly, adults are exposed in small epidemics due to contaminated food or water sources. However, in 40% of people, no known risk factor can be identified. In the United States, approximately 10% to 20% of children have been exposed to hepatitis A by five years of age. Most of these children do not have symptoms when infected. In developing countries, the hepatitis A infection is very common in children (near 100%).
Hepatitis A generally is ingested in contaminated food or water. It is absorbed by the body, and then is taken into the liver cells. Following an incubation period of 15 to 50 days (average of 30 days), the liver cells are injured during the process of the body trying to eliminate the virus.
The incubation period for hepatitis A is about four weeks (i.e., after being exposed to the virus, a patient will not have any symptoms for about four weeks). Then, the patient usually will have flu-like symptoms, including malaise, vomiting, diarrhea, and fatigue. Jaundice (yellow eyes) often develops as the flu-like symptoms lessen; however, many times, particularly in children, jaundice will not be apparent. Liver blood tests, particularly AST and ALT, are abnormal.
After a period of illness, from one to four weeks, the jaundice will clear, the liver blood tests will normalize, and almost all patients will recover. Rarely, patients can have a relapse of jaundice for over six months. Very rarely, hepatitis A can lead to liver failure (less than 1 out of 10,000 cases).
Hepatitis A can be diagnosed by a blood test, which looks for an antibody (anti-hepatitis A IgM) that is produced to the virus. If a patient has abnormal liver blood tests (e.g., bilirubin, AST, or ALT), a physician will suspect hepatitis A.
No medications have been shown to be effective in treating hepatitis A. In fact, most individuals recover from it without any specific treatment. In patients who are deeply jaundiced, a low-fat diet may reduce diarrhea. A Vitamin K supplement may help reduce the risk of bleeding in patients who are jaundiced for a long period of time. In the rare case of liver failure, a liver transplant may be the only treatment option.
The most feared complication is liver failure; however, it very rarely occurs. Other complications, while rare, include pancreatitis, rashes, myocarditis, and relapsing hepatitis for up to six months. Cholestatic hepatitis, with itching as a major symptom, is another rare complication of hepatitis A. It may be treated with corticosteroids.
The primary prevention against hepatitis A is good handwashing and sanitation practices. Post-exposure prophylaxis with immunoglobulin has been the standard method of preventing hepatitis after an individual has been exposed to hepatitis A. Immunoglobulin may not be effective if given more than two weeks after an exposure. However, since hepatitis A can be prevented by vaccination with the hepatitis A vaccine, the use of immunoglobulin is declining. Several inactivated hepatitis A vaccines are available. The hepatitis A vaccination is recommended for those individuals (older than two years)
- who will be traveling to countries where hepatitis A is very prevalent;
- who have a high exposure risk, such as daycare workers;
- who have chronic liver disease;
- who have been exposed to hepatitis A during a community epidemic; or
- who have clotting factor disorders, and are likely to be treated with factor concentrates.
Other high-risk groups include certain Native American populations where hepatitis A may be very prevalent, laboratory workers handling the virus, sewage workers, health care workers, and individuals who work with primates.
Recent research has suggested that the hepatitis A vaccination early in the course of a hepatitis A epidemic may prevent the development of hepatitis A among individuals who are exposed to the virus. After exposure to the virus, gamma globulin can prevent the development of hepatitis A.
Current research efforts have resulted in the licensing of two vaccines. Additional work is concentrated on developing a live, attenuated vaccine that would be useful in third-world countries. Ongoing research also is focused on the use of these vaccines as prophylaxis in epidemics and the development of combination vaccines.
For more information on hepatitis A, log on to the following Web sites:
Innis BL, Snitbhan R, Kunasol, et al. Protection against hepatitis A by an inactivated vaccine. JAMA 1994;271:1328-34.
Katkov WN. Hepatitis vaccines. Med Clin North Am 1996;80:1189-1200.
Keefe EB, Iwarson S, McMahon BJ, et al. Safety and immunogenicity of hepatitis A vaccine in patients with chronic liver disease. Hepatology 1998;27:881-6.
Lemon SM, Thomas DL. Vaccines to prevent viral hepatitis. N Engl J Med 1997;336:196-204.
Koff RS. Hepatitis A. Lancet 1998;341:1643-9.
About the Author
Dr. Narkewicz graduated from the University of Vermont School of Medicine and completed his training in Pediatrics and Pediatric Gastroenterology at the University of Colorado. He holds the Hewit-Andrews Chair in Pediatric Liver Disease and is Associate Professor of Pediatrics at the University of Colorado and the Medical Director of the Pediatric Liver Center and Liver Transplantation at The Children's Hospital, Denver, Colorado.
Copyright 2012 Michael R. Narkewicz, M.D., All Rights Reserved