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.
Hepatitis B is a liver disease. The hepatitis B virus (HBV) causes hepatitis B. This virus is a DNA virus that typically is transmitted by exposure to contaminated blood or other body fluids.
HBV, the virus that causes hepatitis B, is the most common form of acute and chronic viral hepatitis throughout the world. In 1965, HBV was the first virus discovered to cause hepatitis.
In the United States, there are approximately 150,000 new cases of hepatitis B per year, and an estimated 1 to 1.25 million people have chronic infection with HBV. Hepatitis B primarily is transmitted by exposure to contaminated blood or body fluids. In the United States, HBV is spread by intimate contact with individuals who have HBV (e.g., sexual activity or needle sharing among intravenous drug users). The virus can be transmitted from mothers to their babies at the time of delivery.
In developing countries, this is quite common. In the United States, it still may occur, but usually can be prevented if the caregivers are aware of the mother's HBV status. The virus also may be transmitted through small exposures to blood (e.g., minute cuts, abrasions, sharing of toothbrushes, or contaminated piercing equipment or tattooing equipment). Individuals with a high rate of exposure to infected patients, such as health care workers, also are at risk.
HBV acutely infects the liver. There is an incubation period of 28 to 160 days, with an average of 80 days before symptoms may develop. Most adults develop acute hepatitis due to HBV. The body then develops immunity to the virus, and it is eliminated. Approximately 5% to 10% of adults who develop acute HBV infection go on to develop a chronic infection with HBV (i.e., lasting longer than 6 months).
In children, particularly newborns and children less than 1 year of age, about 75% to 90% will develop a chronic HBV infection. Individuals with chronic HBV infection can develop progressive scarring of their liver due to inflammation and are at increased risk for liver cancer.
Many patients (about 50%) with acute hepatitis B infection do not have any symptoms. Those patients who develop acute symptomatic hepatitis have flu-like symptoms, such as fever, malaise, muscle aches, vomiting, diarrhea, and anorexia. Some patients will develop jaundice (yellow eyes), pale stools, and dark urine. These symptoms generally clear over four to six weeks. In most adults, immunity to the virus is developed, and it is eliminated. From 5% to 10% of adults develop chronic HBV infection.
During this phase, they may be without symptoms, or they may have ongoing symptoms that are similar to acute hepatitis; however, the symptoms generally are milder. In children, particularly newborn infants, an acute hepatitis infection usually is without symptoms. Thus, the acute HBV infection generally is silent, and develops into a silent chronic infection in most children under one year of age.
During the acute phase, liver blood tests often are abnormal, particularly AST, ALT, and, less commonly, bilirubin. During a chronic infection, liver blood tests can be normal or abnormal.
HBV is diagnosed by blood tests. These blood tests include:
(a) HBsAg: Hepatitis B surface antigen. This test measures a protein from the virus and indicates that a person is infected with the virus. Persistence of HBsAg for more than six months indicates chronic infection.
(b) Anti-HBs: Antibody to hepatitis B surface antigen. This antibody develops when HBV is cleared from the body, or after the hepatitis B vaccine.
(c) Anti-HBc-IgM. This IgM antibody to the HBV core antigen is present only with an acute infection. IgG develops in any patient who has been infected or is chronically infected.
(d) HBeAg: Hepatitis B e antigen. This measures a protein from the virus, indicating that the virus is replicating (i.e., making a new virus) at a high rate. This often is present early in the course of chronic HBV infection.
(e) Anti-HBe: Antibody to hepatitis B e antigen. This develops when a chronically infected individual begins to build up an immune response to the virus and becomes a chronic carrier of the virus.
There is no treatment for acute HBV, except for supportive care. Liver failure can develop with HBV, and a liver transplant may be required.
Although chronic HBV is difficult to treat, treatments are available. Most patients with chronic HBV have normal liver blood tests and do not require treatment. In general, individuals who receive treatment for chronic HBV show signs of ongoing liver injury by liver blood tests and/or a liver biopsy. The current treatments available include immunomodulatory therapies, such as interferon. This shot is administered 3 times a week for 24 weeks.
Approximately 25% to 30% of children with chronic hepatitis due to HBV will respond to therapy with interferon. Nucleoside analogs, such as Lamivudine, are approved for the treatment of adults, and are currently under study for use in children. A liver transplant may be required for chronic HBV that has progressed to end-stage liver disease.
Acute HBV can be complicated by a serum sickness like illness, arthritis, or a rash. Other complications associated with acute hepatitis B infection include kidney disease (membranous nephropathy), a rash (e.g., papular acrodermatitis, Gianotti syndrome), and aplastic anemia. Rarely, acute HBV can lead to liver failure, requiring a liver transplant, or even causing death.
Chronic HBV infection is associated with various complications, including liver fibrosis or cirrhosis and liver failure. In patients who have chronic HBV infection, there is an increased risk of developing liver cancer. Kidney disease (membranous nephropathy) also may occur.
Avoiding high-risk behaviors can prevent hepatitis B. However, individuals without identified risk factors can acquire HBV.
The hepatitis B vaccine is very effective at protecting fully vaccinated individuals from contracting hepatitis B. It is a series of three shots that is part of the universal vaccination of children in the United States.
The Hepatitis B Immune Globulin (HBIG or NABIļ¿½-HB) can prevent hepatitis B after an acute exposure. It is prepared from hyperimmunized donors who have high levels of anti-HBs. This immune globulin is used in individuals with a known blood exposure to an infected individual.
Active research of hepatitis B is focused on:
- New treatments for chronic hepatitis B infection
- The development of newer vaccine strategies
- The role of HBV in liver cancer
- Treatments for individuals with chronic hepatitis B infection, but who have normal liver blood tests, and are at a high risk of liver cancer
For more information on hepatitis B, log on to the following Web sites:
- CDC Web site
- NIDDK Web site
- Hepatitis Foundation International Web site
- American Liver Foundation Web site
- GI Kids
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Chang MH, Chen CJ, Lai MS, et al. Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children. N Engl J Med 1997;336:1855-9.
Lee PI, Lee CY, Huang LM, Chang MH. Long-term efficacy of recombinant hepatitis B vaccine and risk of natural infection in infants born to mothers with hepatitis B e antigen. J Pediatr 1995;126:716-21.
Lemon SM, Thomas DL. Vaccines to prevent viral hepatitis. N Engl J Med 1997;336:196-204.
Hoofnagle JH, di Bisceglie AM. The treatment of chronic viral hepatitis. N Engl J Med 1997;336:347-56.
Balistreri WF. Acute and chronic viral hepatitis. In: Suchy FJ, ed. Liver disease in children. St. Louis: Mosby, 1994:460-509.
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 Narkewicz, M.D., All Rights Reserved
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