Douglas G. Fish, M.D., Albany Medical College, Albany, N.Y., EE.UU.
Hepatitis B is the most common cause of cirrhosis and heptocellular carcinoma worldwide. Hepatitis B can be transmitted sexually, parenterally and vertically from mother to child. Over 350 million people are chronically infected worldwide with hepatitis B.
The good news is that hepatitis B is largely preventable with a vaccine series. Successful treatments for hepatitis B have lagged behind, but newer drugs with potent activity against hepatitis B make the future look brighter.
The talk will review the serologies for hepatitis B and the significance of each. The hepatitis B surface antigen (HbsAg) becomes positive with acute infection, and usually persists in those who develop chronic infection. The hepatitis B surface antibody (HbsAb) confers immunity, and develops in approximately 90 percent of those infected naturally or vaccinated against hepatitis B. Core antibody develops in the acute phase (HbcAb IgM) of infection, and later the IgG component develops. The hepatitis B core IgG cannot be measured in isolation, so is reflected in a positive total core Ab, which detects both IgM and IgG components. With HIV coinfection, it is common for patients to only show core antibody positivity, with both the surface antigen and surface antibody being negative. Some of these patients are chronically infected, and others are likely immune.
Interferon in high doses for 6 months has been the standard therapy for chronic hepatitis B, with success gauged by conversion from hepatitis e antigen (HbeAg) positive to e antibody (HbeAb) positive. These high doses of interferon required are difficult for HIV-infected patients to tolerate and a challenge to manage along with HAART. Lamivudine has potent activity against hepatitis B, but as a single agent, ultimately fails in the majority of patients over years, due to the development of the YMDD mutation. Tenofovir has activity against both HIV and lamivudine-resistant hepatitis B, and may be synergistic with lamivudine against hepatitis B in untreated patients. Adefovir is now available for those with chronic hepatitis B without HIV. Data with these newer agents will be presented.
Hepatitis D is a defective virus, which only causes disease in those acutely or chronically infected with hepatitis B. Hepatitis A is vaccine-preventable, and occurs in HIV-infected patients largely from contaminated foods, and occasionally between men who have sex with men. Hepatitis A does not have a chronic form. Hepatitis E is an enterically-transmitted form of non-A, non-B hepatitis that occurs primarily in Asia and parts of Africa, and has a high mortality if contracted in the third trimester of pregnancy. Hepatitis G, now called GBV-C, is not felt to cause liver disease, but can be detected in patients by PCR techniques. In those with HIV infection, the co-existence of hepatitis G has been associated with higher CD4+ T-lymphocyte counts and lower HIV loads. The mechanism for this is currently unknown.
In summary, viral hepatitis is common in the world and in patients with HIV infection. The future looks brighter for those with chronic hepatitis B using newer oral agents. Hepatitis C will be reviewed in another presentation.