Hepatitis B and Hepatitis C
The prevalence of combined infections with these two organisms in Canada is unknown. Elsewhere the prevalence ranges between 3.4-18.3% in series of patients with hepatitis C (88-90). Various studies have demonstrated that the outcome of combined infection is more severe than infection with either virus alone (91,92). In most patients one infection predominates, while the other is dormant. Thus in HBV-dominant disease the HBV DNA is detectable, while the HCV RNA is not, and vice versa. Occasionally both diseases may be active. The risk of HCC is also increased compared to the risk with hepatitis B or hepatitis C alone (93-96). There are few reports of treatment (97). In patients with one infection dominant, and the other dormant the indications for treatment and the dose and duration of treatment are identical to when the dominant disease exists on its own. For example, in patients who are HBeAg-positive with detectable HBV DNA, undetectable HCV RNA and elevated aminotransferases, treatment is with interferon 27-36 mu weekly for 4 months. Conversely, if the HBV DNA is undetectable, and HCV RNA is present, the treatment is with interferon and ribavirin for 24 or 48 weeks, as dictated by the hepatitis C genotype.

Hepatitis B and HIV
Since hepatitis B and HIV are spread via similar routes patients often have evidence of infection with both agents. However, only about 10% of HIV-positive subjects are chronic carriers of hepatitis B. In the presence of HIV infection hepatitis B replication is increased, liver disease is more common, and tends to be more rapidly progressive. However, until the advent of highly active anti-retroviral therapy most patients who were co-infected with hepatitis B and HIV died of AIDS, rather than complications of hepatitis B. This may no longer be true now that more effective anti-HIV therapy is available. Interferon treatment of hepatitis B in HIV-positive patients has been largely unsuccessful (31,32,98) Lamivudine therapy is effective in suppressing viral replication, but at present there are no reports of long term outcome after lamivudine therapy in this population. Since lamivudine is a component of highly active anti-retroviral therapy, patients co-infected with both viruses may receive appropriate treatment for the hepatitis B as a fortunate, but not necessarily intended, result of
HIV therapy. Chronic hepatitis B in HIV-infected patients must not be treated with lamivudine monotherapy. Lamivudine
monotherapy will result in the rapid emergence of resistant HIV virus.

Hepatitis C and HIV
Hepatitis C infection occurs in HIV-positive patients with a frequency between 50-90%. Co-infection results in hepatitis C viral loads that are higher than in the absence of HIV (99,100). Progression to cirrhosis is also more rapid (100). Treatment with interferon monotherapy has a success rate not much different than for hepatitis C in the absence of HIV (about15%)(101-104). There are no data on the use of combination therapy with interferon and ribavirin in these patients. There are no recommendations about therapy in patients co-infected with hepatitis C and HIV.

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