Coinfected patients treated with new, successful hepatitis C antivirals drugs face a potentially life-threatening reactivation of their hepatitis B infection—even if their hepatitis B is resolved or inactive.
Up to 30 percent of people infected with hepatitis C are also infected with hepatitis B. In these coinfected patients, hepatitis C becomes the “dominant” virus in the liver and suppresses hepatitis B to barely detectable levels. When the new antiviral drugs, including sofosbuvir (Solvadi) are used, hepatitis B can resurge as hepatitis C retreats.
In the past, hepatitis C treatment used the antiviral ribavirin and pegylated interferon. While ribavirin targeted only hepatitis C, the interferon treatment helped the immune system fight both hepatitis C and B.
Today’s fast-acting hepatitis C treatment contains only antivirals that target only hepatitis C. Once hepatitis C is eradicated, doctors are finding a few cases where coinfected patients quickly experience a dangerous reactivation of their hepatitis B infection, even if they had “inactive” or resolved hepatitis B.
This discovery is significant, according to a report published in the current issue of the journal of Clinical Infectious Diseases, because current hepatitis C treatment guidelines, “do not offer specific guidance on treatment and monitoring of patients coinfected with hepatitis B.”
As a result, doctors don’t know they should be looking for hepatitis B reactivation in patients treated with sofosbuvir and simeprevir. However, coinfected patients may be among the first treated with the new drugs by doctors and Veterans Administration clinics because coinfections can produce more serious liver damage that requires treatment.
The journal article reports on two coinfected patients treated with sofosbuvir and simeprevir. One patient achieved undetectable hepatitis C viral load within four weeks, but seven weeks after starting treatment he developed jaundice and abdominal pain. Doctors at Emory University School of Medicine discovered he had a sudden reactivation of hepatitis B. His hepatitis B viral load, which had been very low before treatment, jumped into the millions and blood tests revealed severe liver damage.
Doctors stopped treatment and started him on the hepatitis B antiviral tenofovir (Viread), which quickly controlled the hepatitis B flare. After 28 weeks, the patient’s hepatitis B remained under control and he remained cured of hepatitis C.
In the second reported case, a patient who had cleared a hepatitis B infection and had hepatitis B surface antibodies, was treated with the same antivirals. This time, doctors monitored his hepatitis B and C viral load every two weeks. As expected, the hepatitis C virus disappeared while the hepatitis B viral load rapidly rose. This time, doctors added tenofovir to the ongoing treatment and 12 weeks later the patient tested undetectable for both viruses.
Researchers urged doctors to screen hepatitis C patients for signs of past or current hepatitis B infections before starting the new treatment, and to monitor hepatitis B viral load during treatment.