No evidence of an interaction between abacavir and ribavirin

There is no evidence of an interaction between the anti-HIV drug abacavir and the anti-hepatitis C agent ribavirin, investigators report in the online edition of AIDS.

Some earlier research reported poorer hepatitis C treatment outcomes in co-infected patients whose antiretroviral regimens included abacavir (Ziagen, also in Kivexa and Trizivir). This was attributed to an interaction between abacavir and ribavirin, leading to sub-optimal levels of the anti-hepatitis C drug.

But French investigators found that this was not the case. Rapid, early and sustained responses to hepatitis C therapy were comparable between patients taking abacavir and non-abacavir combinations. Moreover, trough combinations (C_min) of ribavirin were not adversely affected by abacavir.

“There was no evidence that abacavir affected ribavirin C_min or HCV [hepatitis C virus] treatment outcomes,” comment the investigators.

The retrospective study included 124 co-infected patients enrolled in the larger ANRS CO-13 HEPAVIH study.

Almost all the patients (95%) were taking antiretroviral therapy. Just over a fifth (22%) were treated with a regimen that included abacavir. Over three-quarters (77%) were taking tenofovir (Viread, also in the combination pills Truvada, Atripla and Eviplera). There were no significant HIV- or hepatitis C-related differences between the patients taking abacavir and those who were not taking abacavir.

Hepatitis C therapy consisted of pegylated interferon plus weight-based ribavirin. The median ribavirin dose at baseline was 1000mg per day. This dose was changed in 39% of patients following the first C_min result.

The overall median ribavirin C_min was 1.6 mg/l. This did not differ between abacavir users and non-abacavir patients (1.5 vs 1.7 mg/l).

There was no significant difference between the two groups in terms of the number of individuals who needed to adjust their dose of ribavirin (48 vs 36%).

Comparison between patients treated with abacavir and those taking tenofovir also showed that there was no difference in median C_min (1.5 mg/l vs 1.7 mg/l).

Overall, 52% of patients had a rapid virological response (RVR; undetectable viral load after four weeks) to hepatitis C therapy and 72% had an early virological response (EVR; undetectable viral load at twelve weeks).

Treatment with abacavir did not affect outcomes at these points (RVR: 59 vs 50%; EVR: 72 vs 73%).

Some 45% of patients taking abacavir achieved a sustained virological response (SVR; undetectable viral load 24 weeks after the completion of treatment), considered a cure. This compared to a response rate of 24% among the patients who were not taking abacavir. The difference was just short of significance (p = 0.059).

Virological outcomes were also similar at all time points between patients taking abacavir and patients treated with tenofovir. Once again, the rate of sustained virological response favoured abacavir and almost achieved significance (47 vs 24%; p = 0.053).

“There were no differences in the proportion of patients achieving RVR, EVR or SVR, even when abacavir- and tenofovir-containing regimens were compared,” comment the authors. “It is important to note that the two groups were comparable.”

They therefore conclude: “Our results confirmed that an abacavir-containing regimen is a safe treatment alternative for coinfected patients starting HCV treatment.”