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 (Cmin) of ribavirin were not adversely affected
by abacavir.
“There was no evidence that abacavir affected
ribavirin Cmin 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 Cmin result.
The overall median ribavirin Cmin 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 Cmin (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.”