Early virological response (EVR) to interferon-based
therapy at week 12 and rapid virological response (RVR) at week 4 are known to
predict SVR, or continued undetectable HCV RNA 6 months after completing therapy.
Even earlier response has been shown to predict long-term outcomes in HCV monoinfected
individuals, but there is little data for HIV-HCV coinfected patients.
present analysis included 20 coinfected participants (17 of them men) treated
with pegylated interferon plus ribavirin; 19 were also taking combination antiretroviral
therapy (ART). Patients had well-controlled HIV disease overall, with a median
CD4 count of 545 cells/mm3. Three-quarters had HCV genotype 1 and half had advanced
liver fibrosis or cirrhosis
(Metavir stage F4-F3).
viral load decline 24 hours after starting treatment was significantly higher
among patients who went on to achieve SVR compared with eventual non-responders
(1.6 vs 0.5 logs).|
decrease of less than 0.9 log at 24 hours was the best cut-off level for differentiating
responders and non-responders.|
sensitivity of this cut-of value was 100% and the specificity was 82%. |
cut-off had a negative predictive value (NPV) for SVR of 100% and a positive predictive
value (PPV) of 71%.|
on these findings, the researchers concluded that, "patients who do not reach
0.9 log decay at 24 hours will not achieve SVR."
results suggest that in HIV-HCV coinfected patients HCV therapy could be guided
[by] following very early changes in HCV viral load," they added, suggesting
that this could allow optimization of treatment particularly in resource-limited
settings, as well as for patients with pre-treatment predictors of non-response
or severe toxicity.
Reference Ctr. for AIDS, Buenos Aires, Argentina; Hosp. Juan A. Fernández,
Buenos Aires, Argentina.
Laufer, F Bolcic, E Socias, and others. Early Changes in HCV Viral Load During
the First 24 Hours of Treatment Exhibit a Very High Negative Predictive Value
of Sustained Virological Response in HCV/HIV Coinfected Patients. 49th Interscience
Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2009). San Francisco.
September 12-15, 2009. Abstract H-213.