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Nadir CD4 Count Does Not Predict Response to Pegylated Interferon and Ribavirin in HIV/HCV-co-infected Patients
Susan Hopkins*1,2, O Barry2, J Turner3, M Johnson1, F Mulcahy2, R Gilson3, G Farrell2, S Bhagani1, and C Bergin2
1Royal Free Hosp Cohort, London, UK; 2St James's Hosp, Dublin, Ireland; and 3Mortimer Market Clin, London, UK
Background: The reason for a poorer hepatitis C virus (HCV)
response to pegylated interferon (pegIFN)
+ ribavirin (RBV) is not understood. Recent studies
demonstrated that HCV-related factors and not HIV-related factors predict
response to pegIFN + RBV but did not examine the
effect of nadir CD4 counts. An association between nadir CD4 counts and the
extent of immune restitution suggests that HIV-1 may cause irreparable immune
system damage despite potent HAART. We postulated that a poorer immune response
induced from IFN + RBV in those that have had a low nadir CD4 count might
account for the lack of HCV response to therapy.
Methods: A retrospective analysis was performed on 124
patients who commenced pegIFN + RBV in 3 centers (London and Dublin). Demographics,
HIV (including nadir CD4 count), and HCV factors were analyzed. Those who had
discontinued for adverse reactions were not included in the multivariate
analysis (which was adjusted for the variables in the table; only 1 variable
for CD4 count was included in any analysis).
Results: The median age was 38.5 years; 109 (87.9%)
were male, 104 (95.4%) were Caucasian, and 60 (48.4%) were injecting drug users
(IDU); 70 (58.3%) were on HAART with a baseline median HIV viral load and
median baseline CD4 counts was 440 x 106/L. Median nadir CD4 count
was 208 x 106/L; 63 (51.6%) patients were infected with HCV genotype
non-1 and median log baseline HCV viral load was 6.4; 52% had a sustained viralogical response—25% of genotype 1 and 75% genotype
non-1. On univariate analysis genotype non-1 was the
only statistically significant predictor of response and remained the only
significant predictor in a multivariate analysis. When using a cut-off for
nadir CD4 count of 100 or 350 x 106/L there were minimal differences
in results with nadir CD4 count still having no significant effect and genotype
non-1 remaining significant on multivariate analysis.
 Conclusions: Genotype remains
the only significant predictor of response to pegIFN +
RBV in this HIV/HCV-co-infected cohort. Nadir CD4 count (with cut-offs 100, 250,
and 350 x 106/L) does not predict response to HCV therapy in these
co-infected patients.
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