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Recommended Earlier Initiation of ART Based on Nadir CD4 Cell Count as a Risk Factor for HIV-related Neurocognitive Impairment
Jose A. Muñoz-Moreno*1, C Rodríguez1, A Prats1, M Ferrer1, E Negredo1, M Garolera2, and B Clotet1
1Lluita contra la SIDA Fndn, Germans Trias i Pujol Hosp, Barcelona, Spain and 2Terrassa Hosp, Barcelona, Spain
Background: Nadir CD4 cell count has been proposed as a new
potential risk factor for irreversible HIV-related neurocognitive
impairment. Furthermore, benefits of HAART have been observed to be
insufficient for neurocognitive reversal. We compared
different nadir CD4 cell count cutoffs to study their possible clinical
significance related to the initiation of HAART.
Methods: A total of 64 patients were included in this
observational, cross-sectional study. Demographic, medical, and neurocognitive variables were assessed. We excluded patients
who reported drug abuse, psychiatric treatment, or neurological disorders. The
percentages of patients showing neurocognitive
impairment were compared through different CD4 cell count cutoffs, significant
for HAART initiation: 200, 250, 300, and
350 cells/mL. Neurocognitive and motor functions were also compared among
these study groups. ANOVA, non-parametric, and χ2 tests were
developed.
Results: The percentages of patients showing neurocognitive impairment were: nadir ≤200 cutoff vs
nadir >200 cutoff —73.1% vs 52.6%, respectively;
nadir ≤250 vs nadir >250—66.7% vs 53.3%; nadir ≤300 vs
nadir >300—63.9% vs 56.5%; nadir ≤350 vs nadir >350—57.1% vs 62.5%.
Although differences did not reach statistical significance, the percentage of
impaired patients tended to be higher while the nadir cutoff fell. Supporting
these data, when neurocognitive functions were
compared, statistical differences were found in 2 areas with respect to the
nadir 200 cutoff: attention/working
memory (span backward, p = 0.032); and executive functions (TMT-B, p =
0.020). The functioning was better in the group with >200 cells/mL. By contrast, when functions were studied regarding the
other nadir cutoffs, non-significant differences were found in any function. We
observed a general tendency to present a more protected neurocognitive
functioning in the groups of patients with nadir >200, >250, >300, and
>350 cells/mL, as indicated by higher scores in
most areas assessed in each group.
Conclusions: Our results confirm that the nadir CD4 cell count is a
potential risk factor for HIV-related neurocognitive
impairment. The prevalence of neurocognitive impairment
is higher in those patients with lower nadir counts but, in addition, relevant
differences are found when neurocognitive functioning
is studied considering the nadir CD4 value. Earlier initiation of HAART therapy
is recommended to achieve the major neurocognitive
protection.
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