icon-    folder.gif   Conference Reports for NATAP  
  16th CROI
Conference on Retroviruses and Opportunistic Infections Montreal, Canada
February 8-11, 2009
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HCV Causes Neurcognitive Impairment in HIV+
  Neuradapt: A Prospective Study concerning HIV-related Neurocognitve Impairment
Reported by Jules Levin CROI 2009 Montreal Feb 8-12
Matteo Vassallo*1, A Harvey Langton1, C Pradier1, S Ferrando1, J Cottalorda1, C Caissotti1, J Durant1, G Malandain2, S Chanalet3, and P Dellamonica1 1L'Archet Hospital - CHU Nice - France; 2INRIA - Sophia Antipolis - France; and 3Pasteur Hospital - CHU Nice - France
Background: The HIV Neurobehavioral Research Center (HNRC) recently added the concept of HIV-related asymptomatic neurocognitive impairment (ANI) to HIV-associated dementia (HAD) and minor cognitive disorders (MCD). These 3 categories define the current diagnosis of HIV neurocognitive impairment (HNI). Neuropsychological deficit includes patients with impairment in only one cognitive domain, not included in the definition of HNI. Little is known of the frequency and clinical relevance of neuropsychological deficit. Our aim is to firstly evaluate its prevalence among the HIV-infected population and then correlate the results to imaging.
Methods: Neuradapt is an ongoing, prospective study of HNI prevalence among HIV-1-infected patients followed in Nice University Hospital. From December 2007, we randomly selected patients to undergo neuropsychological testing. We used the HNRC classification (normal tests, neuropsychological deficit, ANI, MCD, and HAD). Test score was adjusted for age, gender, and education. CD4 count, HIV RNA viral load, DNA-proviral load, viral hepatitis, immune activation markers (CD4+CD38+, CD8+CD38+) and cerebral multi-spectral MRI were explored. We also considered current use of psychotropic molecules and HCV therapy, type of ART at inclusion and central nervous system (CNS) drug penetration-effectiveness.
Results: From December 2007 to September 2008, 107 patients (77% male, mean age 44 years, 86% on HAART, mean CD4 cell count 527/mL, 54% of patients with viral load <40 copies/mL, 22% hepatitis C virus [HCV] co-infected) were included; 16% were on benzodiazepines and 8% on antidepressants. HNI accounted for 25% of patients (ANI 11%, MCD 10%, and HAD 4%).. However, 44% of patients presented with neuropsychological deficit. Thus, only 31% had normal tests. HCV infection (p = 0.007) and antidepressants (p = 0.016) were associated with neuropsychological deficit or HNI. Multivariate analysis showed only HCV co-infection to be an independent risk factor for abnormal neuropsychological performance (p = 0.015). Adjusting for current or recent HCV therapy did not modify results.
Conclusions: As many as 69% of subjects have abnormal neuropsychological scores, and neuropsychological deficit accounted for 44% of subjects in our series. Hepatitis C is a risk factor regardless of the degree of cognitive impairment. The clinical relevance of neuropsychological deficit is not known, but the high proportion of subjects needs further evaluation by imaging.