Platelet decline: An avenue for investigation into the pathogenesis of human immunodeficiency virus-associated dementia

Lynn M. Wachtman, Richard L. Skolasky, Patrick M. Tarwater, Deneen Esposito, Giovanni Schifitto, Karen Marder, Michael P. McDermott, Bruce A. Cohen, Avindra Nath, Ned Sacktor, Leon G. Epstein, Joseph L. Mankowski, Justin C. McArthur*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

Background: The identification of biomarkers identifying onset of human immunodeficiency virus-associated dementia (HIV-D) is critical for diagnosis and the elucidation of pathophysiologic pathways. Objective: To examine the association between platelet decline from baseline and HIV-D. Design: Prospective cohort study within the North-East AIDS Dementia cohort. Setting: Four participating referral centers in the United States. Participants: A total of 396 subjects with advanced human immunodeficiency virus (HIV) infection recruited between 1998 and 2003 and undergoing serial neurologic assessments. Eligibility criteria required CD4 cell counts less than 200/μL or less than 300/μL with evidence of cognitive impairment. A cohort subset without prevalent HIV-D at baseline and without incident HIV-D at the visit immediately after baseline was analyzed (n=146). Main Outcome Measure: Time to first diagnosis of HIV-D. Results: After a median follow-up of 31.1 months, 40 subjects developed HIV-D. Platelet decline from baseline was associated with the development of HIV-D when examined as a time-dependent variable lagged by 6 to 12 months before outcome (multivariate hazard ratio [HR], 2.39; 95% confidence interval [CI], 1.14-5.02; P=.02). This association was stronger during the first 2 years of follow-up (multivariate HR, 6.76; 95% CI, 2.36-19.41; P < .001) than during later years (multivariate HR, 0.94; 95% CI, 0.33-2.67; P = .90). Conclusions: These results suggest that individuals with declining platelet counts are at greater risk for HIV-D and that the dynamics of circulating platelets vary with respect to the temporal progression of HIV-D. This highlights an avenue to be explored in the understanding of HIV-D pathogenesis.

Original languageEnglish (US)
Pages (from-to)1264-1272
Number of pages9
JournalArchives of Neurology
Volume64
Issue number9
DOIs
StatePublished - Sep 2007

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

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