XVIII International AIDS Conference

Abstract

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CD4 count trajectories of HIV-infected women in North America with cervical cancer after initiating antiretroviral therapy

Presented by Alison G Abraham (United States).

A.G. Abraham1, S. Gange1, Y. Jing1, R. Bosch2, J.T. Brooks3, R. Dubrow4, J. Eron5, K. Gebo6, M.J. Gill7, N. Hessol8, B. Hogg9, M. Kitahata10, M. Klein11, R. Moore6, S. Rourke12, M. Silverberg13, G. D'Souza1, North American AIDS Cohort Collaboration on Research and Design


1Johns Hopkins Bloomberg School of Public Health, Epidemiology, Baltimore, United States, 2Harvard University, Boston, United States, 3Centers for Disease Control and Prevention, Atlanta, United States, 4Yale University, New Haven, United States, 5University of North Carolina, Chapel Hill, United States, 6Johns Hopkins School of Medicine, Baltimore, United States, 7University of Calgary, Calgary, Canada, 8University of Califorinia at San Francisco, San Francisco, United States, 9BC Centre for Excellence in HIV/AIDS, Vancouver, Canada, 10University of Washington, Seattle, United States, 11McGill University, Montreal, Canada, 12University of Toronto, Toronto, Canada, 13Kaiser Permanente Northern California, Oakland, United States

Background: Immunosuppression resulting from HIV-infection has been hypothesized to promote progression to cervical cancer. Few studies have had sufficient cancer numbers to examine patterns of immune deficiency in relation to invasive cervical cancer (ICC) incidence. We focused on ICC following antiretroviral therapy (ART) initiation.
Methods: Using data from the NA-ACCORD HIV cohort collaboration of IeDEA, thirteen cohorts with clinically confirmed or cancer registry-linked data on ICC were included. Analysis was limited to women who initiated ART during follow-up. Cases were matched at the time of ART initiation (prior to ICC) to controls by CD4 cell count, age, calendar period, cohort and opportunity for ICC (minimum length of follow-up). All appropriate matches were used. The trends in the mean CD4 at various time points prior to ICC diagnosis (starting four years prior to ART initiation) were compared using a piecewise-linear mixed effects model with knots at ART initiation and one year after.
Results: We identified 56 cases of ICC following ART initiation and matched to 590 controls. At ART initiation, the mean CD4 count of all matched samples was 269 cells/mm3. Four years prior to ART, the mean CD4 cell count among cases was 174 cells lower than controls (p=0.02). A year following ART initiation, the average CD4 cell count was 72 cells lower in cases than controls (p=0.04). The mean CD4 counts of controls increased an average of 8 cells/month more in the year following ART than that of the cases (p< 0.01).
Conclusions: In this large North American cohort collaboration, the average CD4 count of treated HIV-infected women diagnosed with ICC was significantly lower than that of comparable HIV-infected women before and after ART initiation, suggesting that poor immune status and a poorer response to ART may contribute to ICC incidence in HIV-infected women.


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