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Cervical cancer diagnosis and CD4+ Count trajectory in HIV-infected women in north america

Cervical cancer diagnosis and CD4+ Count trajectory in HIV-infected women in north america.

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Cervical cancer diagnosis and CD4+ Count trajectory in HIV-infected women in north america

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  1. Cervical cancer diagnosis and CD4+ Count trajectory in HIV-infected women in north america AG Abraham, S Gange, Y Jing, R Bosch, JT Brooks, R Dubrow, J Eron, K Gebo, MJ Gill, N Hessol, R Hogg, M Kitahata, M Klein, R Moore, S Rourke, M Silverberg, &G D’Souza, for the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) IAS 2010 Vienna, Austria WEAB0104 Alison Abraham, PhD Department of Epidemiology Johns Hopkins Bloomberg School of Public Health

  2. Cervical cancer and HIV Human papillomavirus (HPV) is a common sexually transmitted infection causally linked to cervical cancer Most cervical HPV infections clear but in some women they persist and cause cervical cancer Chronic immunosuppression in HIV-infection may promote HPV persistence and increase the risk of cervical cancer IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  3. Does chronic immunosuppression contribute to cervical cancer risk? This study explored whether lower CD4 counts over time could result in higher risk of progression to cervical cancer

  4. NA-ACCORD is • a collaboration of • over 20 existing HIV • research studies and • >110,000 subjects • Part of the NIH/NIAID • IeDEA Network North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) Gange, Kitahata, Saag, …, & Moore. Int J Epi 2007

  5. Study Design &Population • HIV-infected women from 13 North American cohorts contributing to NA-ACCORD • Clinical and interval cohorts • Nested case-control study • Cases: Invasive cervical cancer • Clinically confirmed or cancer registry-linked cervical cancer diagnoses • Occurring after ART initiation • Controls: Women without ICC diagnosis over follow-up IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  6. Methods • Controls were matched at ART initiation on: • CD4+ cell count, Age, Cohort, Calendar Year, Follow-up time • All controls which met the matching criteria were included to maximize available CD4 trajectory information • We modeled trends in average CD4 counts using: • Piecewise-linear mixed effects models • Spline terms added at ART initiation and one year following initiation • Interaction terms to describe differences between cases and controls IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  7. Characteristics at ART initiation No statistically significant differences were noted IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  8. Mean CD4 and 95% CI Controls Cases Areas under the CD4 Curve for Cases approximately 80% of Controls CD4+ Count (cells/μl) Months from ART Initiation IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  9. Estimated CD4 trajectories *p<0.05 for test of equality of case and control parameters IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  10. Modeling CD4 trajectory *p<0.05 IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  11. Viral Load Changes Appeared Similar Geometric mean VL and 95% CI Controls Cases No significant differences in the geometric mean viral loads at any time point tested Viral Load (log base 10), copies/ml Months from ART Initiation IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  12. Conclusions Average CD4 counts were consistently lower over time for women who developed ICC than for similar women who remained free of ICC over follow-up These differences in CD4 trajectory between cases and controls suggest a role of long-term immunosuppression Less robust rebound in CD4 following ART was not explained by differences in viral load (adherence) or prior NRTI exposure (resistance) IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  13. Strengths and Limitations • Large study of cervical cancer among HIV-infected women • The size of NA-ACCORD allowed for both large numbers of cases to be found and the ascertainment of appropriate controls for the current study • Rigorous quality assurance protocol to assemble data from different cohorts into single dataset • Validated data on CD4 history for cases and controls for evaluating trajectory differences • Limited covariate information • No information on Pap screening (potentially heterogeneous between cohorts) or hysterectomy IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

  14. Acknowledgements NA-ACCORD cohorts: VACS: Robert Dubrow, Yale University ALLRT: Ronald Bosch, Harvard; Constance Benson, UCSD; Ann Collier, UW Seattle Montreal: Marina Klein, Montreal Chest Institute HIV Clinic, McGill University HIVRN: Kelly Gebo, Johns Hopkins School of Medicine HOPS: John T. Brooks, CDC JHHCC: Richard Moore, Johns Hopkins School of Medicine KPNC: Michael Silverberg & Michael Horberg, Kaiser Permanente Northern California SAC: M. John Gill, University of Calgary, Southern Alberta UCHCC: Joseph Eron & Sonia Napravnik, University of North Carolina, Chapel-Hill UW: Mari Kitahata, University of Washington at Seattle HOMER:RobertHogg, BC Centre for Excellence and HIV/AIDS; Simon Fraser University OHTN Sean Rourke & Anita Rachlis, University of Toronto, Canada WIHS: Nancy Hessol, UCSF, Women’s Interagency HIV Study THANKS TO: National Institute of Allergy & Infectious Diseases, with supplemental funding from the National Cancer Institute IAS 2010 - Vienna, Austria – Oral Abstract WEAB0104

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