XVIII International AIDS Conference


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Risk factors for cervical intraepithelial neoplasia in HIV-infected women

N.C. Teixeira1, A. Araujo1, C. Lodi2, C. Correa3, A. Alves4, E.D. Murta5, F. Cruz1, G. Alvarenga6, D. del Castillo7, N. Carvalho7, I. Oliveira8, R. Campos6, V. Melo5, Women and HIV Research Group, Belo Horizonte, Brazil.

1Prefeitura Municipal, Belo Horizonte, Brazil, 2Medical Science School of Minas Gerais, Belo Horizonte, Brazil, 3Prefeitura Municipal, Tres Rios, Brazil, 4Prefeitura Municipal, Conselheiro Lafaiete, Brazil, 5Federal University of Minas Gerais, Belo Horizonte, Brazil, 6Prefeitura Municipal, Betim, Brazil, 7Center for Research and Diagnostics (NUPAD), Belo Horizonte, Brazil, 8Prefeitura Municipal, Barbacena, Brazil

Background: HIV-infected women are at increased risk for developing dysplastic genital lesions and cervical cancer. Prevalence of cervical intraepithelial neoplasia (CIN) among these women ranges from 20 to 60%. Cervical cancer and Human Papillomavirus (HPV) association has been confirmed and HPV/HIV co-infection on the cervix is very frequent (60 to 80%). Current data suggest that HIV infection can increase cervical HPV persistence and the development of CIN lesions, probably associated to a weak local immune response. Our objective was to find predictive markers of CIN among these women.
Methods: This is a cross-sectional study comprising HIV- infected women from five cities of Minas Gerais (Brazil), enrolled from 1998 to 2008. Gynecologic exam was performed and cervical samples were collected (HPV-DNA and Pap smear). Colposcopy, cervical biopsy and treatment of lesions were performed as part of routine medical care. Biopsy results, TCD4+ cells count, DNA-HPV and antiretroviral therapy (ART) were compared with cervical dysplasia. Univariate and multivariate statistical analysis were used to detect independent risk factors for CIN.
Results: 523 HIV-infected women were enrolled. CIN prevalence was 22.1% (6.1% of severe dysplasia and 16% of mild dysplasia). Risk of CIN was significantly increased among women with TCD4+ cells count bellow 200cells/mL (OR = 2.7; 95%CI = 1.2- 6.1; P=.012). There was also a positive association of high risk HPV DNA (16,18, 31 and 35) and cervical dysplasia (OR = 2.3; 95%CI = 1.2- 4.2; P = .007). There was not a protective effect against any cervical dysplasia in women taking ART.
Conclusions: A history of immunosuppression, determined by TCD4+ cells count, and the presence of high risk HPV DNA, were predictors of genital dysplasia in HIV infected women.

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