Sexual behaviour and papillomavirus exposure in cervical intraepithelial neoplasia: a population-based case-control study

L Kjellberg, Z Wang, F Wiklund, K Edlund, T Angstrom, P Lenner, I Sjoberg, G Hallmans, KL Wallin, M Sapp, J Schiller, G Wadell, CG Mahlck and J Dillner Department of Obstetrics and Gynecology, University Hospital of Northern Sweden, Umea. Sexual history is an established risk determinant for cervica...

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Veröffentlicht in:Journal of general virology 1999-02, Vol.80 (2), p.391-398
Hauptverfasser: Kjellberg, L, Wang, Z, Wiklund, F, Edlund, K, Angstrom, T, Lenner, P, Sjoberg, I, Hallmans, G, Wallin, KL, Sapp, M, Schiller, J, Wadell, G, Mahlck, CG, Dillner, J
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Sprache:eng
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Zusammenfassung:L Kjellberg, Z Wang, F Wiklund, K Edlund, T Angstrom, P Lenner, I Sjoberg, G Hallmans, KL Wallin, M Sapp, J Schiller, G Wadell, CG Mahlck and J Dillner Department of Obstetrics and Gynecology, University Hospital of Northern Sweden, Umea. Sexual history is an established risk determinant for cervical neoplasia. It is not clear if human papillomavirus (HPV) exposure entirely explains the sexual behaviour-related risk or if other sexually transmitted agents may act as cofactors for HPV in carcinogenesis. The aim of this study was to elucidate whether HPV exposure or HPV persistence explains the sexual history-related risk of high-grade cervical intraepithelial neoplasia (CIN) using a population- based case-control study of most of the 254 women referred to colposcopy in the Vasterbotten county in Sweden because of an abnormal cervical smear during October 1993 to December 1995 and 320 age-matched women from the general population. The women were interviewed for sexual history and tested for presence of serum antibodies to HPV-16, - 18 and -33 as well as for presence of HPV DNA in cervical brush samples. HPV-16, -18 and -33 seropositivity was specific for the corresponding type of HPV DNA, dependent on the lifetime sexual history and associated with a two- to threefold increased risk of CIN 3. There was no sexual history-related risk of CIN among HPV-seropositive women and adjustment for HPV DNA presence explained the sexual history- related risk of CIN. In conclusion, HPV exposure appeared to explain the sexual history-related risk of high-grade CIN.
ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-80-2-391