HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica

A Hildesheim, R Herrero, P E Castle, S Wacholder, M C Bratti, M E Sherman, A T Lorincz, R D Burk, J Morales, A C Rodriguez, K Helgesen, M Alfaro, M Hutchinson, I Balmaceda, M Greenberg, M Schiffman, A Hildesheim, R Herrero, P E Castle, S Wacholder, M C Bratti, M E Sherman, A T Lorincz, R D Burk, J Morales, A C Rodriguez, K Helgesen, M Alfaro, M Hutchinson, I Balmaceda, M Greenberg, M Schiffman

Abstract

We examined factors associated with high-grade squamous intraepithelial lesions (HSIL) and cervical cancer among human papillomavirus (HPV)-infected women in a prevalent case-control study conducted within a population-based cohort of 10 077 women in Costa Rica. We compared 146 women with HPV-positive HSIL or cancer (HSIL/CA) against 843 HPV-positive women without evidence of HSIL/CA. Subjects completed a risk factor questionnaire. We evaluated the associations between exposures and HSIL/CA among women positive for any HPV and restricted to those positive for high-risk HPV types. Risk of HSIL/CA increased with increasing number of live births (P(trend)= 0.04). Women who smoked 6+ cigarettes/day had a RR for HSIL/CA of 2.7 (95% CI = 1.1-6.7) compared to non-smokers. Current use of barrier contraceptives was associated with a reduction in risk of HSIL/CA (RR = 0.39; 95% CI = 0.16-0.96). Sexual behaviour and a self-reported history of sexually transmitted diseases (STDs) other than HPV were not associated with HSIL/CA. Oral contraceptive use was associated with HSIL/CA among women with <3 pregnancies. Effects were similar in analysis restricted to women positive for high-risk HPV types. Among women positive for high-risk HPV types, 44% of HSIL/CA could be attributed to multiparity (>/=3 pregnancies) and/or smoking. Among HPV-positive women, multiparity and smoking are risk factors for HSIL/CA. Oral contraceptive use may be associated with HSIL/CA in subgroups of women.

Copyright 2001 Cancer Research Campaign http://www.bjcancer.com.

References

    1. JAMA. 2000 Jan 5;283(1):87-93
    1. Cancer Detect Prev. 1991;15(5):397-402
    1. Obstet Gynecol. 1993 Jan;81(1):5-12
    1. J Natl Cancer Inst. 1993 Jun 16;85(12):958-64
    1. Cancer Epidemiol Biomarkers Prev. 1993 Sep-Oct;2(5):423-31
    1. J Infect Dis. 1994 Feb;169(2):235-40
    1. Int J Epidemiol. 1994 Oct;23(5):913-22
    1. Am J Obstet Gynecol. 1995 Mar;172(3):946-54
    1. J Natl Cancer Inst. 1995 Jun 7;87(11):796-802
    1. Cancer Epidemiol Biomarkers Prev. 1995 Jul-Aug;4(5):459-67
    1. Int J Cancer. 1996 Mar 1;65(5):601-6
    1. J Immunol. 1996 Apr 1;156(7):2384-90
    1. Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2930-5
    1. Cancer. 1995 Nov 15;76(10 Suppl):1888-901
    1. Cancer Res. 1997 Mar 1;57(5):937-42
    1. Rev Panam Salud Publica. 1997 May;1(5):362-75
    1. J Natl Cancer Inst. 1997 Jun 18;89(12):868-73
    1. J Natl Cancer Inst. 1998 Jan 7;90(1):43-9
    1. J Natl Cancer Inst. 1998 Jan 7;90(1):50-7
    1. Int J Cancer. 1998 Feb 9;75(4):546-54
    1. Epidemiology. 1998 May;9(3):346-9
    1. Int J Cancer. 1998 May 29;76(5):613-9
    1. Acta Obstet Gynecol Scand. 1998 Jul;77(6):678-82
    1. Int J Cancer. 1998 Oct 29;78(3):281-5
    1. Am J Obstet Gynecol. 1999 May;180(5):1110-4
    1. Lancet. 1999 Jul 3;354(9172):20-5
    1. J Natl Cancer Inst. 2000 Mar 15;92(6):464-74
    1. Br J Cancer. 1980 Sep;42(3):359-69
    1. Int J Cancer. 1987 Aug 15;40(2):198-201
    1. Int J Cancer. 1987 Oct 15;40(4):450-4
    1. J Infect Dis. 1987 Dec;156(6):904-11
    1. Nature. 1988 Oct 27;335(6193):832-5
    1. Am J Obstet Gynecol. 1989 Jul;161(1):50-5
    1. J Gen Virol. 1989 Aug;70 ( Pt 8):2227-32
    1. Int J Cancer. 1990 Jul 15;46(1):5-7
    1. Crit Rev Toxicol. 1990;20(5):369-95
    1. Biometrics. 1990 Dec;46(4):991-1003
    1. Int J Cancer. 1992 Nov 11;52(5):750-8

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