Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia

Nicolas F. Schlecht, Sophie Kulaga, Juliette Robitaille, Silvaneide Ferreira, Monica Santos, Romulo A. Miyamura, Eliane Duarte-Franco, Thomas E. Rohan, Alex Ferenczy, Luisa L. Villa, Eduardo L. Franco

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Abstract

Context Human papillomavirus (HPV) infection is believed to be the central cause of cervical cancer, although most of the epidemiological evidence has come from retrospective, case-control studies, which do not provide information on the dynamics of cumulative or persistent exposure to HPV infection. Objective To assess the risks of cervical neoplasia related to prior persistent HPV infections. Design and Setting Longitudinal study of the natural history of HPV infection and cervical neoplasia in women residing in the city of São Paulo, Brazil, which was conducted between November 1993 and March 1997 and involved repeated measurements of HPV and lesions with follow-up until June 2000. Participants A total of 1611 women with no cytological lesions at enrollment and HPV test results available from the first 2 visits. Main Outcome Measure Cervical specimens taken for Papanicolaou cytology and HPV testing every 4 months in the first year and twice yearly thereafter. Incident cervical cancer precursor lesions ascertained by expert review of all cytology smears. Results The incidence rate of squamous intraepithelial lesions (SILs) was 0.73 per 1000 women-months (95% confidence interval [CI], 0.5-0.9) among women free of HPV at the 2 initial visits and 8.68 (95% CI, 2.3-15.1) among women with HPV type 16 or 18 infections persisting over both visits. Relative to those negative for HPV oncogenic types at both initial visits, the relative risk (RR) of incident SIL was 10.19 (95% CI, 5.9-17.6) for persistent infections with any known oncogenic HPV types. The equivalent RR of incident high-grade SIL was 11.67 (95% CI, 4.1-33.3). The RRs of lesions were considerably higher for persistent infections with HPV type 16 or 18. Conclusion A strong relationship exists between persistent HPV infections and SIL incidence, particularly for HPV types 16 and 18.

Original languageEnglish (US)
Pages (from-to)3106-3114
Number of pages9
JournalJournal of the American Medical Association
Volume286
Issue number24
StatePublished - Dec 26 2001

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Cervical Intraepithelial Neoplasia
Papillomavirus Infections
Human papillomavirus 18
Human papillomavirus 16
Confidence Intervals
Uterine Cervical Neoplasms
Cell Biology
Infection
Incidence
Natural History
Brazil
Longitudinal Studies
Case-Control Studies
Neoplasms
Outcome Assessment (Health Care)

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Schlecht, N. F., Kulaga, S., Robitaille, J., Ferreira, S., Santos, M., Miyamura, R. A., ... Franco, E. L. (2001). Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia. Journal of the American Medical Association, 286(24), 3106-3114.

Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia. / Schlecht, Nicolas F.; Kulaga, Sophie; Robitaille, Juliette; Ferreira, Silvaneide; Santos, Monica; Miyamura, Romulo A.; Duarte-Franco, Eliane; Rohan, Thomas E.; Ferenczy, Alex; Villa, Luisa L.; Franco, Eduardo L.

In: Journal of the American Medical Association, Vol. 286, No. 24, 26.12.2001, p. 3106-3114.

Research output: Contribution to journalArticle

Schlecht, NF, Kulaga, S, Robitaille, J, Ferreira, S, Santos, M, Miyamura, RA, Duarte-Franco, E, Rohan, TE, Ferenczy, A, Villa, LL & Franco, EL 2001, 'Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia', Journal of the American Medical Association, vol. 286, no. 24, pp. 3106-3114.
Schlecht NF, Kulaga S, Robitaille J, Ferreira S, Santos M, Miyamura RA et al. Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia. Journal of the American Medical Association. 2001 Dec 26;286(24):3106-3114.
Schlecht, Nicolas F. ; Kulaga, Sophie ; Robitaille, Juliette ; Ferreira, Silvaneide ; Santos, Monica ; Miyamura, Romulo A. ; Duarte-Franco, Eliane ; Rohan, Thomas E. ; Ferenczy, Alex ; Villa, Luisa L. ; Franco, Eduardo L. / Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia. In: Journal of the American Medical Association. 2001 ; Vol. 286, No. 24. pp. 3106-3114.
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abstract = "Context Human papillomavirus (HPV) infection is believed to be the central cause of cervical cancer, although most of the epidemiological evidence has come from retrospective, case-control studies, which do not provide information on the dynamics of cumulative or persistent exposure to HPV infection. Objective To assess the risks of cervical neoplasia related to prior persistent HPV infections. Design and Setting Longitudinal study of the natural history of HPV infection and cervical neoplasia in women residing in the city of S{\~a}o Paulo, Brazil, which was conducted between November 1993 and March 1997 and involved repeated measurements of HPV and lesions with follow-up until June 2000. Participants A total of 1611 women with no cytological lesions at enrollment and HPV test results available from the first 2 visits. Main Outcome Measure Cervical specimens taken for Papanicolaou cytology and HPV testing every 4 months in the first year and twice yearly thereafter. Incident cervical cancer precursor lesions ascertained by expert review of all cytology smears. Results The incidence rate of squamous intraepithelial lesions (SILs) was 0.73 per 1000 women-months (95{\%} confidence interval [CI], 0.5-0.9) among women free of HPV at the 2 initial visits and 8.68 (95{\%} CI, 2.3-15.1) among women with HPV type 16 or 18 infections persisting over both visits. Relative to those negative for HPV oncogenic types at both initial visits, the relative risk (RR) of incident SIL was 10.19 (95{\%} CI, 5.9-17.6) for persistent infections with any known oncogenic HPV types. The equivalent RR of incident high-grade SIL was 11.67 (95{\%} CI, 4.1-33.3). The RRs of lesions were considerably higher for persistent infections with HPV type 16 or 18. Conclusion A strong relationship exists between persistent HPV infections and SIL incidence, particularly for HPV types 16 and 18.",
author = "Schlecht, {Nicolas F.} and Sophie Kulaga and Juliette Robitaille and Silvaneide Ferreira and Monica Santos and Miyamura, {Romulo A.} and Eliane Duarte-Franco and Rohan, {Thomas E.} and Alex Ferenczy and Villa, {Luisa L.} and Franco, {Eduardo L.}",
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T1 - Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia

AU - Schlecht, Nicolas F.

AU - Kulaga, Sophie

AU - Robitaille, Juliette

AU - Ferreira, Silvaneide

AU - Santos, Monica

AU - Miyamura, Romulo A.

AU - Duarte-Franco, Eliane

AU - Rohan, Thomas E.

AU - Ferenczy, Alex

AU - Villa, Luisa L.

AU - Franco, Eduardo L.

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N2 - Context Human papillomavirus (HPV) infection is believed to be the central cause of cervical cancer, although most of the epidemiological evidence has come from retrospective, case-control studies, which do not provide information on the dynamics of cumulative or persistent exposure to HPV infection. Objective To assess the risks of cervical neoplasia related to prior persistent HPV infections. Design and Setting Longitudinal study of the natural history of HPV infection and cervical neoplasia in women residing in the city of São Paulo, Brazil, which was conducted between November 1993 and March 1997 and involved repeated measurements of HPV and lesions with follow-up until June 2000. Participants A total of 1611 women with no cytological lesions at enrollment and HPV test results available from the first 2 visits. Main Outcome Measure Cervical specimens taken for Papanicolaou cytology and HPV testing every 4 months in the first year and twice yearly thereafter. Incident cervical cancer precursor lesions ascertained by expert review of all cytology smears. Results The incidence rate of squamous intraepithelial lesions (SILs) was 0.73 per 1000 women-months (95% confidence interval [CI], 0.5-0.9) among women free of HPV at the 2 initial visits and 8.68 (95% CI, 2.3-15.1) among women with HPV type 16 or 18 infections persisting over both visits. Relative to those negative for HPV oncogenic types at both initial visits, the relative risk (RR) of incident SIL was 10.19 (95% CI, 5.9-17.6) for persistent infections with any known oncogenic HPV types. The equivalent RR of incident high-grade SIL was 11.67 (95% CI, 4.1-33.3). The RRs of lesions were considerably higher for persistent infections with HPV type 16 or 18. Conclusion A strong relationship exists between persistent HPV infections and SIL incidence, particularly for HPV types 16 and 18.

AB - Context Human papillomavirus (HPV) infection is believed to be the central cause of cervical cancer, although most of the epidemiological evidence has come from retrospective, case-control studies, which do not provide information on the dynamics of cumulative or persistent exposure to HPV infection. Objective To assess the risks of cervical neoplasia related to prior persistent HPV infections. Design and Setting Longitudinal study of the natural history of HPV infection and cervical neoplasia in women residing in the city of São Paulo, Brazil, which was conducted between November 1993 and March 1997 and involved repeated measurements of HPV and lesions with follow-up until June 2000. Participants A total of 1611 women with no cytological lesions at enrollment and HPV test results available from the first 2 visits. Main Outcome Measure Cervical specimens taken for Papanicolaou cytology and HPV testing every 4 months in the first year and twice yearly thereafter. Incident cervical cancer precursor lesions ascertained by expert review of all cytology smears. Results The incidence rate of squamous intraepithelial lesions (SILs) was 0.73 per 1000 women-months (95% confidence interval [CI], 0.5-0.9) among women free of HPV at the 2 initial visits and 8.68 (95% CI, 2.3-15.1) among women with HPV type 16 or 18 infections persisting over both visits. Relative to those negative for HPV oncogenic types at both initial visits, the relative risk (RR) of incident SIL was 10.19 (95% CI, 5.9-17.6) for persistent infections with any known oncogenic HPV types. The equivalent RR of incident high-grade SIL was 11.67 (95% CI, 4.1-33.3). The RRs of lesions were considerably higher for persistent infections with HPV type 16 or 18. Conclusion A strong relationship exists between persistent HPV infections and SIL incidence, particularly for HPV types 16 and 18.

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