Elsevier

The Journal of Pediatrics

Volume 132, Issue 2, February 1998, Pages 277-284
The Journal of Pediatrics

The natural history of human papillomavirus infection as measured by repeated DNA testing in adolescent and young women,☆☆,,★★

https://doi.org/10.1016/S0022-3476(98)70445-7Get rights and content

Abstract

Objectives: The objectives of this study were to describe the early natural history of human papillomavirus (HPV) infection by examining a cohort of young women positive for an HPV test and to define within this cohort (1) the probability of HPV regression, (2) the risk of having a squamous intraepithelial lesion, and (3) factors that were associated with HPV regression.

Study design: The study was a cohort analytic design. An inception cohort of 618 women positive for HPV participated. HPV testing, cytologic evaluation, and colposcopic evaluation were performed at 4-month intervals. HPV testing was characterized for two groups: low risk (five types rarely associated with cancers) and high risk (nine types most commonly associated with cancers).

Results: Estimates provided by Kaplan-Meier curves showed that ~70% of women were found to have HPV regression by 24 months. Women with low-risk HPV type infections were more likely to show HPV regression than were women with high-risk HPV type infections (log rank test p = 0.002). The relative risk for the development of high-grade squamous intraepithelial lesion (HSIL) was 14.1 (95% confidence interval: 2.3, 84.5) for women with at least three positive tests for high-risk HPV preceding the development of the HSIL compared with that for women with negative tests for high-risk HPV. However, 88% of women with persistent positive HPV tests have not had HSIL to date. No factors associated with high-risk HPV type regression were identified except for a negative association with an incident history of vulvar condyloma (relative risk = 0.5 [95% confidence interval: 0.3 to 0.8]).

Conclusion: Most young women with a positive HPV test will become negative within a 24-month period. Persistent positive tests with oncogenic HPV types represented a significant risk for the development of HSIL. However, we found that most young women with persistent positive HPV tests did not have cytologically perceptible HSIL over a 2-year period. Factors thought to be associated with the development of HSIL were found not to be important in HPV regression. (J Pediatr 1998;132:277-84)

Section snippets

Study Population

Beginning in October 1990, young women 13 to 22 years old were recruited from two clinic sites: Planned Parenthood and a university student health clinic. Demographics of Planned Parenthood have been described in detail previously.1 The university is a state-subsidized university located in San Francisco; ethnic and racial distribution for young women attending the university student health clinic as shown by university enrollment records at the time of recruitment was 56% white, 30%

RESULTS

Fig. 1 describes the recruitment algorithm, number of subjects screened, and final number of subjects who participated in the cohort.

. Algorithm for participating cohort.

The demographic and behavioral characteristics of the HPV-positive women participating in the final cohort are outlined in Table I.

. Demographic and behavioral characteristic of the women positive for HPV participating in the cohort study by site

Planned Parenthood (n = 325)University Health Clinic (n = 293)p Value
Age at entry (yr)

DISCUSSION

Our data suggest that most young women (60% to 75%) who test positive for HPV DNA appear to become negative for that viral group type within a 20to 30-month observation period. We suggest that the prolonged DNA negativity in this study reflects actual viral elimination of a specific viral type in most women. Our data also emphasize the difficulty in defining virus negativity for purposes of epidemiologic study. With a dot-blot method with recognized limited sensitivity, negative status after

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    From the Division of Adolescent Medicine, Department of Pediatrics, the Department of Epidemiology and Biostatistics, the Department of Laboratory Medicine and Stomatology, and the Department of Anatomic Pathology, University of California, San Francisco.

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    Supported in part by National Cancer Institute No. R01CA51323 and No. R01CA54053, NIAIDS No. P01A121912, National Institutes of Health grant No. M01 RR01271, Maternal and Child Health Bureau Training Grant No. MCJ000978, the Cigarette and Tobacco Surtax Fund of the State of California through the Tobacco-related Research Program of the University of California, grant No. RT 487 and grant No. RT 484, AIDS Clinical Research Center, University of California, San Francisco.

    Reprint requests: Anna-Barbara Moscicki, MD, 400 Parnassus Ave., Room AC-01, Box 0503, San Francisco, CA 94143.

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