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American Journal of Epidemiology Vol. 151, No. 12: 1158-1171
Copyright © 2000 by The Johns Hopkins University School of Hygiene and Public Health


other

Mathematical Model for the Natural History of Human Papillomavirus Infection and Cervical Carcinogenesis

Evan R. Myers1,2,, Douglas C. McCrory2,3,4, Kavita Nanda1,2, Lori Bastian2,3,4 and David B. Matchar2,3,4

1Department of Obstetrics and Gynecology, Duke University Medical Center Durham, NC.
2Evidence-based Practice Center, Center for Clinical Health Policy Research, Duke University Medicine, Department of Medicine, Duke University Medical Center Durham, NC.
3Division of General Internal Medicine, Department of Medicine, Duke University Medical Center Durham, NC.
4Durham Veteran's Affairs Medical Center Durham, NC.

Reprint requests to Dr. Evan R. Myers, DUMC 3279, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC 27710 (e-mail: myers008@mc.duke.edu).

The authors constructed a Markov model as part of a systematic review of cervical cytology conducted at the Duke University Evidence-based Practice Center (Durham, North Carolina) between October 1997 and September 1998. The model incorporated states for human papillomavirus infection (HPV), low- and high-grade squamous intraepithelial lesions, and cervical cancer stages I–IV to simulate the natural history of HPV infection in a cohort of women from ages 15 to 85 years. The age-specific incidence rate of HPV, and regression and progression rates of HPV and squamous intraepithelial lesions, were obtained from the literature. The effects of varying natural history parameters on cervical cancer incidence were evaluated by using sensitivity analysis. The base-case model resulted in a lifetime cervical cancer risk of 3.67% and a lifetime cervical cancer mortality risk of 1.26%, with a peak incidence of 81/100, 000 at age 50 years. Age-specific distributions of precursors were similar to reported data. Lifetime risk of cancer was most sensitive to the incidence of HPV and the probability of rapid HPV progression to high-grade lesions (two- to threefold variations in risk). The model approximates the age-specific incidence of cervical cancer and provides a tool for evaluating the natural history of HPV infection and cervicai cancer carcinogenesis as well as the effectiveness and cost-effectiveness of primary and secondary prevention strategies. Am J Epidemiol 2000; 151: 1158-71.

cervical intraepithelial neoplasia; cervix neoplasms; models; theoretical; papillomavirus; human


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