This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Insinga, R. P. Articles by Madeleine, M. M. PubMed PubMed Citation Articles by Insinga, R. P. Articles by Madeleine, M. M.

A Systematic Review of the Prevalence and Attribution of Human Papillomavirus Types among Cervical, Vaginal, and Vulvar Precancers and Cancers in the United States

Departments of ¹ Health Economic Statistics and ² Epidemiology, Merck Research Laboratories, North Wales, Pennsylvania and ³ Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, Washington

Requests for reprints: Ralph P. Insinga, Merck & Co., Inc., UG1C-60, P.O. Box 1000, North Wales, PA 19454-1099. Phone: 267-305-7992; Fax: 267-305-6455. E-mail: ralph_insinga{at}merck.com

Objectives: To describe prevalence and estimated attribution of human papillomavirus (HPV) types in U.S. cervical, vaginal, and vulvar precancers and cancers.

Methods: U.S. studies reporting HPV typing for cervical intraepithelial neoplasia (CIN), vulvar intraepithelial neoplasia (VIN), and vaginal intraepithelial neoplasia (VaIN) and/or invasive cancers of those sites were gathered from the PubMed database (http://www.ncbi.nlm.nih.gov/sites/entrez/). Selected studies had PCR testing data for 10 cases for a disease endpoint. Analytic methods augmented prior reviews of cervical disease with an updated and expanded analysis (including vulvar and vaginal disease), new selection criteria for specimens, and adjustment for histologic type, where possible, among pooled cancer cases. In addition, for analyses of estimated attribution of HPV types, we incorporated accounting methods for lesions infected with multiple HPV types.

Results: Data from 22 U.S. studies meeting review eligibility criteria were tabulated. Following adjustment for the presence of multiple HPV types in a single specimen, the top two HPV types contributing to disease were CIN 1 (HPV 16/66; 15.3%), CIN 2/3 (HPV 16/31; 61.9%), cervical cancer (HPV 16/18; 79.2%), VIN 1 (HPV 6/11; 41.7%), VIN 3 (HPV 16/18; 84.0%), vulvar cancer (HPV 16/33; 55.5%), VaIN 3 (HPV 16/18; 65.1%), and vaginal cancer (HPV 16/18; 72.7%).

Conclusions: The HPV type distribution and proportion of cases testing positive for any HPV type were observed to vary among U.S. cervical, vulvar, and vaginal neoplasias and by grade of disease. Adjustment for the presence of multitype HPV infections can have an important effect on the estimated attribution of HPV types to disease, particularly for types other than HPV 16. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1611–22)