SS 13-02PREVALENCE OF HUMAN PAPILLOMAVIRUS IN SQUAMOUS VULVAR CANCER AND VULVAR INTRAEPITHELIAL NEOPLASIA: A SYSTEMATIC REVIEW AND META-ANALYSIS

02. Epidemiology and natural history
M.T. Faber 1, F.L. Sand 1, V. Albieri 2, B. Norrild 3, J. Junge 4, S.K. Kjær 5, F. Verdoodt 1.
1Danish Cancer Society Research Center, Virus, Lifestyle and Genes, Copenhagen (Denmark), 2Danish Cancer Society Research Center, Statistics, Bioinformatics and Registry, (Denmark), 3Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen (Denmark), 4Department of Pathology, Hvidovre Hospital, University of Copenhagen, Copenhagen (Denmark), 5Danish Cancer Society Research Center, Virus, Lifestyle and Genes, Copenhagen and Department of Gynecology, Rigshospitalet, University of Copenhagen, Copenhagen (Denmark)

Background / Objectives

A causal role of human papillomavirus (HPV) has been suggested for a subset of vulvar carcinomas and for the majority of vulvar intraepithelial neoplasia (VIN). A number of studies have investigated HPV prevalence and HPV type distribution in vulvar cancer and VIN, and the findings have been summarized in review articles. Since publication of these reviews, a considerable number of new studies on the association between HPV and vulvar lesions have been published. We conducted an updated systematic review and meta-analysis to estimate the pooled prevalence of HPV DNA and HPV type distribution in vulvar cancer and VIN.


Methods

Through a systematic literature search, studies published between 1990 and 2015 were identified in PubMed and Embase databases, and the Cochrane Library. Studies using a PCR-based or hybrid capture test to evaluate the presence of HPV DNA in invasive squamous cell carcinoma of the vulva or VIN were eligible for inclusion. Pooled estimates of the HPV prevalence with corresponding 95% confidence intervals (CI) were calculated based on a random effects model.


Results

We identified 93 eligible papers examining the prevalence of HPV DNA in vulvar cancer (65 papers) and/or VIN (48 papers) comprising altogether 5106 cases of vulvar cancer and 2415 cases of VIN. The pooled prevalence of HPV in vulvar cancer was 40.1% (95% CI: 35.8–44.7), while the pooled HPV prevalence in VIN was 77.0% (95% CI: 70.7–82.3). Among HPV-positive cases the predominant HPV type was HPV16 (70.9% in vulvar cancer; 81.4% in VIN), followed by HPV33 (13.5% in vulvar cancer; 12.7% in VIN) and HPV18 (10.9% in vulvar cancer; 3.5% in VIN).


Conclusion

HPV prevalence was higher in VIN than in vulvar cancer and HPV16 accounted for the majority of HPV-positive cases. In subsequent meta-regression and stratified analyses, we will evaluate potential sources of between-study heterogeneity such as geographical region, publication year, histological classification, HPV DNA detection method and tissue type.


References