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. 2021 Jul 5:37:100828.
doi: 10.1016/j.gore.2021.100828. eCollection 2021 Aug.

Prevalence and type distribution of human papillomavirus infections in Danish patients diagnosed with vulvar squamous cell tumors and precursors

Annemarie Brusen Villadsen  1   2 , Caspar Bundgaard-Nielsen  1   2 , Lea Ambühl  1   2 , Majbritt Tang Svendsen  1   2 , Inge Søkilde Pedersen  2   3   4 , Estrid Stæhr Hansen  5 , Ulrik Baandrup  1   2 , Jan Blaakær  6   7 , Suzette Sørensen  1   2
Affiliations

Prevalence and type distribution of human papillomavirus infections in Danish patients diagnosed with vulvar squamous cell tumors and precursors

Annemarie Brusen Villadsen et al. Gynecol Oncol Rep. .

Abstract

Objective: To study the prevalence and type distribution of human papillomavirus (HPV) in patients with vulvar high-grade precancerous lesions and vulvar squamous cell carcinoma (VSCC).

Methods: Formalin-fixed and paraffin-embedded (FFPE) tissue samples from Danish patients diagnosed with vulvar precancerous lesions or VSCC in the period from 2010 to 2012 were obtained. HPV-DNA detection was carried out by the use of polymerase chain reaction (PCR) using GP5+/GP6+ primers and genotyped by sequencing. A systematic literature search on the PubMed database was performed to investigate the prevalence and genotype distribution worldwide.

Results: In the present study population (n = 149) 52 vulvar high-grade squamous intraepithelial lesions (HSIL), 2 differentiated vulvar intraepithelial neoplasia (dVIN), and 95 VSCC cases were identified. HPV was detected in 85 patients (57.0%). Overall, a higher proportion of the vulvar high-grade precancerous lesions were HPV positive compared to VSCC (83.6% vs. 42.1%, p < 0.001). Additionally, HSIL had a significantly higher HPV-positive rate compared to keratinizing VSCC (84.6% vs. 33.3%, p < 0.001). However, the HPV positivity was comparable between HSIL and non-keratinizing VSCC (84.6% vs. 82.4%, p = 0.825). One dVIN was HPV positive whereas the other was HPV negative. HPV-16 was the most common HPV type (68.2%), followed by HPV-33 (18.8%) and HPV-18 (8.2%).

Conclusions: Most vulvar HSIL and non-keratinizing VSCCs appear to be HPV associated. However, we find a high HPV association in keratinizing VSCC, which needs to be further studied. HPV-16 remains the predominant genotype, but HPV-33 also seems to play a role in the development of VSCC.

Keywords: HPV-16; HPV-33; Human papillomavirus; Vulvar high-grade squamous intraepithelial lesions; Vulvar intraepithelial neoplasia; Vulvar squamous cell carcinoma.

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References

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