A Clinical and Pathological Overview of Vulvar Condyloma Acuminatum, Intraepithelial Neoplasia, and Squamous Cell Carcinoma

Abstract

Condyloma acuminatum, intraepithelial neoplasia, and squamous cell carcinoma are three relatively frequent vulvar lesions. Condyloma acuminatum is induced by low risk genotypes of human papillomavirus (HPV). Vulvar intraepithelial neoplasia (VIN) and squamous cell carcinoma have different etiopathogenic pathways and are related or not with high risk HPV types. The goal of this paper is to review the main pathological and clinical features of these lesions. A special attention has been paid also to epidemiological data, pathological classification, and clinical implications of these diseases.

Anogenital Condyloma: Epidemiological, Clinical, Therapeutic and Evolutionary Aspects of 74 Cases in Benin

“…This assessment consists in looking for other locations in the patient and his partners depending on the context and the sexual practices. The findings should be broadened to the systematic search for other STIs such as HIV infection, viral hepatitis B and C according to context, syphilis, genital herpes, chancroid, gonorrhea and chlamydia [5] [6]. Therapeutically, three types of therapeutic methods were recently published in the annals of dermatology and venereology of October 2016 by Bouscarat et al [7].…”

Giant condyloma acuminatum of vulva

“…Types 6 and 11 are not oncogenic and contribute to about 90% of anogenital warts. 1 In the general population, the prevalence of HPV infection among asymptomatic women ranges from 2 to 44% and among men from 2.3 to 34.8%. Although there is no exact data but it is rare in our country.…”

Stathmin is a highly sensitive and specific biomarker for vulvar high-grade squamous intraepithelial lesions

“…The subtle clinical and histological changes make recognition and diagnosis difficult, which might contribute to the low prevalence 5 11 12. Importantly, the malignant potential of untreated dVIN lesions is probably as high as 80% 9 12 13. Given the malignant potential of HSILs and dVIN, it is important to treat these patients adequately and to ensure close follow-up.…”

“…However, p16 staining can be less specific for differentiating between vulvar LSIL and HSIL lesions, since these lesions sometimes show similar p16 expression patterns. Furthermore, the p16 staining pattern is sometimes difficult to interpret due to differential staining intensity and patterns that can also be found in inflammatory vulvar disorders 9 13 19–21. Ki67, a cell proliferation marker, is widely used to differentiate between cervical LSILs and HSILs 9 13 20 22.…”