Abstract
Background: vulvar intraepithelial neoplasia is a non-invasive precursor lesion found in 50–70% of patients affected by vulvar squamous cell carcinoma. In the past, radical surgery was the standard treatment for vulvar intraepithelial neoplasia, however, considering the psychological and physical morbidities related to extensive surgery, several less aggressive treatment modalities have been proposed since the late 1970s. Photodynamic therapy is an effective and safe treatment for cutaneous non-melanoma skin cancer, with favorable cosmetic outcomes. Methods: in the present paper, the results of selected studies on photodynamic therapy in the treatment of vulvar intraepithelial neoplasia are reported and discussed. Results: Overall, complete histological response rates ranged between 20% and 67% and symptom response rates ranged between 52% and 89% according to different studies and case series. Conclusions: the real benefit of photodynamic therapy in the setting of vulvar intraepithelial neoplasia lies in its ability to treat multi-focal disease with minimal tissue destruction, preservation of vulvar anatomy and excellent cosmetic outcomes. These properties explain why photodynamic therapy is an attractive option for vulvar intraepithelial neoplasia treatment.
Highlights
Vulvar intraepithelial neoplasia (VIN) is a non-invasive precursor lesion usually found in50–70% of patients affected by vulvar squamous cell carcinoma (VSCC) [1]
VIN is a non-invasive precursor lesion usually found in 50–70% of patients affected by vulvar squamous cell carcinoma (VSCC)
Two different pathogenetic pathways may lead to VSCC, through the development of two distinct vulvar pre-cancerous lesions: (i) VIN of usual type, referred as classic or bowenoid
Summary
Vulvar intraepithelial neoplasia (VIN) is a non-invasive precursor lesion usually found in. VIN 1 was usually represented by flat condylomatous lesions and associated with low-risk (LR) HPV genotypes, especially 6 and 11. VIN 2 and 3 were usually related to risk of progression to VSCC and associated with high-risk (HR) HPV genotypes [6]. Due to the negligible progression risk of VIN 1, in 2004, the ISSVD proposed a new classification, including (i) uVIN that comprehended lesions previously classified as VIN 2 and VIN 3; and (ii) dVIN [7]. The 2014 World Health Organization (WHO) and the 2015 ISSVD classifications accepted the LAST, but included dVIN as an additional category [9] The incidence of both uVIN, nowadays named vulvar H-SIL (vH-SIL), and dVIN has risen over the last three decades, even if the incidence of VSCC has remained relatively stable. Gave their informed consent for inclusion before they participated in the study
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