Nonsurgical Treatment of Preneoplastic Vulvar Conditions
Five to eighteen percent of biopsies of vulvar intraepithelial lesions can have unsuspected stromal invasion on the final specimen. Therefore, a meticulous examination is important before applying a nonsurgical treatment, such as imiquimod, cidofovir, pho
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Mario Preti, Gianluigi Radici, and Leonardo Micheletti
57.1 Introduction Using the keywords “vulvar intraepithelial neoplasia” or “VIN” and “treatment” or “therapy” for PubMed search, we found at February 1, 2018, more than 1200 articles. In this chapter, we report the guiding principles and comments on the most relevant publications. The recent ISSVD classification [1], includes the following three conditions: • Low-grade squamous intraepithelial lesions (L-SIL) [flat condyloma or HPV effect] • High-grade squamous intraepithelial lesions (H-SIL) [VIN usual type] • Differentiated type VIN (dVIN) It allows us to consider for treatment only the lesions for which a risk of neoplastic progression is demonstrated: vulvar high-grade squamous intraepithelial lesion (VHSIL) and differentiated vulvar intraepithelial neoplasia (dVIN). The classification clearly highlights that there are two vulvar preneoplastic conditions. They have different oncogenic pathways, separated by etiology, epidemiology, and pathogenesis: HPV related (VHSIL) and not HPV related (dVIN) [1].
M. Preti (*) · G. Radici · L. Micheletti Department of Gynecology and Obstetrics, University of Torino, Torino, Italy
Vulvar low-grade squamous intraepithelial lesions (VLSIL-flat condyloma or HPV effect) do not have a malignant potential. This condition should be observed or treated only if symptomatic. Because of the different pathogenetic mechanisms behind VHSIL and dVIN (Table 57.1, Figs. 57.1 and 57.2), we can consider nonsurgical therapies only for VHSIL (Figs. 57.3 and 57.4) [2]. dVIN (Fig. 57.5) is difficult to diagnose, due to the high degree of cellular differentiation and absence of widespread nuclear pleomorphism and atypia. If a dVIN is suspected in a field of chronic dermatosis, we must biopsy and communicate to the pathologist our suspicion. Due to the short intraepithelial phase of dVIN and its rapid progression to VSCC. Its genesis, its risk of progression to invasive carcinoma, and its risk to harbor, in some parts of the lesion, invasive lesions missed at initial biopsy, this lesion is not appropriate to medical treatment. These concepts are underlined in Table 57.1.
57.2 Assessment of Coexistent Invasion Five to eighteen percent of biopsies of vulvar intraepithelial lesions can have unsuspected stromal invasion on the final specimen. Therefore we must exclude any focus of invasion before
© Springer International Publishing AG, part of Springer Nature 2019 J. Bornstein (ed.), Vulvar Disease, https://doi.org/10.1007/978-3-319-61621-6_57
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M. Preti et al.
386 Table 57.1 Characteristics to consider in VHSIL and dVIN treatment planning Patient/lesion characteristic Age Comorbidity Symptoms Smoking HIV positivity Etiology Size of lesion LSA on adjacent pathology HPV on adjacent pathology Multifocality Synchronous or metachronous VaIN or CIN or AIN Unrecognized invasive carcinoma Recurrence Risk of progression to invasive carcinoma Not surgical therapies
HOST FACTORS: Age, Immunity, Smoking, Environment and Diet Sexual behaviour
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