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Neoplasia in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Carcinoma of the vulva represents only about 4% of gynecologic malignancies and is quite rare in pregnancy, because the vast majority of vulvar malignancies occur in postmenopausal patients. Approximately 15% of vulvar cancers are found in women less than 40 years of age. Of these, about 90% of the cases are squamous cell cancers. Other cell types include melanoma, adenocarcinoma, basal cell carcinoma, and sarcoma. Presenting symptoms are similar to those of the nonpregnant state and include itching, irritation, discharge, and occasionally bleeding. The etiology of vulvar cancer is unknown, but common patient characteristics include obesity, diabetes, hypertension, and perhaps less-than-optimal vulvar hygiene. Recent evidence suggests that HPV infection is a causative or associative factor in preinvasive vulvar intraepithelial neoplasia as well as in invasive vulvar cancer. Examination of the vulva will demonstrate areas of ulceration, exophytic growth, hyper- or hypopigmentation, or red or white discoloration. The key to early diagnosis is biopsy. All abnormal areas of the vulva, including raised, depressed, discolored, or warty lesions, deserve consideration for biopsy. Biopsy may be performed in the office under local anesthesia by simple excision or by utilizing the Keyes punch biopsy instrument. Toluidine blue staining and colposcopy may be used as adjunctive procedures, but should not substitute for biopsies, even in lieu of pregnancy.
Carcinoma of the Vagina and Vulva
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Sadaf Ghaem-Maghami, Kostas Lathouras
Human papilloma virus (HPV) is found in association with vaginal carcinoma, indicating a role in its etiology.2 Also, seropositivity to HPV 16 increases the risk of developing vaginal carcinoma by a factor of 4.5, and seropositivity for HPV 18 increases the risk of developing VAIN by a factor of 12.3 A field effect, in the lower genital tract, has been suggested by the observation of multicentric neoplasia involving cervix, vagina, and vulva4; however, Sugase and Matsukura found high copy numbers of HPV virus in vaginal biopsies of patients with VAIN, a large proportion of whom had no associated CIN or vulvar intraepithelial neoplasia (VIN).5
Cidofovir and Brincidofovir
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Graciela Andrei, Robert Snoeck
The activity, safety, and feasibility of CDV and imiquimod (an immunomodulatory) for treatment of vulvar intraepithelial neoplasia have been recently evaluated in a multicenter open-label randomized phase II trial (Tristram et al., 2014). Patients were allocated to topical treatment with either 1% CDV or 5% imiquimod to be self-applied three times a week for a maximum of 24 weeks. The primary end point was a histologically confirmed complete response at the posttreatment assessment visit 6 weeks after the end of treatment (a maximum of 30 weeks after treatment started). Analysis of the primary end point was by intention to treat. A total of 180 participants were enrolled in the study: 89 patients were randomly allocated CDV and 91 were assigned imiquimod. At the posttreatment assessment visit, a complete response had been achieved by 41% patients allocated CDV and by 42% patients assigned imiquimod. Adverse events were reported in 37% of CDV-treated patients and 46% of patients allocated imiquimod. Thus CDV and imiquimod proved active, safe, and feasible for treatment of vulval intraepithelial neoplasia and warrant further investigation in a phase III setting and represent effective alternatives to surgery for female patients with vulval intraepithelial neoplasia after exclusion of occult invasive disease.
Identification of potential prognostic biomarkers in vulval squamous cell carcinoma based on human papillomavirus infection Status-Analysis of GSE183454
Published in Journal of Obstetrics and Gynaecology, 2023
Ruxing Xi, Donghong Li, Shuanque Yang, Hui Zhang, Lijuan Hu, Xiaowei Wang, Guoqing Wang, Yan Wang
It has been reported that HPV-associated carcinoma accounts for 40% of all VSCC and is considered to be the cause of the recent increase worldwide. Both Low-Grade Squamous Intraepithelial Lesion (LSIL) and High-Grade Squamous Intraepithelial Lesion (HSIL) are precancerous lesions of VSCC and could be caused by high-risk HPV, which is also called oncogenic HPV based on its extreme carcinogenic capability. Among this, HPV16 is related with more than 77% cases of HSIL, whereas HPV 33 and 18 are related with 11% and 2.6% cases of cases, respectively (Leonard et al.2014). As previously mentioned, the preneoplastic of another HPV independent type of VSCC is differentiated vulval intraepithelial neoplasia (VIN) which occurs frequently in elderly females with inflammatory dermatosis, mostly lichen scleroses. Furthermore, it is also reported that the aberrant of Interferon regulatory factor-6 (IRF6) promoter methylation promote the occurrence of lesions from vulva normal skin to vulvar lichen sclerosus, VIN and VSCC (Rotondo et al.2016). Meanwhile, smoking, multiple sexual partners, young age of first intercourse and immunosuppression are additional risk factors for VSCC in general (Reyes and Cooper 2014, American Cancer Society 2022).
Low genitourinary tract risks in women living with the human immunodeficiency virus
Published in Climacteric, 2023
F. R. Pérez-López, A. M. Fernández-Alonso, E. Mezones-Holguín, P. Vieira-Baptista
Vulvar cancer can be derived from two pathways: one associated with vulvar dermatosis (lichen sclerosus or lichen planus) and one associated with HPV infection. According to the International Society for the Study of Vulvovaginal Diseases, the associated precursor lesions are differentiated vulvar intraepithelial neoplasia and vulvar high-grade squamous intraepithelial lesion, respectively [84,85]. Most vulvar cancers are associated with vulvar dermatosis, while most cases of vulvar intraepithelial neoplasia are associated with HPV infection. More recently, the World Health Organization (WHO) proposed that the terminology ‘HPV-independent vulvar intraepithelial neoplasia’ and ‘HPV-associated vulvar intraepithelial neoplasia’ should be adopted [86]. Vulvar cancer and its precursors are less frequent than their cervical counterparts. The cancers associated with lichen sclerosus or lichen planus tend to occur in older women and have a worse prognosis, while the associated HPV is often seen in younger women, and smokers, with other lesions of the anogenital tract and immunodepression.
Is 2045 the best we can do? Mitigating the HPV-related oropharyngeal cancer epidemic
Published in Expert Review of Anticancer Therapy, 2022
Ari Schuman, Karen S. Anderson, Andrew T. Day, Jay Ferrell, Erich M. Sturgis, Kristina R. Dahlstrom
For oropharyngeal cancer, where there is no premalignant lesion, the primary goal of screening is to identify patients who have already developed a malignancy in early stages, where treatment has minimal morbidity. However, screening for other cancers, like cervical or vulvar, involves the detection of precancerous lesions. These can then be treated, either with excision or medical options. The key medical option, which may hold promise for OPC, is immunoprevention through therapeutic vaccination. One such method was developed by Kenter et al., who used a vaccine against HPV16 E6 and E7 proteins as a treatment for high grade vulvar intraepithelial neoplasia (VIN). They found that 79% (95% CI 54%–94%) responded, with complete response in 47% (95% CI 24%–71%) [119]. In another immune-modulating approach, imiquimod, which activates toll-like receptor 7, has been used to treat VIN [120]. Additionally, multiple authors have attempted adjuvant HPV vaccination after excision of cervical intraepithelial neoplasia (CIN) in unvaccinated women, reducing the risk of recurrent CIN 1 or greater by one-third (RR 0.67, 95% CI 0.52–0.85) and CIN 2 or greater by 59% (RR 0.41, 95% CI 0.20–0.85) in a meta-analysis. It is possible that therapies similar to these – either targeted vaccination to other aspects of HPV, or another type of immunoprevention – will be valuable for the patients with persistent oral HPV infection or otherwise identified as high risk by screening who do not yet have an oropharyngeal lesion amenable to surgical removal [121].