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Peter Hillemanns - One of the best experts on this subject based on the ideXlab platform.
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evaluation of different treatment modalities for Vulvar Intraepithelial Neoplasia vin co2 laser vaporization photodynamic therapy excision and vulvectomy
Gynecologic Oncology, 2006Co-Authors: Peter Hillemanns, Xiuli Wang, Stefanie Staehle, Wolfgang Michels, Christian DanneckerAbstract:Abstract Objectives. To evaluate various treatment modalities for Vulvar Intraepithelial Neoplasia (VIN) in relation to possible risk factors for recurrence. Methods. Retrospective review of 93 patients with VIN treated by CO 2 laser vaporization, photodynamic therapy with aminolevulinic acid (PDT), excision or vulvectomy. Results. 40.4% of the 47 patients with laser vaporization, 48.1% of 27 patients with PDT, 42% of 12 patients with local excision and none of the 7 patients treated by vulvectomy experienced a relapse within a mean follow-up of 53.7 months. The risk for recurrence significantly increased with VIN grade ( P = 0.02), multifocal VIN disease ( P = 0.01), multicentric Intraepithelial Neoplasia ( P = 0.05) and high-risk HPV infection ( P P = 0.012) and, if HPV testing is not available, multifocality ( P = 0.03). The lowest rate of postoperative side effects was noted in patients after PDT. There was one (1%) case of progression to Vulvar cancer. Conclusions. Vulva preserving treatment methods for VIN have high recurrence rates, especially in patients with HPV infection and multifocal disease. Therefore, careful long-term surveillance is mandatory.
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integration of hpv 16 and hpv 18 dna in Vulvar Intraepithelial Neoplasia
Gynecologic Oncology, 2006Co-Authors: Peter Hillemanns, Xiuli WangAbstract:Abstract Objective. Vulvar Intraepithelial Neoplasia (VIN) is a premalignant disease of the lower genital tract. The increased occurrence of high-risk human papillomavirus (HPV) infection seems to be associated with the increasing frequency of VIN. Integration of HPV DNA into host chromosome has been hypothesized to be a critical step in the carcinogenesis of cervical Neoplasia resulting in altered expression of two viral transforming genes E6 and E7. Method. We analyzed HPV-16 and HPV-18 DNA, and integrated transcripts of HPV-16 and HPV-18 genomes in 30 VIN cases with 53 lesions using a PCR-based protocol for the amplification of papillomavirus oncogene transcripts (APOT). Result. 24 of 30 VIN lesions (80%) harbored HPV-16 (in 23 cases) and HPV-18 DNA. Integration of HPV-16 and HPV-18 genome was observed in eight (38.1%) of 21 HPV-16/18 positive VIN III cases. All eight VIN were multifocal and had multicentric disease (CIN/VAIN) including one case that progressed to Vulvar carcinoma. Five of eight lesions were found to have E7 specific viral–cellular fusion transcripts only, two of eight showed E7–E4 viral–cellular fusion transcripts, and one of eight had both episomally derived and E7–E4 viral–cellular fusion transcripts. In 10 (83.3%) of 12 multifocal VIN III patients, all specimens derived from the same patient harbored the same HPV type and HPV transcript pattern suggesting monoclonality. Conclusion. HPV-16 is the most prevalent type among VIN II/III. HPV-16 and HPV-18 DNA integration into host cell genome seems to be related to the progression stage of Vulvar dysplasia and, therefore, may be necessary for development of HPV-associated invasive Vulvar carcinoma.
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evaluation of different treatment modalities for Vulvar Intraepithelial Neoplasia vin co 2 laser vaporization photodynamic therapy excision and vulvectomy
Gynecologic Oncology, 2006Co-Authors: Peter Hillemanns, Xiuli Wang, Stefanie Staehle, Wolfgang Michels, Christian DanneckerAbstract:Abstract Objectives. To evaluate various treatment modalities for Vulvar Intraepithelial Neoplasia (VIN) in relation to possible risk factors for recurrence. Methods. Retrospective review of 93 patients with VIN treated by CO 2 laser vaporization, photodynamic therapy with aminolevulinic acid (PDT), excision or vulvectomy. Results. 40.4% of the 47 patients with laser vaporization, 48.1% of 27 patients with PDT, 42% of 12 patients with local excision and none of the 7 patients treated by vulvectomy experienced a relapse within a mean follow-up of 53.7 months. The risk for recurrence significantly increased with VIN grade ( P = 0.02), multifocal VIN disease ( P = 0.01), multicentric Intraepithelial Neoplasia ( P = 0.05) and high-risk HPV infection ( P P = 0.012) and, if HPV testing is not available, multifocality ( P = 0.03). The lowest rate of postoperative side effects was noted in patients after PDT. There was one (1%) case of progression to Vulvar cancer. Conclusions. Vulva preserving treatment methods for VIN have high recurrence rates, especially in patients with HPV infection and multifocal disease. Therefore, careful long-term surveillance is mandatory.
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photodynamic therapy of Vulvar Intraepithelial Neoplasia using 5 aminolevulinic acid
International Journal of Cancer, 2000Co-Authors: Peter Hillemanns, Michael Untch, Christian Dannecker, Reinhold Baumgartner, Herbert Stepp, Joachim Diebold, Helmut Weingandt, Florian Prove, M KorellAbstract:Photodynamic (PDT) therapy is a relatively new technique with unique properties that make it attractive for the local treatment of superficial epithelial disorders. The objective of this study was to investigate the clinical response of PDT with the photosensitizing agent 5-aminolevulinic acid (5-ALA) in patients with Vulvar Intraepithelial Neoplasia (VIN) grades 1 to 3. Twenty-five patients with 111 lesions of VIN 1–3 were topically sensitized with 10 ml of a 20% solution of 5-ALA and treated with 57 cycles of laser light at 635 nm (100 J/cm2). Seventy (64%) of the 111 VIN lesions regressed after various PDT cycles. A complete response was achieved in 13 patients (52%) with 27 lesions. All patients with VIN 1 and mono- and bifocal VIN 2–3 showed complete clearance. However, a complete response could be achieved in only 4 (27%) of 15 women with multifocal VIN 2–3, whereas a partial response was noted in 9 of these patients with a total of 70 lesions, out of which 44 (63%) lesions disappeared. No response was seen in 2 patients with multifocal VIN 3. Histological assessment of the fluorescence-directed biopsies revealed that increased pigmentation and hyperkeratosis of the lesions were associated with low response rates. PDT using 5-ALA represents an alternative treatment modality for VIN which is easy to perform and has the advantage of minimal tissue destruction, low side effects and excellent cosmetic results. However, multifocal VIN disease with pigmented and hyperkeratinic lesions remains difficult to treat. Int. J. Cancer 85:649–653, 2000. © 2000 Wiley-Liss, Inc.
Ronald W Jones - One of the best experts on this subject based on the ideXlab platform.
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the natural history of Vulvar Intraepithelial Neoplasia differentiated type evidence for progression and diagnostic challenges
International Journal of Gynecological Pathology, 2016Co-Authors: Susan M Bigby, Lois Eva, Kah Leng Fong, Ronald W JonesAbstract:Squamous cell carcinoma of the vulva (SCCV) develops through either human papillomavirus (HPV)-dependent or HPV-independent pathways. Approximately 60% of SCCV arise independently of HPV, commonly in a background of an inflammatory dermatosis, particularly lichen sclerosus. The likely direct precursor to most of these lesions is Vulvar Intraepithelial Neoplasia (VIN), differentiated type (dVIN), although the evidence is largely circumstantial. There are few reports of progression to carcinoma, and the natural history of this pathway is not well understood. Nevertheless, dVIN is widely regarded as a potentially aggressive lesion. We identified dVIN adjacent to SCCV in 97 of 212 women (45.8%). Twenty-four of the 97 women (24.7%) had biopsies performed at least 6 mo before presentation with SCCV; slides for 47 biopsies from 21 women were available for review. dVIN was identified in 18 biopsies from 8 women (38.1%), which in 14 biopsies had been previously unrecognized. The subsequent cancer developed in the same region as the previous biopsy showing dVIN in 6 of the 8 women. The median interval between biopsy and invasive cancer was 43.5 mo (range, 8-102 mo). dVIN-associated SCCV was strongly associated with both lichen sclerosus, and HPV-negative status compared with usual type VIN (relative risk=38.35 (9.755-150.8) and 0.06485 (0.02764-0.1522), respectively). This study adds to the evidence linking dVIN with SCCV, and indicates that both clinical and histologic underrecognition contribute to the apparent rarity of dVIN as a solitary diagnosis. The morphologic spectrum of dVIN is likely to be wider than commonly appreciated; however, histologically defining the lower threshold is difficult and controversial.
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squamous Vulvar Intraepithelial Neoplasia 2004 modified terminology issvd Vulvar oncology subcommittee
Obstetrical & Gynecological Survey, 2006Co-Authors: Mario Sideri, Mario Preti, James Scurry, Edward J Wilkinson, Ronald W Jones, Debra S. Heller, Hope K Haefner, Sallie NeillAbstract:ABSTRACT The terminology for squamous Vulvar Intraepithelial Neoplasia (VIN) was established in 1986 by the International Society for the Study of Vulvar Disease (ISSVD). In this classification, abnormal changes in Vulvar tissue seen on cytology are categorized as VIN 1, VIN 2, or VIN 3. Although the grading is similar to that used for cervical Intraepithelial lesions (CIN), there is no evidence that VIN and CIN have a similar natural history or that the grading of VIN represents a biologic continuum. It is now accepted that VIN 1 has a low malignant potential and is not a precursor to VIN 2 or 3. As originally described, VIN 1 denotes basally cellular changes in the basal epithelial that are relatively uncommon and are an effect of exposure to human papillomavirus (HPV). Its diagnosis varies from pathologist to pathologist and is not reproducible. The categories of VIN 2 and VIN 3 have been useful in describing high-grade disease, but they do not differentiate between lesions usually associated with high-risk HPV types (VIN, usual type) and other lesions not resulting from exposure to HPV (VIN, differentiated). The ISSVD proposal for Vulvar Intraepithelial Neoplasia uses the term VIN for all high-grade squamous lesions. Two different categories of VIN are to be used VIN, usual type, is related to HPV. It is further subdivided into 3 histologic subtypes: warty, basaloid, and mixed. These lesions are unifocal or multifocal and may present clinically as patches, erosion, plaques, papules, and nodules with hyperkeratotic, verrucous, pigmented red or white changes. The progression of VIN, usual type, to invasive cancer in untreated patients has been unequivocally demonstrated, especially in women over 30 years of age or immunocompromised women. A variant of VIN, usual type, associated with genital warts or pregnancy is seen in some younger women and can regress spontaneously. VIN, differentiated type, is not associated with HPV and is related to lichen sclerosa and/or squamous cell hyperplasia. It is a less common diagnosis usually seen in older women. It usually presents as a warty papule or hyperkeratotic plaque. It is commonly seen during follow up of women who have been treated for lichen sclerosus or invasive Vulvar cancer. Rarely, a pagetoid type of VIN is seen that cannot be classified as either VIN, usual type, or VIN, differentiated type. This type of VIN can be termed VIN, unclassified.
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squamous Vulvar Intraepithelial Neoplasia 2004 modified terminology issvd Vulvar oncology subcommittee
Journal of Reproductive Medicine, 2005Co-Authors: Mario Sideri, Mario Preti, James Scurry, Edward J Wilkinson, Ronald W Jones, Debra S. Heller, Hope K Haefner, Sallie NeillAbstract:In the current classification, squamous Vulvar Intraepithelial Neoplasia (VIN) is categorized as VIN 1, 2 and 3 according to the degree of abnormality. There is neither evidence that the VIN 1-3 morphologic spectrum reflects a biologic continuum nor that VIN 1 is a cancer precursor. The VIN 2 and 3 category includes 2 types of lesion, which differ in morphology, biology and clinical features. VIN, usual type (warty, basaloid and mixed), is HPV related in most cases. Invasive squamous carcinomas of warty or basaloid type is associated with VIN, usual type. VIN, differentiated type, is seen particularly in older women with lichen sclerosus and/or squamous cell hyperplasia in some cases. Neither VIN, differentiated type, nor associated keratinizing squamous cell carcinoma is HPV related. The term VIN should apply only to histologically high grade squamous lesions (former terms, VIN 2 and VIN 3 and differentiated VIN 3). The term VIN 1 will no longer be used. Two categories should describe squamous VIN: VIN, usual type (encompassing former VIN 2 and 3 of warty, basaloid and mixed types) and VIN, differentiated type (VIN 3, differentiated type).
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spontaneous regression of Vulvar Intraepithelial Neoplasia 2 3
Obstetrics & Gynecology, 2000Co-Authors: Ronald W Jones, Darion M RowanAbstract:Abstract Objective: To determine the background and clinical features of a group of women who experienced spontaneous regression of Vulvar Intraepithelial Neoplasia (VIN) 2-3 before treatment was undertaken. Methods: A retrospective review was made of the records of 14 women who experienced spontaneous regression of VIN 2-3. Results: The women were 15–27 years of age (median 19.5 years). Ninety-three percent were non-white. All women were seen initially in a sexual health clinic, and with one exception, all had been treated previously for genital condyloma acuminata. Four of the 14 cases were pregnancy-associated. Half of the women were asymptomatic. The transit time to regression of VIN 2-3 was 3–30 months (median 9.5 months). The median follow-up was 3 years. All lesions were multiple and pigmented. Conclusion: Spontaneous regression of VIN 2-3 can occur in young women with multifocal pigmented lesions.
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trends in squamous cell carcinoma of the vulva the influence of Vulvar Intraepithelial Neoplasia
Obstetrics & Gynecology, 1997Co-Authors: Ronald W Jones, Judith Baranyai, S StablesAbstract:Objective: To determine trends in the clinicopathology of Vulvar squamous cell carcinoma over the past 2 decades, with particular reference to the possible effects of the increasing incidence of Vulvar Intraepithelial Neoplasia (VIN) during this time. Methods: Two cohorts of 56 and 57 women with squamous cell carcinoma of the vulva and separated by at least 2 decades were reviewed retrospectively. Pathologic specimens were analyzed concurrently. Results: In the 1965–1974 cohort, only one of 56 patients was younger than 50 years of age at the time of presentation, whereas in the 1990–1994 cohort, 12 of 57 (21%) were younger than 50 years of age (P = .001). Ten of 13 women younger than 50 years of age, compared with 13 of 100 of women 50 years of age or older, had warty or basaloid VIN associated with their invasive carcinoma (P < .001). Cigarette smoking and multiple lower genital tract Neoplasia were both significantly more common in women younger than 50 years of age (P < .001). Conclusion: Over the past 2 decades, a subset of women younger than 50 years of age with squamous cell carcinoma of the vulva has emerged. Most of these carcinomas appear to arise in a field of warty or basaloid VIN. This suggests that the increasing incidence of VIN seen in young women during the past 2 decades is being reflected now in VIN-associated squamous cell carcinoma of the vulva in younger women.
Bastiaan Nuijen - One of the best experts on this subject based on the ideXlab platform.
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HPV16 E7 DNA tattooing: safety, immunogenicity, and clinical response in patients with HPV-positive Vulvar Intraepithelial Neoplasia
Cancer Immunology Immunotherapy, 2017Co-Authors: Sanne Samuels, Marij J P Welters, Henry J M A A Zijlmans, Daisy Philips, Pia Kvistborg, Ilina Ehsan, A. Marijne Heeren, Joost H. Berg, Suzy M. E. Scholl, Bastiaan NuijenAbstract:Background Usual type Vulvar Intraepithelial Neoplasia (uVIN) is caused by HPV, predominantly type 16. Several forms of HPV immunotherapy have been studied, however, clinical results could be improved. A novel intradermal administration route, termed DNA tattooing, is superior in animal models, and was tested for the first time in humans with a HPV16 E7 DNA vaccine (TTFC-E7SH). Methods The trial was designed to test safety, immunogenicity, and clinical response of TTFC-E7SH in twelve HPV16^+ uVIN patients. Patients received six vaccinations via DNA tattooing. The first six patients received 0.2 mg TTFC-E7SH and the next six 2 mg TTFC-E7SH. Vaccine-specific T-cell immunity was evaluated by IFNγ-ELISPOT and multiparametric flow cytometry. Results Only grade I-II adverse events were observed upon TTFC-E7SH vaccination. The ELISPOT analysis showed in 4/12 patients a response to the peptide pool containing shuffled E7 peptides. Multiparametric flow cytometry showed low CD4^+ and/or CD8^+ T-cell responses as measured by increased expression of PD-1 (4/12 in both), CTLA-4 (2/12 and 3/12), CD107a (5/12 and 4/12), or the production of IFNγ (2/12 and 1/12), IL-2 (3/12 and 4/12), TNFα (2/12 and 1/12), and MIP1β (3/12 and 6/12). At 3 months follow-up, no clinical response was observed in any of the twelve vaccinated patients. Conclusion DNA tattoo vaccination was shown to be safe. A low vaccine-induced immune response and no clinical response were observed in uVIN patients after TTFC-E7SH DNA tattoo vaccination. Therefore, a new phase I/II trial with an improved DNA vaccine format is currently in development for patients with uVIN.
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hpv16 e7 dna tattooing safety immunogenicity and clinical response in patients with hpv positive Vulvar Intraepithelial Neoplasia
Cancer Immunology Immunotherapy, 2017Co-Authors: Sanne Samuels, Marij J P Welters, Marijne A Heeren, Henry J M A A Zijlmans, Joost H Van Den Berg, Daisy Philips, Pia Kvistborg, Ilina Ehsan, S Scholl, Bastiaan NuijenAbstract:Background Usual type Vulvar Intraepithelial Neoplasia (uVIN) is caused by HPV, predominantly type 16. Several forms of HPV immunotherapy have been studied, however, clinical results could be improved. A novel intradermal administration route, termed DNA tattooing, is superior in animal models, and was tested for the first time in humans with a HPV16 E7 DNA vaccine (TTFC-E7SH).
Mario Preti - One of the best experts on this subject based on the ideXlab platform.
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Diagnostic Criteria for Differentiated Vulvar Intraepithelial Neoplasia and Vulvar Aberrant Maturation.
Journal of lower genital tract disease, 2020Co-Authors: Debra S. Heller, James Scurry, Tania Day, Jill Allbritton, Gianluigi Radici, Kathryn C. Welch, Mario PretiAbstract:OBJECTIVE The aim of the study was to describe the features required for diagnosis of differentiated Vulvar Intraepithelial Neoplasia (dVIN) and Vulvar aberrant maturation (VAM). MATERIALS AND METHODS The International Society of the Study of Vulvovaginal Diseases tasked the difficult pathologic diagnoses committee to develop consensus recommendations for clinicopathologic diagnosis of Vulvar lichen planus, lichen sclerosus, and dVIN. The dVIN subgroup reviewed the literature and formulated diagnostic criteria that were reviewed by the committee and then approved by the International Society of the Study of Vulvovaginal Diseases membership. RESULTS Differentiated Vulvar Intraepithelial Neoplasia is the immediate precursor of human papillomavirus (HPV)-independent Vulvar squamous cell carcinoma and shows a spectrum of clinical and microscopic appearances, some overlapping with HPV-related Neoplasia. The histopathologic definition of dVIN is basal atypia combined with negative or nonblock-positive p16 and basal overexpressed, aberrant negative, or wild-type p53. The most common pattern of dVIN is keratinizing with acanthosis, aberrant rete ridge pattern, and premature maturation. The morphologic spectrum of keratinizing dVIN includes hypertrophic, atrophic, acantholytic, and subtle forms. A few dVIN cases are nonkeratinizing, with basaloid cells replacing more than 60% of epithelium. Vulvar aberrant maturation is an umbrella term for lesions with aberrant maturation that arise out of lichenoid dermatitis and lack the basal atypia required for dVIN. CONCLUSIONS Evaluation of women at risk for dVIN and VAM requires a collaborative approach by clinicians and pathologists experienced in Vulvar disorders. Close surveillance of women with lichen sclerosus and use of these recommendations may assist in prevention of HPV-independent squamous cell carcinoma through detection and treatment of dVIN and VAM.
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Vulvar Intraepithelial Neoplasia
Best practice & research. Clinical obstetrics & gynaecology, 2014Co-Authors: Mario Preti, James Scurry, Claudia Marchitelli, Leonardo MichelettiAbstract:Vulvar Intraepithelial Neoplasia (VIN) is a high-grade Intraepithelial squamous lesion and precursor of invasive squamous cell carcinoma (SCC). The 2004 International Society for the Study of Vulvovaginal Disease (ISSVD) classification distinguished two types of VIN: usual type (human papillomavirus (HPV)-related) and differentiated type (not HPV-related). The incidence of usual-type VIN is higher in younger women, while differentiated-type VIN is more common in older patients with chronic dermatologic conditions. Differentiated-type VIN has a greater invasive potential and shorter time between diagnosis and SCC than usual-type VIN. The diagnosis of VIN is carried out by identifying a lesion by visual inspection and confirming by performing a biopsy. Screening tests are not available. Patients with usual-type VIN are at a higher risk of developing another HPV-related malignancy of the anogenital tract; therefore, examination from the cervix to the perianal area is mandatory. The therapeutic approach to VIN balances the invasive potential with the need to be as conservative as possible. Current prophylactic HPV vaccines offer protection against usual-type VIN and related invasive carcinoma.
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squamous Vulvar Intraepithelial Neoplasia 2004 modified terminology issvd Vulvar oncology subcommittee
Obstetrical & Gynecological Survey, 2006Co-Authors: Mario Sideri, Mario Preti, James Scurry, Edward J Wilkinson, Ronald W Jones, Debra S. Heller, Hope K Haefner, Sallie NeillAbstract:ABSTRACT The terminology for squamous Vulvar Intraepithelial Neoplasia (VIN) was established in 1986 by the International Society for the Study of Vulvar Disease (ISSVD). In this classification, abnormal changes in Vulvar tissue seen on cytology are categorized as VIN 1, VIN 2, or VIN 3. Although the grading is similar to that used for cervical Intraepithelial lesions (CIN), there is no evidence that VIN and CIN have a similar natural history or that the grading of VIN represents a biologic continuum. It is now accepted that VIN 1 has a low malignant potential and is not a precursor to VIN 2 or 3. As originally described, VIN 1 denotes basally cellular changes in the basal epithelial that are relatively uncommon and are an effect of exposure to human papillomavirus (HPV). Its diagnosis varies from pathologist to pathologist and is not reproducible. The categories of VIN 2 and VIN 3 have been useful in describing high-grade disease, but they do not differentiate between lesions usually associated with high-risk HPV types (VIN, usual type) and other lesions not resulting from exposure to HPV (VIN, differentiated). The ISSVD proposal for Vulvar Intraepithelial Neoplasia uses the term VIN for all high-grade squamous lesions. Two different categories of VIN are to be used VIN, usual type, is related to HPV. It is further subdivided into 3 histologic subtypes: warty, basaloid, and mixed. These lesions are unifocal or multifocal and may present clinically as patches, erosion, plaques, papules, and nodules with hyperkeratotic, verrucous, pigmented red or white changes. The progression of VIN, usual type, to invasive cancer in untreated patients has been unequivocally demonstrated, especially in women over 30 years of age or immunocompromised women. A variant of VIN, usual type, associated with genital warts or pregnancy is seen in some younger women and can regress spontaneously. VIN, differentiated type, is not associated with HPV and is related to lichen sclerosa and/or squamous cell hyperplasia. It is a less common diagnosis usually seen in older women. It usually presents as a warty papule or hyperkeratotic plaque. It is commonly seen during follow up of women who have been treated for lichen sclerosus or invasive Vulvar cancer. Rarely, a pagetoid type of VIN is seen that cannot be classified as either VIN, usual type, or VIN, differentiated type. This type of VIN can be termed VIN, unclassified.
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squamous Vulvar Intraepithelial Neoplasia 2004 modified terminology issvd Vulvar oncology subcommittee
Journal of Reproductive Medicine, 2005Co-Authors: Mario Sideri, Mario Preti, James Scurry, Edward J Wilkinson, Ronald W Jones, Debra S. Heller, Hope K Haefner, Sallie NeillAbstract:In the current classification, squamous Vulvar Intraepithelial Neoplasia (VIN) is categorized as VIN 1, 2 and 3 according to the degree of abnormality. There is neither evidence that the VIN 1-3 morphologic spectrum reflects a biologic continuum nor that VIN 1 is a cancer precursor. The VIN 2 and 3 category includes 2 types of lesion, which differ in morphology, biology and clinical features. VIN, usual type (warty, basaloid and mixed), is HPV related in most cases. Invasive squamous carcinomas of warty or basaloid type is associated with VIN, usual type. VIN, differentiated type, is seen particularly in older women with lichen sclerosus and/or squamous cell hyperplasia in some cases. Neither VIN, differentiated type, nor associated keratinizing squamous cell carcinoma is HPV related. The term VIN should apply only to histologically high grade squamous lesions (former terms, VIN 2 and VIN 3 and differentiated VIN 3). The term VIN 1 will no longer be used. Two categories should describe squamous VIN: VIN, usual type (encompassing former VIN 2 and 3 of warty, basaloid and mixed types) and VIN, differentiated type (VIN 3, differentiated type).
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inter observer variation in histopathological diagnosis and grading of Vulvar Intraepithelial Neoplasia results of an european collaborative study
British Journal of Obstetrics and Gynaecology, 2000Co-Authors: Mario Preti, Maura Mezzetti, Chris Robertson, Mario SideriAbstract:Objective To evaluate the inter-observer variability of Vulvar Intraepithelial Neoplasia diagnosis and grading system. Design Prospective study. Sample Histological sections of 66 Vulvar biopsies. Methods Six consultant pathologists working at different European institutions independently reviewed 66 Vulvar biopsies. The following variables were investigated: specimen adequacy, gross categorisation into benign or neoplastic changes, presence of atypical cytological pattern, presence of neoplastic architectural pattern, grade of Vulvar Intraepithelial Neoplasia, presence of histopathologic associated findings for human papillomavirus infection. Main outcome measures The degree of inter-observer variation for each histopathologic parameter was assessed by Kappa (κ) statistics. The frequency and the degree of disagreement were calculated by a symmetrical agreement matrix showing the number paired classifications. Results A good agreement (overall weighted κ= 0.65, unweighted κ= 0.46) was observed for grading Vulvar Intraepithelial Neoplasia. Human papillomavirus infection associated findings and specimen adequacy were the variables with less inter-observer agreement (overall weighted κ 0.26 and 0.22, respectively). Exact agreement between two pathologists for grade of Vulvar Intraepithelial Neoplasia was observed in 63.6% of paired readings; the rate of paired agreement reached 73.9% considering Vulvar Intraepithelial Neoplasia 2 and 3 as a single class. Conversely, only 5.0% of Vulvar Intraepithelial Neoplasia 1 diagnoses were concordant in paired analysis. Conclusions Current terminology offers a reproducible tool in the hands of expert pathologists. While on the diagnosis of ‘high grade’ Vulvar Intraepithelial Neoplasia (Vulvar Intraepithelial Neoplasia 2 and 3) there is good agreement, the diagnostic category of Vulvar Intraepithelial Neoplasia 1 is not reproducible.
James Scurry - One of the best experts on this subject based on the ideXlab platform.
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Diagnostic Criteria for Differentiated Vulvar Intraepithelial Neoplasia and Vulvar Aberrant Maturation.
Journal of lower genital tract disease, 2020Co-Authors: Debra S. Heller, James Scurry, Tania Day, Jill Allbritton, Gianluigi Radici, Kathryn C. Welch, Mario PretiAbstract:OBJECTIVE The aim of the study was to describe the features required for diagnosis of differentiated Vulvar Intraepithelial Neoplasia (dVIN) and Vulvar aberrant maturation (VAM). MATERIALS AND METHODS The International Society of the Study of Vulvovaginal Diseases tasked the difficult pathologic diagnoses committee to develop consensus recommendations for clinicopathologic diagnosis of Vulvar lichen planus, lichen sclerosus, and dVIN. The dVIN subgroup reviewed the literature and formulated diagnostic criteria that were reviewed by the committee and then approved by the International Society of the Study of Vulvovaginal Diseases membership. RESULTS Differentiated Vulvar Intraepithelial Neoplasia is the immediate precursor of human papillomavirus (HPV)-independent Vulvar squamous cell carcinoma and shows a spectrum of clinical and microscopic appearances, some overlapping with HPV-related Neoplasia. The histopathologic definition of dVIN is basal atypia combined with negative or nonblock-positive p16 and basal overexpressed, aberrant negative, or wild-type p53. The most common pattern of dVIN is keratinizing with acanthosis, aberrant rete ridge pattern, and premature maturation. The morphologic spectrum of keratinizing dVIN includes hypertrophic, atrophic, acantholytic, and subtle forms. A few dVIN cases are nonkeratinizing, with basaloid cells replacing more than 60% of epithelium. Vulvar aberrant maturation is an umbrella term for lesions with aberrant maturation that arise out of lichenoid dermatitis and lack the basal atypia required for dVIN. CONCLUSIONS Evaluation of women at risk for dVIN and VAM requires a collaborative approach by clinicians and pathologists experienced in Vulvar disorders. Close surveillance of women with lichen sclerosus and use of these recommendations may assist in prevention of HPV-independent squamous cell carcinoma through detection and treatment of dVIN and VAM.
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distinguishing erosive lichen planus from differentiated Vulvar Intraepithelial Neoplasia
Journal of Lower Genital Tract Disease, 2016Co-Authors: Tania Day, Nikola A Bowden, Ken Jaaback, Geoff Otton, James ScurryAbstract:ObjectiveErosive lichen planus (LP) and differentiated Vulvar Intraepithelial Neoplasia (dVIN) may display overlapping histopathologic features.Materials and MethodsWe searched the local pathology database for Vulvar biopsies reported as dVIN or erosive vulvitis during 2011 to 2013 inclusive. After
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Vulvar Intraepithelial Neoplasia
Best practice & research. Clinical obstetrics & gynaecology, 2014Co-Authors: Mario Preti, James Scurry, Claudia Marchitelli, Leonardo MichelettiAbstract:Vulvar Intraepithelial Neoplasia (VIN) is a high-grade Intraepithelial squamous lesion and precursor of invasive squamous cell carcinoma (SCC). The 2004 International Society for the Study of Vulvovaginal Disease (ISSVD) classification distinguished two types of VIN: usual type (human papillomavirus (HPV)-related) and differentiated type (not HPV-related). The incidence of usual-type VIN is higher in younger women, while differentiated-type VIN is more common in older patients with chronic dermatologic conditions. Differentiated-type VIN has a greater invasive potential and shorter time between diagnosis and SCC than usual-type VIN. The diagnosis of VIN is carried out by identifying a lesion by visual inspection and confirming by performing a biopsy. Screening tests are not available. Patients with usual-type VIN are at a higher risk of developing another HPV-related malignancy of the anogenital tract; therefore, examination from the cervix to the perianal area is mandatory. The therapeutic approach to VIN balances the invasive potential with the need to be as conservative as possible. Current prophylactic HPV vaccines offer protection against usual-type VIN and related invasive carcinoma.
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pathologic audit of 164 consecutive cases of Vulvar Intraepithelial Neoplasia
International Journal of Gynecological Pathology, 2006Co-Authors: James Scurry, Michael Campion, Bonnie Scurry, Soo Nyung Kim, Neville F HackerAbstract:Summary:There are 2 types of Vulvar Intraepithelial Neoplasia (VIN): warty-basaloid and differentiated. Differentiated VIN is uncommon and seldom diagnosed prior to carcinoma and, traditionally, is not graded. There are currently 3 grading systems for warty-basaloid VIN: the World Health Organizatio
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squamous Vulvar Intraepithelial Neoplasia 2004 modified terminology issvd Vulvar oncology subcommittee
Obstetrical & Gynecological Survey, 2006Co-Authors: Mario Sideri, Mario Preti, James Scurry, Edward J Wilkinson, Ronald W Jones, Debra S. Heller, Hope K Haefner, Sallie NeillAbstract:ABSTRACT The terminology for squamous Vulvar Intraepithelial Neoplasia (VIN) was established in 1986 by the International Society for the Study of Vulvar Disease (ISSVD). In this classification, abnormal changes in Vulvar tissue seen on cytology are categorized as VIN 1, VIN 2, or VIN 3. Although the grading is similar to that used for cervical Intraepithelial lesions (CIN), there is no evidence that VIN and CIN have a similar natural history or that the grading of VIN represents a biologic continuum. It is now accepted that VIN 1 has a low malignant potential and is not a precursor to VIN 2 or 3. As originally described, VIN 1 denotes basally cellular changes in the basal epithelial that are relatively uncommon and are an effect of exposure to human papillomavirus (HPV). Its diagnosis varies from pathologist to pathologist and is not reproducible. The categories of VIN 2 and VIN 3 have been useful in describing high-grade disease, but they do not differentiate between lesions usually associated with high-risk HPV types (VIN, usual type) and other lesions not resulting from exposure to HPV (VIN, differentiated). The ISSVD proposal for Vulvar Intraepithelial Neoplasia uses the term VIN for all high-grade squamous lesions. Two different categories of VIN are to be used VIN, usual type, is related to HPV. It is further subdivided into 3 histologic subtypes: warty, basaloid, and mixed. These lesions are unifocal or multifocal and may present clinically as patches, erosion, plaques, papules, and nodules with hyperkeratotic, verrucous, pigmented red or white changes. The progression of VIN, usual type, to invasive cancer in untreated patients has been unequivocally demonstrated, especially in women over 30 years of age or immunocompromised women. A variant of VIN, usual type, associated with genital warts or pregnancy is seen in some younger women and can regress spontaneously. VIN, differentiated type, is not associated with HPV and is related to lichen sclerosa and/or squamous cell hyperplasia. It is a less common diagnosis usually seen in older women. It usually presents as a warty papule or hyperkeratotic plaque. It is commonly seen during follow up of women who have been treated for lichen sclerosus or invasive Vulvar cancer. Rarely, a pagetoid type of VIN is seen that cannot be classified as either VIN, usual type, or VIN, differentiated type. This type of VIN can be termed VIN, unclassified.
