Human Papillomavirus Infections and Vulvar Disease Development

Garland, Suzanne M.; Insinga, Ralph P.; Sings, Heather L.; Haupt, Richard M.; Joura, Elmar A.

doi:10.1158/1055-9965.epi-09-0067

Cited by 40 publications

(24 citation statements)

References 35 publications

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“…For precancerous lesions, a high prevalence of HPV is detected for VaIN2/3 (95.8%), VIN2/3 (86.7%) and AIN2/3 (100.0%). Results are similar to previous studies [1,9,30].…”

Section: Discussionsupporting

confidence: 92%

Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions

Serrano

Sanjosé

Tous

et al. 2015

European Journal of Cancer

193

159

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“…For precancerous lesions, a high prevalence of HPV is detected for VaIN2/3 (95.8%), VIN2/3 (86.7%) and AIN2/3 (100.0%). Results are similar to previous studies [1,9,30].…”

Section: Discussionsupporting

confidence: 92%

Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions

Serrano

Sanjosé

Tous

et al. 2015

European Journal of Cancer

193

159

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“…A study from the U.S. found the median time from the first detection of an HPV infection to the development of CIN 2–3 was 14.1 months [16,21], similar to our data (18.8 months); indeed, the median time from vulvar HPV infection to VIN might be comparable to that of CIN.…”

Section: Discussionsupporting

confidence: 90%

“…HPV DNA testing performed 6 months after treatment was more predictive than was abnormal cervical cytology. A probable predictive value of the HPV DNA test for the monitoring of patients treated for VIN was observed [16], although the use of the HPV DNA test is not standardized in the management of the vulva.…”

Section: Introductionmentioning

confidence: 99%

The re-infection rate of high-risk HPV and the recurrence rate of vulvar intraepithelial neoplasia (VIN) usual type after surgical treatment

et al. 2011

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SummaryBackgroundVIN usual type appears to be related to the HPV’s oncogenic types. The aim of this prospective multicenter study was to evaluate the re-infection rate of high-risk HPV and the recurrence rate of VIN usual type after surgical treatment.Material/MethodsThe study enrolled 103 women affected by VIN usual type. They underwent wide local excision by CO2 laser. The patients were investigated by clinical evaluation and HPV DNA test 6 months after surgical treatment, and then were followed-up at 12, 18, 24, and 36 months. The recurrences were treated with re-excision.ResultsThe rate of HPV infection after surgical treatment was 34% at 6 months, 36.9% at 12 months, 40% at 18 months, 41.7% at 24 months and 44.7% at 36 months. The mean time from HPV infection to the development of VIN was 18.8 months.ConclusionsHPV testing in the follow-up of VIN usual type patients might be useful for identifying those patients with a higher risk of recurrence after surgical treatment, although more studies are needed. These preliminary data suggest that the test, in addition to clinical examination, can improve the efficacy of the follow-up.

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“…Unlike the ISSVD, the WHO continues to recommend grading of UVIN as VIN 1-3, because a significant number of VIN 1 lesions are associated with the presence of high-risk HPV. 35,36 The third grading system is the Bethesda-like system, which is not widely accepted internationally.…”

Section: Current Definitions Of Vinmentioning

confidence: 99%

Is Differentiated Vulval Intraepithelial Neoplasia the Precursor Lesion of Human Papillomavirus–Negative Vulval Squamous Cell Carcinoma?

Kokka

Singh

Faruqi

et al. 2011

International Journal of Gynecological Cancer

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Vulval squamous cell carcinoma appears to arise via 2 distinct pathways. A significant minority are associated with oncogenic human papillomavirus (HPV) infection and undifferentiated vulval intraepithelial neoplasia (VIN). However, the majority arises in the absence of HPV, on a background of chronic inflammation. Until recently, it was assumed that lichen sclerosus was the underlying inflammatory condition in the majority of HPV-negative cancers. This pathway of carcinogenesis has been less well studied than the HPV pathway. Emerging evidence implicates differentiated VIN (DVIN), rather than lichen sclerosus, as the most likely precursor lesion in HPV-negative vulval squamous cell carcinoma. Here we discuss the clinical and molecular evidence that implicates DVIN as a lesion with a high malignant potential. This lesion is probably underdiagnosed and may be undertreated. Better recognition of DVIN by gynecologists and pathologists may therefore offer an opportunity to prevent some vulval cancers.

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Human Papillomavirus Infections and Vulvar Disease Development

Cited by 40 publications

References 35 publications

Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions

Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions

The re-infection rate of high-risk HPV and the recurrence rate of vulvar intraepithelial neoplasia (VIN) usual type after surgical treatment

Is Differentiated Vulval Intraepithelial Neoplasia the Precursor Lesion of Human Papillomavirus–Negative Vulval Squamous Cell Carcinoma?

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