Squamous Vulvar Intraepithelial Neoplasia: 2004 Modified Terminology, ISSVD Vulvar Oncology Subcommittee

European Institute of Oncology, Milan, Italy.
The Journal of reproductive medicine (Impact Factor: 0.7). 12/2005; 50(11):807-10. DOI: 10.1097/01.ogx.0000201921.69949.10
Source: PubMed


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).

Download full-text


Available from: Hope Haefner,
    • "Vulvar cancer in pre-menopausal women, as found in communities within the East Arnhem district and several communities bordering that district (hereafter referred to as Arnhem Land), is associated with persistent human papillomavirus (HPV) infection, particularly genotype 16, whereas in older women it is more usually associated with a dermatological condition called lichen sclerosus [3] [4] [5]. The precursor lesion to HPV-related invasive vulvar cancer is vulvar intraepithelial neoplasia (VIN) usual type (warty, basaloid and mixed) [6], and the incidence of VIN in this population is similarly high (34.7 per 100 000 in women aged less than 50 years) [2]. Previous work with the Arnhem Land population, however, found no evidence that higher rates of HPV infection [7] or that particularly virulent strains of HPV [8] could explain the excess incidence of vulvar cancer in this population, suggesting the possible involvement of additional environmental and/or genetic factors that may impair host immunity . "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective A cluster of vulvar cancer exists in young Aboriginal women living in remote communities in Arnhem Land, Australia. A genetic case–control study was undertaken involving 30 cases of invasive vulvar cancer and its precursor lesion, high-grade vulvar intraepithelial neoplasia (VIN), and 61 controls, matched for age and community of residence. It was hypothesized that this small, isolated population may exhibit increased autozygosity, implicating recessive effects as a possible mechanism for increased susceptibility to vulvar cancer. Methods : Genotyping data from saliva samples were used to identify runs of homozygosity (ROH) in order to calculate estimates of genome-wide homozygosity. Results No evidence of an effect of genome-wide homozygosity on vulvar cancer and VIN in East Arnhem women was found, nor was any individual ROH found to be significantly associated with case status. This study found further evidence supporting an association between previous diagnosis of CIN and diagnosis of vulvar cancer or VIN, but found no association with any other medical history variable. Conclusions These findings do not eliminate the possibility of genetic risk factors being involved in this cancer cluster, but rather suggest that alternative analytical strategies and genetic models should be explored.
    Gynecologic Oncology 06/2014; 133(3). DOI:10.1016/j.ygyno.2014.03.566 · 3.77 Impact Factor
  • Source
    • "The International Society for the Study of Vulvovaginal disease (ISSVD) has proposed that VIN should not be graded but described as high-grade VIN lesions only (VIN 2 or VIN 3). The ISSVD has also recommended that the term low-grade VIN (VIN 1, or mild dysplasia) should not be used anymore and that such lesions should be classified as flat condyloma acuminatum, or given an appropriate descriptive term [49]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Condyloma acuminatum, intraepithelial neoplasia, and squamous cell carcinoma are three relatively frequent vulvar lesions. Condyloma acuminatum is induced by low risk genotypes of human papillomavirus (HPV). Vulvar intraepithelial neoplasia (VIN) and squamous cell carcinoma have different etiopathogenic pathways and are related or not with high risk HPV types. The goal of this paper is to review the main pathological and clinical features of these lesions. A special attention has been paid also to epidemiological data, pathological classification, and clinical implications of these diseases.
    02/2014; 2014(1):480573. DOI:10.1155/2014/480573
  • Source
    • "Patients with the diagnosis of invasive cancer within one year from initial diagnosis of IN were also excluded in order to minimize falsely detecting preexisting invasive disease due to incorrect initial diagnosis. Low grade IN (formerly VIN I) was not considered an inclusion criterion since it had been omitted from the classification system for VIN developed by the International Society for the Study of Vulvovaginal Diseases (ISSVD) in 2005 [3]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The malignant potential of intraepithelial neoplasia of the vulva and vagina after treatment is not well defined. Our objective was to examine risk factors for recurrence and invasive disease. Four hundred sixty-four women with biopsy proven high-grade intraepithelial neoplasia of the vulva and vagina were identified in the electronic databases of four colposcopy clinics. Inclusion criteria were a follow-up of more than one year, no history of invasive cancer and no invasive cancer within the first year after initial treatment. We investigated the potential factors associated with recurrence and progression using a logistic regression analysis to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Of the 411 eligible patients, 123 patients (29.9%) recurred later than one year after initial treatment and 24 patients (5.8%) progressed to invasive disease. According to multivariate analyses, the risk factors associated with recurrence were multifocality (OR, 3.33; 95% CI, 2.02 to 5.51), immunosuppression (OR, 2.51; 95% CI, 1.09 to 5.81), excision as initial treatment (vs. laser evaporation; OR, 1.79; 95% CI, 1.11 to 2.91) and smoking (OR, 1.61; 95% CI, 1.02 to 2.55). Risk factors for progression to invasive disease were immunosuppression (OR, 4.00; 95% CI, 1.30 to 12.25), multifocality (OR, 3.05; 95% CI, 1.25 to 7.43) and smoking (OR, 2.97; 95% CI, 1.16 to 7.60), but not treatment modality. Laser evaporation combined with extensive biopsy is at least as efficacious as initial treatment of intraepithelial neoplasia with excision. Smoking is a risk factor for both recurrence and progression to invasive disease. Hence, smoking cessation should be advised and maintaining a long follow-up period due to late relapses is necessary.
    Journal of Gynecologic Oncology 07/2013; 24(3):236-41. DOI:10.3802/jgo.2013.24.3.236 · 2.49 Impact Factor
Show more