VinN90.0-N90.2

Vulval Intraepithelial Neoplasias (VIN) are incipient precursor lesions for squamous cell carcinomas of the vulva. S.a. spinocellular carcinoma, vulvar carcinoma. It is the most common prein vasi ve disease of the vulva and is defined by cellular atypia of the squamous epithelium with disturbance of the tissue structure.

• Classification according to histological criteria (ISSVD). A distinction is made:
  • Squamous type (vulvar intraepithelial neoplasia)
  • Non-squamous guy.
• The squamous type (VIN) is divided into 3 grades of severity:
  • VIN I: Mild intraepithelial neoplasia
  • VIN II: Moderate intraepithelial neoplasia
  • VIN III: Severe intraepithelial neoplasia:
    • differentiated (2-10% of cases), no association with HPV infection
    • undifferentiated (90% of cases), evidence of high-risk HV!
• The non-squamous type includes pathogenetically different clinical pictures, e.g.:
  • Extramammary Paget's disease
  • Melanoma in situ of the vulva.

In this classification, terms such as M. Bowen, erythroplasia queyrat and bowenoid papulose are no longer used, they are classified as stage VIN III. S.a. AIN (anal intraepithelial neoplasia).

Etiologically, two groups of patients can be distinguished:

• Predominantly older patients > 60 years, in whom a differentiated type VIN III or a vulvar carcinoma develops.
• Pat. < 50 years with undifferentiated type VIN III (basaloid or condylomatous type) or vulvar carcinoma . Frequent detection of HPV-DNA (HPV-16)! After therapy 35% recurrence rate (Satmary W et al. 2018)

Common association with HPV disease. The incidence of HPV DNA increases as the severity of VIN increases. Depending on the method used, HPV can be detected in 50-90% of cases. The most common type of HPV DNA is type 16.

• Initially, patients complain of no or unspecific symptoms such as itching, pain and soreness. This often leads to self-treatment and protraction of the disease.
• Leukoplakia: Very variable and dependent on the stage of VIN, with sharply defined, flat or bumpy leukoplakia;
• In addition, reddish-brownish or deep red, occasionally also brown-black, moderately indurated plaques with or without scaling, sharply separated from the normal skin or mucous membrane.
• Erosions: Often flat erosions or macerations are found.
• Erythroplasia: Rarely is the pure erythematous type (older nomenclature: Erythroplasia Queyrat) with a weeping, velvety surface. This non-cornifying variant of VIN III usually develops on the non-cornifying squamous epithelium of the introitus vaginae and on the inner sides of the small labia.
• Indurated ulcerations may be an indication of infiltrating growth.
• A particular diagnostic and therapeutic problem are the multifocal lesions occurring at the vulva. They are more prone to recurrence than the unifocal variants.

• basaloid type
• Condylomatous type (warty type)
• Differentiated type.

• Clinic, Biopsy
• HPV detection from biopsy
• Papanicolaou smears: The material obtained by Papanicolaou smears or the grading based on it correlates relatively poorly with histologically confirmed lesions.

Notice! Suspect areas must be biopsied!

• Extensive lesions / high grade VIN III: excision with primary closure, possibly split skin grafts.
• Small lesions: cauterization, erbium YAG laser or CO ₂ laser ablation, cryosurgery, podophyllotoxin. The less radical the therapy chosen, the higher the risk of recurrence.
• Topical therapy with Imiquimod, where complete eradication of the underlying HPV type was observed.

1. Campagne G et al (2003) Successful treatment of a high-grade intraepithelial neoplasia with imiquimod, with vulvar pemphigus as a side effect. Eur J Obstet Gynecol Reprod Biol 109: 224-227
2. Fehr MK et al (2002) Photodynamic therapy of vulvar and vaginal condyloma and intraepithelial neoplasia using topically applied 5-aminolevulinic acid. Lasers Surg Med 30: 273-279
3. Gupta J (1987) Association of human papillomavirus type 16 with neoplastic lesions of the vulva and other genital sites by in situ hybridization. On J catholic 127: 206-209
4. Jayne CJ et al (2002) Treatment of vulvar intraepithelial neoplasia 2/3 with imiquimod. J Reprod Med 47: 395-398
5. Küppers V (1997) Risk factors for recurrent VIN: role of multifocality and grade of disease. J Reprod Med. 42: 140-147
6. Penna C et al (2002) CO2 laser surgery for vulvar intraepithelial neoplasia. Excisional, destructive and combined techniques. J Reprod Med 47: 913-918
7. Rodolakis A et al (2003) Vulvar intraepithelial neoplasia (VIN)--diagnostic and therapeutic challenges. Eur J Gynaecol Oncol 24: 317-322
8. Saravanamuthu J (2003) The role of angiogenesis in vulvar cancer, vulvar intraepithelial neoplasia, and vulvar lichen sclerosus as determined by microvessel density analysis. Gynecol Oncol 89: 251-258
9. Satmary W et al(2018) Vulvar intraepithelial neoplasia: Risk factors for recurrence.
   Gynecol Oncol 148:126-131.
10. Speck LM (2006) Vaccines for the prevention of human papillomavirus infections. Skin Therapy Lett 11: 1-3
11. Travis LB (2002) Successful treatment of vulvar intraepithelial neoplasia with topical imiquimod 5% cream in a lung transplanted patient. Acta Derm Venereol 82: 475-476
12. Villa LL et al (2006) High sustained efficacy of a prophylactic quadrivalent human papillomavirus types 6/11/16/18 L1 virus-like particle vaccine through 5 years of follow-up. Br J Cancer 95: 1459-1466
13. Wilkinson EJ (1992) Normal histology and nomenclature of the vulva and malignant neoplasms, including VIN. Dermatol Clin 10: 238-244
14. Van Seters M et al (2008) Treatment of vulvar intraepithelial neoplasia with topical imiquimod. N Engl J Med 358: 1465-1473