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ORIGINAL RESEARCH |
From the Vulvar Clinic, Department of Gynecologic Oncology, National Women’s Hospital, Auckland, New Zealand.
Address reprint requests to: Ronald W. Jones, FRCS, FRCOG PO Box 26090 EPSOM Auckland 3 New Zealand
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Abstract |
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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.
The heterogeneous nature of vulvar intraepithelial neoplasia (VIN) 2-3 is now widely accepted.1 Whereas the potential for VIN to progress to invasive vulvar cancer is the prime concern of physicians, spontaneous regression of the lesion is recognized. Evidence for spontaneous regression in gynecologic literature is based largely on case reports2,3 and a small number of poorly documented cases in older published series.4,5 Scant information exists in recent gynecologic literature on spontaneous regression of VIN 2-3, the background of the subjects, or the clinical features associated with it.
Our previous experience suggests that untreated VIN 3 is a lesion with a significant invasive potential.6 There is evidence that the increasing incidence of VIN in younger women is now being reflected in an increasing incidence of VIN-related vulvar cancers in women younger than 50 years of age.7 It has therefore been our policy to recommend treatment either by surgical or laser excision or laser vaporization for all women with histologically proven VIN 2-3. However, an increasingly conservative approach to management is advocated by some, with observation alone in asymptomatic women.8 We report the clinical details of 14 women with VIN 2-3 who experienced spontaneous regression of the lesion without treatment.
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Materials and Methods |
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Results |
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Ten lesions were characterized histologically as VIN 3 and four lesions as VIN 2. All lesions were examples of warty/basaloid VIN.
A diagnosis of complete regression was established by vulvoscopy. The median (range) interval between diagnosis and complete disappearance of the lesions was 9.5 (3–30) months. This interval was more than 2 years in only one patient who failed to attend the clinic for 24 months, and it is possible that spontaneous resolution occurred much earlier than recorded. The median (range) follow-up interval since complete regression was 3 years (6 months to 5 years, 3 months). Twelve of the 14 cases were followed for at least 2 years. There have been no recurrences of VIN 2-3 after spontaneous regression of the lesion. There were no examples of invasive vulvar carcinoma after either earlier treatment or nontreatment of multifocal pigmented VIN 2-3 during the study period.
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Discussion |
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The striking features of the examples of spontaneous regression of VIN 2-3 reported in the present study are the uniformity of the background of the subjects and the clinical appearance of the lesions. Regression occurred exclusively in women younger than 30 years of age. The median age of 19.5 years compares with a median age of 35 years for all women with VIN 2-3 attending our clinic.6 Previous reports have noted that regression often occurs in black women.1,2 In the present study, there were no black women; with one exception, all were non-white, mainly Polynesian.
Symptoms occur in the majority of women with VIN. Half of the women in the present study had no symptoms, and it is therefore possible that such lesions frequently pass unnoticed. In some cases, the diagnosis of VIN was established only after biopsy of an atypical condyloma. The excess number of women presenting during pregnancy and the puerperium has been noted by others.12 This may be related to the altered immunologic tolerance of pregnant women. The role of the immune system may be a central event in the processes associated with both progression to invasion and spontaneous regression of VIN.
All study subjects were referred from a sexual health clinic and, with one exception, had a history of genital condyloma. Others13 have noted a coexistence of condyloma with human papillomavirus 16 VIN lesions found in the pigmented vulvar papules of young women.
Time to progression or regression of VIN lesions must be considered when constructing management strategies. A notable feature of the present study is the median regression time of 9.5 months and, with one exception, complete regression within 2 years. The earlier view that there was unlikely to be a relationship between VIN and vulvar cancer because of the 30-year interval between the mean ages of women with these conditions has now been disproved. Indefinite persistence of VIN 2-3 has not been reported. Recent studies have noted that progression to invasion usually occurs within 8 years.6,14 Our policy of promptly treating all women with VIN may have excluded a number of women who would have experienced spontaneous regression. The presence of occult invasion in surgical specimens considered to have VIN 3 alone15 and the relatively short time to invasion in some cases support our usual policy of treating high-grade VIN both in symptomatic and asymptomatic women.
The frequency of spontaneous regression of VIN 2-3 cannot be estimated because of our policy of treating VIN and the nature of the referral patterns to our tertiary-level vulvovaginal clinic. The present study highlights one facet of the heterogeneous nature of VIN. The findings should be of assistance to those who selectively manage certain cases on an expectant basis. Clinicians may consider an observational policy for a period of 12 months in asymptomatic women who are younger than 30 years of age and who present with multifocal pigmented VIN 2-3 lesions. Further research in this area should focus on a comparison of the clinical, molecular, and immunologic differences between cases of high-grade VIN which regress spontaneously and cases that progress to invasive vulvar cancer.
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Footnotes |
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Received December 13, 1999. Received in revised form March 20, 2000. Accepted March 30, 2000.
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References |
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2. Friedrich EG. Reversible vulvar atypia. Obstet Gynecol 1972;39: 173–81.
3. Skinner MS, Sternberg WH, Ichinose H, Collins J. Spontaneous regression of Bowenoid atypia of the vulva. Obstet Gynecol 1973;42:40–6.[Medline]
4. Friedrich EG, Wilkinson EJ, Fu YS. Carcinoma in situ of the vulva: A continuing challenge. Am J Obstet Gynecol 1980;136:830–43.[Medline]
5. Bernstein SG, Kovacs BR, Townsend DE, Morrow CP. Vulvar carcinoma in situ. Obstet Gynecol 1983;61:304–7.
6. Jones RW, Rowan DM. Vulvar intraepithelial neoplasia III: A clinical study of the outcome in 113 cases with relation to the later development of invasive vulvar carcinoma. Obstet Gynecol 1994; 84:741–5.
7. Jones RW, Baranyai J, Stables S. Trends in squamous cell carcinoma of the vulva: The influence of vulvar intraepithelial neoplasia. Obstet Gynecol 1997;90:448–52.[Abstract]
8. van Beurden M, van Der Vange N, Ten Kate FJ, de Craen AJ, Schilthuis MS, Lammes FB. Restricted surgical management of vulvar intraepithelial neoplasia 3: Focus on exclusion of invasion and on relief of symptoms. Int J Gynecol Cancer 1998;8:73–7.[Medline]
9. Wade TR, Kopf AW, Ackerman AB. Bowenoid papulosis of the genitalia. Arch Dermatol 1979;115:306–8.[Abstract]
10. Bergeron C, Naghashfar Z, Canaan C, Shah K, Fu Y, Ferenczy A. Human papillomavirus type 16 in intraepithelial neoplasia (Bowenoid papulosis) and coexistent invasive carcinoma of the vulva. Int J Gynecol Pathol 1987;6:1–11.[Medline]
11. Planner RS, Andersen HE, Hobbs JB, Williams RA, Fogarty LF, Hudson PJ. Multifocal invasive carcinoma of the vulva in a 25-year-old woman with Bowenoid papulosis. Aust N Z J Obstet Gynaecol 1987;27:291–5.[Medline]
12. Ulbright TM, Stehman FB, Roth LM, Ehrlich CE, Ransburg RC. Bowenoid dysplasia of the vulva. Cancer 1982;50:2910–9.[Medline]
13. Inagaki H, Nonaka M, Eimoto T. Bowenoid papulosis showing polyclonal nature. Diagn Mol Pathol 1998;7:122–6.[Medline]
14. Herod JJ, Shafi MI, Rollason TP, Jordan JA, Luesley DM. Vulvar intraepithelial neoplasia: Long term follow up of treated and untreated women. Br J Obstet Gynaecol 1996;103:446–52.[Medline]
15. Chafe W, Richards A, Morgan L, Wilkinson E. Unrecognized invasive carcinoma in vulvar intraepithelial neoplasia. Gynecol Oncol 1988;31:154–62.[Medline]
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