How should you evaluate a patient who has a cytologic diagnosis of atypical glandular cells (AGC)?
Charles J. Dunton, MD (Examining the Evidence; August 2011)
What is optimal surveillance after treatment for high-grade cervical intraepithelial neoplasia (CIN)?
Alan G. Waxman, MD, MPH (Examining the Evidence; June 2011)
2 HPV vaccines, 7 questions that you need answered
Neal M. Lonky, MD, MPH, and an expert panel (August 2010)
Dr. Massad reports no financial relationships relevant to this article.
The societal shifts of the 1960s generated many changes—among them, permanently altered sexual mores. That may be a primary reason why the incidence of vulvar intraepithelial neoplasia (VIN) increased more than 400% between 1973 and 2000, says L. Stewart Massad, Jr, MD, chairman of the Practice Committee of the American Society for Colposcopy and Cervical Pathology (ASCCP) and member of the ACOG Committee on Gynecologic Practice—and one of the authors of a new joint Committee Opinion on the management of VIN.1 This precancer is often associated with carcinogenic types of human papillomavirus (HPV), the most common sexually transmitted disease in the nation.
The 400% statistic caught the attention of OBG Management. The editors invited Dr. Massad to discuss the subject of VIN at length, elaborating on key issues such as its prevention, identification, treatment, and surveillance.
How to identify a VIN lesion
OBG Management: What is VIN? What does it look like?
Dr. Massad: VIN is a premalignant condition of the vulva that may present as unifocal or multifocal lesions. These lesions may be flesh-colored, hypopigmented, or hyperpigmented (FIGURE). They also may be erythematous, flat, or raised. They can be found on any part of the vulva. The dysplastic cells may extend into hair shafts or sweat glands; they don’t penetrate the basement membrane, however, so, by definition, they aren’t invasive.
A. This warty lesion is hyperpigmented around the periphery, hypopigmented in the center. B. Another warty lesion. Both images reflect the application of acetic acid.OBG Management: Why has the incidence increased so considerably?
Dr. Massad: The data we have on incidence comes from the Surveillance, Epidemiology and End Results (SEER) program of the National Cancer Institute, as reported by Judson and colleagues.2 Although better reporting of findings of VIN may play a role, the rising incidence seems to be attributable to changes in sexual behavior over the past half century. The incidence of vulvar cancer rose during the same period—about 20%.3 The much slower growth in the incidence of vulvar cancer suggests that treatment of VIN has blunted the risk of cancer.
OBG Management: Is VIN associated with any particular type of HPV?
Dr. Massad: Yes, more than 80% of VIN lesions are associated with HPV 16.
OBG Management: One study from 2005 noted that the mean age of women with VIN decreased from 50 years before 1980 to 39 years in subsequent years.4 Why are more younger women developing VIN?
Dr. Massad: The study that showed that age shift was from New Zealand. The authors speculated that the change was due to earlier sexual activity among women who smoke: HPV, especially HPV 16, and smoking are important risk factors for VIN. The question hasn’t been definitively answered.
OBG Management: What are the risk factors for VIN?
Dr. Massad: Smoking is a big one. More than 50% of women who have VIN are smokers. Thirty percent have concurrent or prior cervical intraepithelial neoplasia (CIN) or vaginal intraepithelial neoplasia (VAIN). The risk of invasion rises with age at the time of the initial diagnosis and with longer follow-up. I can talk about surveillance a little later.
Are some lesions more worrisome than others?
OBG Management: Are VIN lesions categorized similarly to CIN lesions—that is, using three different grades of severity?
Dr. Massad: Until recently, that was the case, but it is no longer so. Broadly, there are now two classes of VIN, according to the International Society for the Study of Vulvovaginal Disease (ISSVD): usual-type VIN and differentiated VIN.
ACOG and ASCCP have embraced this classification system, although not all pathologists have done so, and clinicians may still see reports using the old three-tier system.
Usual-type VIN is associated with infection with high-risk types of HPV—most notably, HPV 16, as I mentioned. Histologically, usual-type VIN can mimic common genital warts, and the warty subtype shows keratosis at the surface, a spiky or undulating surface, and vertical maturation of cells in the lesion but with pleomorphic cells filling half or more of the epithelial thickness. The basaloid subtype of usual VIN shows little maturation.