Vulvar Intraepithelial Neoplasia
Special Feature
Vulvar Intraepithelial Neoplasia
By Kenneth Noller, MD
During the past 20 years, i have had the opportunity to attend and teach well over 100 colposcopy/lower genital tract neoplasia courses. This has afforded me the opportunity to listen to the greatest minds in the field describe their research and approach to the evaluation and treatment of lower genital tract neoplasia. One of the most interesting areas covered in these courses is intraepithelial neoplasia of the vulva (VIN).
Unlike cervical intraepithelial neoplasia (CIN), much less is known about the natural history of VIN. The lesion was not recognized as early as cervical dysplasia and is rarer, so no large series of patients with VIN have been followed prospectively without therapy. Nonetheless, there is now a general consensus concerning the management of most patients with VIN. In many cases, the current management recommendations are not widely known.
VIN III is a Cancer Precursor
There is now no doubt that VIN III (carcinoma in situ) is a precursor to invasive cancer of the vulva. Enough cases of VIN III have been followed without treatment, and invasive cancer has developed to state definitively that VIN III always should be treated.
For some years, some investigators did not believe VIN III was a cancer precursor, especially in younger women. In retrospect, that position makes little sense. Virtually, no one would now leave VIN III untreated.
VIN I is not a Cancer Precursor
There are virtually no data published in the literature that support the premise that VIN I (mild dysplasia of the vulva) is a precursor to invasive cancer. This fact, when presented at a colposcopy course, often surprises some members of the audience. Nonetheless, it is a fact. I have not heard a speaker at a national course for at least a decade support treatment for VIN I. VIN I should not be treated.
There is a difference between the diagnoses of VIN I and CIN I. While most of us do not favor treatment of CIN I unless it persists for two or more years or progresses to CIN II (something that happens in only about 30% of cases), there is general agreement that VIN I should not be treated regardless of persistence. The reason for this lies in the inaccuracy of the pathologic diagnosis of intraepithelial neoplasia of the vulva. On the cervix, basal cell hyperplasia and early nuclear atypia do not routinely occur spontaneously unless HPV infection has occurred. On the vulva, similar changes are called VIN I but are probably most often due to irritation, repair, or some unknown mechanism. The vulva is much more likely to be traumatized through normal activity and sexual intercourse than is the cervix. In addition, although HPV infection of the vulva is common, the virus does not seem to be able to transform the vulvar epithelium into a self-perpetuating neoplastic lesion as easily as it can change the cervical epithelium.
HPV of the Vulva?
Unlike the cervix, it is difficult to diagnose the presence of HPV infection on the vulva if clinically evident warts are not present. The presence of acetowhite epithelium is not a sensitive or specific predictor of the presence of HPV. Also, it has been shown that biopsies of the vulvar epithelium, which are interpreted by competent gynecologic pathologists as showing HPV infection, are often found not to contain HPV when the tissue samples are subjected to HPV-DNA testing. When a competent gynecologic pathologist sees koilocytic changes with nuclear atypia on a cervical biopsy and diagnoses HPV infection, there is almost always HPV-DNA present. That is not true with vulvar biopsies. Thus, HPV infection of the vulva is grossly over-diagnosed. Although the role of HPV-DNA testing in the presence of cervical disease is still open to debate concerning its usefulness, it may have a role in vulvar disease, primarily to rule out the presence of an HPV infection despite a biopsy showing HPV-type changes.
What to do about VIN II?
It is clear that VIN III should be treated and VIN I should be ignored. What about VIN II? The short answer is that no one knows for sure. No prospective studies have been performed. However, we do know that if VIN II is present, and even if it is a precursor to invasive vulvar cancer, it will likely be several decades before invasion occurs. On the vulva, transition from intraepithelial disease to invasive disease occurs at a glacial pace. There is certainly no reason why VIN II cannot be followed in a patient who is reliable. On the other hand, if a patient has a history of poor compliance with follow-up instructions or has immune suppression for any reason (transplantation, HIV, inherited), it might be appropriate to treat VIN II when it is discovered.
I would strongly encourage, though, that VIN II never be treated in a young woman (teenage-25 years). VIN II tends to regress in this age group and treatment often leads to vulvar deformity and sometimes dyspareunia. It is easy to cause more harm than good.
References
1. Küpper V, et al. J Reprod Med 1997;42:140-144.
2. Jones RS, Rowan DM. Obstet Gynecol 1994;84: 741-745.
3. Haefner HK, et al. Hum Pathol 1995;26:147-154.
4. Wilkinson EJ, Stone IK. Atlas of Vulvar Disease, Baltimore, MD: Williams and Wilkins; 1995:101-110.
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