Vulvar intraepithelial neoplasia
Background
Vulvar intraepithelial neoplasia (VIN) is a common vulvar lesion with malignant potential if left untreated. While named for uniformity with the more common cervical intraepithelial neoplasia (CIN), differences in clinical behavior do exist. First, the biologic continuum from VIN I to VIN III to invasive cancer has not been proven. Second, the association with the human papilloma virus is significant but it is not universal, as in CIN. Even though MORE than 30% of women with VIN present with pruritis, pain, a palpable mass or dysuria, the diagnosis is often delayed. Routine examination, high suspicion, and low threshold for biopsy are essential to appropriate management of this condition. Factors that put patients at highest risk are cigarette smoking, immunocompromised conditions such as those requiring steroids, poor hygiene, and pregnancy.
Evaluation
Evaluation consists of careful inspection of the entire vulva and perineum. Appearance can vary widely depending on the degree of keratinization, the patient’s race or complexion, and the type of lesion. The most common locations are the labia minora and the introitus between 3 and 9 o’clock. While disease involving the anal canal and intergluteal cleft can occur in up to 30% of cases, VIN of the glans clitoris and urethra is rare.
Whereas colposcopic examination can aid in defining the extent of VIN, acetic acid (vinegar) staining is also useful. Multiple biopsies may be required to define the extent of the disease and to exclude invasion. Squamous dysplasia and carcinoma tend to involve all organs of the lower genital tract sequentially or simultaneously. Consequently, the cervix and vagina must also be evaluated for squamous neoplasia whenever the vulva is involved.
Treatment
The treatment of VIN has undergone major changes in the past two decades. The most important difference is the general recognition that total or even simple vulvectomy is seldom warranted and usually is contraindicated. In addition, treatment planning must take into consideration that spontaneous regression can occur, especially if the dysplasia is low grade. In general, women with mild vulvar dysplasia can be followed with close examination every 6 months, assuming compliance is not an issue. If the patient is very bothered by the lesion (either because of pruritis or for esthetic reasons), treatment can be offered. Patients with moderate or severe vulvar dysplasia should be offered treatment as these lesions have a greater potential for progression than low-grade lesions. An exception is the woman who is either pregnant or in the puerperium. Even severe vulvar dysplasia may regress once the immune-inhibiting effects of pregnancy dissipate.
The two options for treatment for VIN are laser ablation and wide local excision. The former is generally preferred as it gives excellent cosmetic results in an area where preservation of appearance is important. It is essential to rule out invasive disease before laser ablation is performed. As invasive disease in association with VIN is more likely to occur in a postmenopausal patient than a younger woman, the preferred treatment method has been excision for the older woman and laser ablation for the younger woman. However, there is room for individualization. Though rare, invasive cancer of the vulva has been reported even in very young women (less than 25 years old), where it has frequently been misdiagnosed as condyloma. It is essential to thoroughly biopsy, if not excise, suspicious vulvar lesions (markedly papillary, ulcerated or indurated) in young women prior to laser ablation. In postmenopausal women, laser ablation may be used in conjunction with excision to allow primary closure and to avoid excision at problematic sites such as the urethral or clitoral areas. It should also be kept in mind that the sites most likely to harbor invasive disease are the posterior perineal and perianal areas; both should be thoroughly examined prior to laser treatment. The failure rate of both excision and laser in the treatment of VIN ranges from 15% up to 40%.
Vaginal intraepithelial neoplasia
Etiology
Preinvasive lesions of the vaginal squamous epithelium occur in only 1–3% of the patients with cervical neoplasia. The majority of women with this lesion, however, have had CIN. In a series of over 50 cases of vaginal intraepithelial neoplasia (VAIN) reviewed at our institution, 40% had prior and 15% co-existing cervical or vulvar neoplasia. As discussed earlier, human papilloma virus is thought to be a major etiologic factor in VAIN, as well as in CIN and VIN. Other predisposing causes of VAIN are radiation and immunosuppressive therapy. It has been suggested that postmenopausal atrophy of the vagina is also conducive to the development of VAIN; however, it is more likely that exfoliated cells from the atrophic vaginal epithelium often are interpreted incorrectly as intraepithelial neoplasia, exaggerating the true association of these factors.
Detection and evaluation
The Papanicolaou (Pap) smear is the single most important means of bringing the preinvasive vaginal lesion to the attention of the physician. A spatula or brush is used for cytologic sampling of the vaginal mucosa as the speculum is withdrawn and rotated.
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