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HPV is often found to be a factor in the occurrence of VIN. Other reasons are smoking and poor immunity. Abnormalities in the vulvar skin tissue (presence of lesions) cause intense pain and itching sensation and also create psychosexual problems affecting normal sexual activity. The development of this premalignant condition to vulval cancer is dependent on its severity.
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Vulval intraepithelial neoplasia (VIN) is a predecessor of squamous cell cancer of the vulva, which results in the formation of lesions in the vulvar (external genital area of women) skin regions.
It can be categorized into two types: usual-type and differentiated-type. The usual-type VIN is caused by prolonged viral infection with human papillomavirus (HPV), while differentiated VIN occurs in the absence of HPV and is normally associated with inflammatory lichen sclerosus and lichen chronicus.
The usual-type VIN, also called vulval high-grade squamous intraepithelial lesion, is characterized by a thickened epidermis, disordered keratinocytes and nuclear atypia, and irregular mitotic figures in skin tissue together with a high nucleus-cytoplasm ratio seen all over the epidermis.
Hence, the usual-type VIN is pronounced and can be easily misdiagnosed for squamous cell carcinoma. Also, in cases of VIN, corps ronds, pyknotic nuclei, and dyskeratotic cells with thick eosinophilic cytoplasm can be seen.
In the warty subtype of usual VIN, the surface of the epidermis has a papillary arrangement and the koilocytes, multinucleated cells, and dyskeratotic cells are mostly present here. Comparatively, the basaloid subtype of usual-type VIN has a somewhat flat surface and the epidermis is substituted with small, poorly differentiated cells having a high nucleus–cytoplasm ratio.
Finally, the mixed subtype of usual-type VIN combines both the properties of warty and basaloid subtype. The presence of lesions in usual-type is multifocal and multicentric.
Differential VIN is less characterized and is identified close to an invasive SCC. The differentiated type is characterized by a dense epidermis, enlarged keratinocytes with a disordered maturation pattern, surface parakeratosis, and elongated rete ridges.
Above the basal epidermis layer, there is no or little observed atypia. The presence of lesions is unifocal and unicentric, with white or gray discoloration and a roughened surface, white elevated nodules and plaques, or red lesions that are ulcerous or erythematous.
The labia majora, labia minora, and posterior margin of the vulva (fourchette) are usually affected with lesions; fewer reported lesions are found in the mons pubis (lies above vulva), clitoris, and perineum (the area below vulva).
A large irregularity is seen in the visual aspect of lesions in usual-type VIN. White or red plaques are common, but they may seem polypoid, papular, pigmented or verruciform. Usual-type VIN has almost well-defined lesions, whereas the differentiated-type VIN lesions are less noticeable. The differentiated type has unclear, often ill-defined, elevated areas with grayish white lesions together with either lichen sclerosus or lichen planus.
About 66% of women are affected by VIN encounter pruritus. Ulceration, pain, and leukoplakia are less common symptoms present either separately or together with pruritus. Roughly 20% of the women stay asymptomatic to the disease, which is diagnosed by chance during internal medical examination.
Common symptoms are the presence of raised patches of red, gray, white, or dark color, warty skin, itching in the vulvar skin tissue, burning sensation while urinating, and pain in the vulvar skin.
The affected part in the vulvar skin tissue is seen as a recalcitrant condylomata acuminata or a vulval lump. The presence of a well-defined mass and symptoms like ulceration and bleeding strongly state VIN to be an invasive disease.
The prevalence of VIN seems to have increased in the past several years, perhaps due to the increase in occurrence of high-grade squamous intraepithelial lesions (HSIL) caused by HPV. The certain types of HPV that affects the genital region in women and causes VIN are Types 16, 18, and 31. HPV spreads through sexual contact with an infected person.
The immune system in women helps to eliminate HPV infection naturally. All women with HPV infection do not develop VIN. Hence, HPV infection is not the only factor that causes VIN; the body’s poor immune system increases the risk of contracting VIN.
In most cases, the HSIL (VIN usual-type) has multifocal presence and dominates about 90% of the total VIN affected cases. Cigarette smoking mainly causes HSIL. Even after treatment, continued smoking together with the presence of HPV infection will increase the risk of recurrence of VIN. Smoking tends to react with HPV and the immune system.
Women infected by the Human Immunodeficiency virus (HIV) are at high risk to develop VIN. Usual-type VIN is more frequent among premenopausal younger women, while differentiated-type VIN is seen more often in women in the postmenopausal stage. Differentiated VIN will cause vulvar dermatoses like lichen sclerosus and lichen chronicus.