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New Treatments for Diseases of the Vulva

Squamous cell carcinoma of the vulva. Squamous cell carcinoma is the most common malignant tumor of the vulva. All other carcinomas are a distant second to squamous cell carcinoma. Until proven otherwise, if there is a malignancy in the vulva, it is a squamous cell carcinoma. If you get any other diagnoses on a vulvar biopsy of malignancy, unless you see a pigmented lesion that is a melanoma, call the pathologist. The incidence of vulvar carcinoma is low; endometrial carcinomas are much more common. In the rest of the world, cervical carcinoma is much more common. Ovarian carcinoma is much more common in the United States than vulvar carcinoma. You do not have to die from a vulvar cancer, if it is picked up early. The reason is that you can see the lesion. Keep in mind that there are many other types of vulvar carcinoma.

In invasive squamous cell carcinoma, you have the stroma, keratin pearl formation, destruction of the stroma (invasive cancer) and most of the time in the vulva they are either well-differentiated or moderately-differentiated, but usually well-differentiated. Stage and grade determine how a tumor is going to behave.

Condyloma is associated with HPV 6 and 11 most of the time. In dyskeratosis, you see cells that look very typical with what appears to be some keratin in them. Acanthosis usually means thick - the epidermis is thick. In hyperkeratosis you get the little keratin top with no nuclei. In parakeratosis, you have the keratin on top with nuclei. Papillomatosis has a lot of vessels - it is thick. Koilocytosis has some viral changes characterized by a halo and irregular nuclei. They usually have these finger-like projections. Lichen sclerosis - atrophicus has been dropped - is just the opposite; it is thin , with no rete's pegs or rete's ridges. There is subepithelial edema, or loosening of the stroma. You will see lymphocytes. You will not see melanocytes. Squamous cell hyperplasia is the term that I would like you to use. In squamous cell hyperplasia, the epidermis is thick. In hyperkeratosis, there is a thick layer of keratin with nuclei. By definition, there is no nuclear atypia.

You still have to remember the old terminology, because many people still use it. In hyperparakeratosis, you can see mitotic figures in the basal layer, this normal, because the cells have to proliferate, but nothing beyond that; you will not see any mitotic figures beyond the basal layer. When there is edema in between the cells, the cells separate and that is how you get intercellular bridges. In cancer, you have edema. The intercellular bridges are thick, big, there is hyperkeratosis, inflammation and there is no atypia. The point I want to make is the idea that you have squamous hyperplasia and then VIN and cancer happens very rarely.

Chances are that if you see a vulvar squamous cell carcinoma with adjacent vulvar intraepithelial neoplasia, it is probably a better prognosis cancer, if you have to have an invasive cancer. This one is somewhat indolent in the sense that chances are the lymph nodes are going to be free and if you do the right procedure, the lady will be around a bit longer than somebody who has a garden-variety invasive squamous cell carcinoma. Stage, grade and depth of invasion of any skin lesion is important . So VIN is no different than CIN in the sense that CIN is cervical intraepithelial neoplasia and VIN is vulvar intraepithelial neoplasia. In the future, this CIN terminology will disappear. It is going to be low-grade squamous intraepithelial lesion and high-grade squamous intraepithelial lesion. You could say that we have this already in the Pap. smear. smear. It will disappear officially in the biopsies as well. It will start with low-grade squamous intraepithelial lesion in biopsy (CIN-I) and the high grades are going to be called high-grade squamous intraepithelial lesion (CIN-II or CIN-III).

Another thing that is going to happen - right now, we say VIN-I, VIN-II, VIN-III; in the future, it is just going to be vulvar intraepithelial neoplasia. The reason is that all VINs are treated the same way. A low of people at other institutions watch the low grades and do nothing. The high-grade cervicals you treat. All VINs are treated the same.

In vulvar intraepithelial neoplasia, the first thing that you see that you did not see in any of the other lesions, except for squamous cell carcinoma, is pleomorphism. Secondly, there is hyperchromasia - the cells are big and blue. You see mitotic figures. There is lack of maturation, meaning that the cells on the surface look the same as the cells in the base - they are not progressing accordingly. If you look at the cells individually, you would see high nuclear to cytoplasmic ratio. The nucleus gets big and the cytoplasm stays the same. On low power, you see increased cellularity and you can start to wonder what is going on. The differential diagnosis is usually condyloma versus VIN. Condylomas are verrucous and papillary and there are usually no mitotic figures. There is no nuclear pleomorphism in the condylomas, except possibly in HPV.