|Vulva — Squamous Hyperplasia|
Squamous cell hyperplasia (formerly called hyperplastic dystrophy or leukoplakia) represents about 40 to 45% of patients with non-neoplastic epithelial disorders. Approximately two thirds of the patients are premenopausal. It is related to chronic irritation. Squamous cell hyperplasia is not a distinct entity, it is only a description of a morphologic alteration of vulvar skin. Since the causes of vulvar epithelial hyperplasia are many, each of them should be properly identified, diagnosed and treated accordingly. Such conditions as lichen sclerosus, psoriasis, lichen planus, lichen simplex chronicus, eczema, seborrheic dermatosis, HPV infection, Candida infection may show squamous cell hyperplasia, but need to be properly identified.
The skin of the vulvar area is particular permeable to water in respect to the skin of other body sites. In this way the vulvar region is moist and prone to adsorb many compounds which occasionally come in the area. Almost any irritative condition may lead to hyperplastic changes. Among the factors implicated in the pathogenesis of hyperplasia, we can recognize intrinsic (physiologic sweat, psychogenic sweat, psychogenic pruritus, pruritus as the result of systemic disease) and extrinsic factors (physical, mechanical and chemical factors).
Squamous cell hyperplasia is characterized by a pink-red vulva with overlying gray-white keratin. Areas most frequently involved on the vulva are the prepuce, labia majora, interlabial sulci, outer aspect of the labia minora, and the posterior commissure. Lesions may be present to the adjacent thighs. There is a range in size. Pruritis is generally present. Itching, scrubbing and scratching are consequence of the initial event and contribute to sustain and promote the circle leading to squamous cell hyperplasia.
Microscopic findings consist of elongation, widening of the rete ridges and irregular thickening of the Malpighian layer of rete ridges (acanthosis), hyperkeratosis, and chronic inflammation in dermis. Parakeratosis may also be present. Inflammatory reactions within the dermis consist of lymphocytes and a small number of plasma cells. These are all nonspecific dermotopathologic features that may be found in many pathological vulvar conditions as. The recent change in the nomenclature points out to describe squamous cell hyperplasia when other causes of hyperplastic epithelial changes are excluded on the basis of specific anatomical-clinical features.
The relief of itching seems therefore the first aim of any therapy. If symptoms of anxiety and irritability re present, oral tranquillizers may be used, especially at bedtime. Topical corticosteroids are the mainstay of therapy for squamous cell hyperplasia. The fluorinated compounds in cream or ointment vehicles, applied twice daily will generally cure the lesion. If the vulva is extremely thickened and a large area is involved with squamous cell hyperplasia, a Class 1 topical steroid may be required. Generally though, squamous cell hyperplasia can be treated with a short term Class IV steroid. When using potent steroids in the vulvar area, as usually, care should be taken to avoid rebound effects; the patient should be checked at close intervals and therapy switched to a less potent steroid as soon as the symptomatology starts to improve. If an antihistamine is added, the antipruritic effect will be improved. Rarely it is necessary to inject triamcinolone acetonide. Once the relief of itching has been achieved, the identification and removal of any irritant cause should be undertaken.
Squamous cell hyperplasia is sometimes observed next to invasive squamous cell cancer although the risk of development of invasive cancer for women treated for squamous cell hyperplasia without intraepithelial neoplasia is minimal. It has been found that women with squamous cell hyperplasia occurring in a background of lichen sclerosus constitute a distinct group at higher risk of developing invasive cancer and require histologic assessment.