Implications of the vulvar sensitive skin syndrome after menopause

Abstract

Many women suffer from vulvar burning and skin sensitivity. The fragile nature of the skin in that area is reflected by high transepidermal water loss and a high friction coefficient, in comparison to other body sites. Abrasion from clothing and harsh toilet paper, chemical injury from urine and various medicated creams and lubricants, hard water, and soap are a few of the persistent irritants that cause burning and vulvar pain. Irritant avoidance may be a difficult challenge for women with sensitive vulvar skin. Sensitive vulvar skin is at high risk for development of spongiotic dermatitis. Elevated estrogen in pregnancy enhances the risk for spongiotic reaction. Vulvar spongiotic dermatitis further compromises vulvar skin barrier function. Spongiotic dermatitis is also a significant contributing factor for secondary yeast infection, which further compromises skin barrier function. Thus, many women with sensitive vulvar skin find themselves in a repetitive cycle of vulvar burning, yeast infection, and irritating cream application. The significant postmenopausal decline in vulvar Langerhans cell population and the decreased cytokine response associated with aging may give some relief for women with spongiotic vulvar changes. After menopause, this immune reactivity is blunted unless topical estrogen is applied. The simultaneous loss of intercellular lipids and the rise in vulvar skin pH compromise the vulvar skin barrier. This may result in a greater tendency for skin sensitivity in some cases. Thus, sensitivity of postmenopausal vulvar skin is impacted by a wide range of environmental and intrinsic factors. Vulvar sensitive skin may become more symptomatic after menopause if the overriding factor is loss of skin barrier function with the decline in estrogen and rise in vulvovaginal pH. In contrast, the ability of vulvar skin to react symptomatically to environmental insults may decline with lack of estrogen support for skin metabolism and immune responsiveness.