Six common dermatologic disorders of the vulva and vagina can present considerable challenges:
- Allergic contact dermatitis: 100% of the population may be at risk for this disorder, and the vulvar skin is especially vulnerable.
- Irritant contact dermatitis: Skin-barrier compromise due to chronic, low-level vulvar irritant dermatitis likely contributes to the acquisition of sexually transmitted disease.
- Lichen sclerosus: Women with this condition are at increased risk for persistent vulvar yeast infection and squamous vulvar cancer.
- Lichen planus: Antibiotic therapy is ineffective against this disorder; symptoms reappear as soon as antibiotics are stopped.
- Yeast infection: Yeast organisms release proteins that activate a local allergic response and perpetuate an environment that supports infection.
- Human papillomavirus (HPV): The small HPV particle easily gains entry to minimally traumatized vulvar skin.
These common conditions sometimes compromise the skin barrier and prevent an adequate immune response to invading microbes. Some degree of skin immune dysfunction is generally associated with each genital dermatologic disorder. Identifying and treating the underlying dermatologic disorder, then, often corrects the associated immune dysfunction and may restore the skin barrier and prevent further microbial invasion.
Allergic contact dermatitis
Allergic dermatitis, or atopic dermatitis (formerly called eczema), is a highly prevalent skin disorder (FIGURE 1). Depending on the environment and genetic factors, as many as 40% of adults have a history of atopic dermatitis, and essentially 100% of the population may be at risk. Women have a higher rate of atopic dermatitis than men do.
Recognized vulvar allergens or triggers include dry climate, elastic, latex, fragrances in soaps or body lotions, and residues of detergent and fabric softener in clothing. In most biopsy-proven cases of vulvar eczema, the patient is unable to identify specific allergens. Such a patient often has a history of asthma, allergic rhinitis, sinusitis, or atopic dermatitis on other parts of the body.
Patch testing is no help in identifying specific allergens in the pelvic area. Testing the tougher skin of the back may not disclose all vulvar sensitivities.
But biopsy is useful. Women with vulvar allergic contact dermatitis often complain of persistent itching. A history of allergy elsewhere on the body is diagnostically helpful, but a biopsy submitted to a dermatopathologist confirms the diagnosis.
Not all women with vulvar allergic dermatitis have atopy at other body sites. Hyperkeratosis and spongiosis in the pathology specimen are characteristic. A small (3-or 4-mm) biopsy at the most symptomatic site is appropriate in any woman with chronic vulvar pruritis.
Local immune dysfunction is involved. Allergic vulvar dermatitis is characterized by a locally dysfunctional cell-mediated immune response. Langerhans cells are involved in this allergic reaction, directed away from their normal protective role.1 (Read about the role of Langerhans cells in “Three barriers to microbial infection: The skin’s built-in defense system,”) Viruses, bacteria, and yeast that gain entry into the skin have greater freedom to proliferate and persist, and skin-cancer surveillance by Langerhans cells is also compromised, with an increased risk for squamous carcinoma. This may account for a large portion of the 50% of vulvar carcinomas that cannot be attributed to HPV infection. Langerhans-cell dysfunction also contributes to the progression of HPV-associated carcinoma.
Allergic dermatitis inhibits the production of human cathelicidin and the ß-defensins, natural skin microbicides. As a result, vulvar skin affected by allergic dermatitis has a higher yeast and bacterial colonization rate.
FIGURE 1 Allergic contact dermatitis
This case of severe allergic contact dermatitis has been aggravated by chronic scratching, especially of the left labia. Cases typically are much more subtle.
Look for telltale flaking skin
Allergic dermatitis involves flaking of the skin, probably due to allergic stimulation of epithelial cell proliferation. Flakes of skin are exfoliated before the desmosomes that hold individual skin cells together deteriorate. The flaking compromises the stratum corneum barrier, and likely facilitates skin invasion of yeast and bacteria that have colonized the surface.
Because the background rate of dermatitis in the general population is relatively high, skin flakes often appear in the saline wet prep and are referred to as “reactive, reparative” changes in the Papanicolaou smear.2
Other diagnostic clues. Chronic vulvar pruritus with a history of asthma, hay fever, sinusitis, atopic dermatitis, or dry skin is vulvar dermatitis until it is proved otherwise. Recurrent yeast infection is often reported as well.