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Zedde, P. Contact Dermatitis of the Vulva. Encyclopedia. Available online: (accessed on 02 March 2024).
Zedde P. Contact Dermatitis of the Vulva. Encyclopedia. Available at: Accessed March 02, 2024.
Zedde, Pierantonia. "Contact Dermatitis of the Vulva" Encyclopedia, (accessed March 02, 2024).
Zedde, P. (2021, November 15). Contact Dermatitis of the Vulva. In Encyclopedia.
Zedde, Pierantonia. "Contact Dermatitis of the Vulva." Encyclopedia. Web. 15 November, 2021.
Contact Dermatitis of the Vulva

The vulvar area is a common site of contact dermatitis due to the thin skin, easily traversable by irritant and allergic substances. The nonkeratinized vulvar vestibule is likely to be more permeable than the keratinized portions of the vulva and thus more susceptible to exogenous topical agents. The vulva is an area of occlusion due to both its intrinsic anatomical structure and the frequent use of occlusive napkins or underwear, which increase penetration or absorption of both irritants and allergens. Furthermore, women at different ages, due to urine and feces as children and to vaginal mucosal atrophy and the increase in the vulvar pH in menopause, may have an altered barrier function and, in incontinent elderly subjects, the use of diapers may contribute to increased susceptibility to irritants and allergens.

contact dermatitis vulvar dermatitis allergic dermatitis

1. Irritant Contact Dermatitis

Irritant contact dermatitis (ICD) is the result of a direct damage to the skin by various chemical or physical stimuli. The initiating event is the disruption of the epidermal barrier (i.e., the stratum corneum), with consequent increased skin permeability. This results in an inflammatory cutaneous reaction, caused by proinflammatory mediators released from keratinocytes and by the activation of innate immunity [1][2]. Risk factors for vulvar ICD are multifactorial and include the type of irritant, the length of exposure, the presence of previous dermatoses, and the host’s susceptibility. Women with an atopic diathesis (particularly atopic dermatitis) are more susceptible to ICD as a result of the impaired barrier function of their skin. Furthermore, vulvar skin shows an increased susceptibility to some irritants (maleic acid and benzalkonium chloride) [3]. ICD is more common than allergic contact dermatitis, but the exact prevalence is unknown. The most common vulvar irritants are reported in Table 1.
Table 1. List of the most common irritants responsible for vulvar ICD.
Vulvar Irritants  
Strong Irritants Weak Irritants
Imiquimod Friction/rubbing
Trichloroacetic acid Urine/feces/vaginal secretions/sweat/semen/saliva
Podophyllin Sanitary napkins
5-fluorouracil Soaps/detergents
  Antiseptic or scented wipes
Sodium hypochlorite Deodorants
Irritant contact dermatitis from strong irritants (caustics, topical medicaments) can have a rapid onset within minutes or hours of being exposed and presents with erythema, patches, papules, vesicles, bullae, and scaling. In chronic diseases (mostly due to weak cumulative allergens such as detergents or friction), lichenification and fissuring are more typical features. The main symptoms of ICD are burning, stinging, and, less frequently, itching or pain. In most cases the dermatitis is localized to the site of contact. In particular, when due to napkins ICD is located on the convex areas of the vulva, sparing the folds.
Avoiding use of the offending agents and providing patients education, together with the prescription of potent topical steroids to reduce inflammation, are crucial to the control of symptoms and signs.

2. Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) is the consequence of a T-lymphocytes mediated immune reaction to small, molecular weight chemicals (haptens) that penetrate the skin and activate innate immunity and then the adaptive immunity [2]. During the sensitization phase, naive T cells are activated in a process that involves Langerhans cells and dermal dendritic cells; in the elicitation phase, T cells migrate into the skin and induce skin damage through the release of proinflammatory cytokines and by killing hapten-loaded keratinocytes.
The sensitization phase of ACD results in the expansion of skin-homing hapten-specific T cells that, upon subsequent hapten challenge, migrate into the skin and induce the skin damage through the release of proinflammatory cytokines and by killing hapten-loaded keratinocytes. Vulvar ACD may occur as a primary disorder or may complicate an underlying vulvar dermatosis. The risk of ACD increases in the case of pre-existing ICD and with the use of multiple topical treatments.
Vulvar ACD may develop as an acute eczema where the allergen was applied. In that case an itching vesicular or exudative eczema develops on previously healthy skin. However, the onset is often a complication of previous different cutaneous dermatoses (lichen sclerosus, psoriasis, atopic dermatitis, etc.) presenting as a local aggravation or exacerbation of symptoms and signs (Figure 1). The diagnosis may not be easy because of the confounding clinical aspects related to the preexisting dermatosis. In this case, history and the clinical aspect are very important in differentiating a lichen flare-up with an allergic dermatitis. The appearance of acute inflammatory lesions as erythema, edema, and vesiculation suggests contact sensitization. Furthermore, a poor response to an appropriate topical corticosteroid therapy could be indicative of contact sensitization to these molecules. The prolonged contact with the allergen can cause lichenification. (Figure 2).
Figure 1. A case of psoriasis complicated by allergic contact dermatitis due to topical medications.
Figure 2. Lichenification following persistent allergic contact dermatitis.
ACD can often severely affect quality of life for women who already suffer from a debilitating vulvar disease.
Sometimes the area of involvement spreads over the borders of the vulva not only due to the spread of inflammation but also because of the modality of contact with the allergens [4]. (Figure 3).
Figure 3. A case of allergic contact dermatitis in which the area of involvement spreads over the borders of the vulva.
Distant localizations may also develop due to inadvertent hand transfer or rubbing of the adjacent areas (e.g., thighs). The contamination of clothing or napkins may lead to persistent dermatitis. Furthermore, a rapid spread to distant sites (auto-eczematization) may also result from the absorption and diffusion of allergens inducing a sort of id-dermatitis.
Clinically, vulvar irritation and allergic dermatitis can be difficult to distinguish, and diagnosis is made on the basis of history, clinical investigation, and patch testing.
A particular situation in vulvar ACD may be represented by the so-called “Connubial dermatitis”, a dermatitis that occurs because of contact with substances transferred to the patients’ skin by her partner. The diagnosis of connubial dermatitis should be considered in cases of probable allergic contact eczema when patch test results are apparently inconsistent with the patient’s clinical history. In these situations, it may be necessary to extend medical investigation to the patient’s partner as well, in order to clarify the source of allergic contacts when no obvious exposures can be found.
Vulvar ACD is frequently linked to direct contact with cosmetics and detergents or medicaments. Less frequently textiles or dyes are described. Sometimes unsuspected allergens such as nail varnish (ectopic contact dermatitis) can be the cause.
A review of the studies concerning vulvar ACD is reported in Table 2 [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19].
Table 2. Review of the studies concerning vulvar ACD.
Authors   Pathologies N° Patients %
Relevant p.t.
Doherty et al. 1990 Vulvar itching 50 78 - nickel, fragrances, neomycin, local anesthetics
Marren et al. 1992 Vulvar dermatoses 135 47 29 nickel, fragrances, preservatives, ethylenediamine, topical medicaments
Brenan et al. 1996 Chronic vulvar symptoms 700 42 - nickel, fragrances, ethylenediamine
Goldsmith et al. 1997 Anogenital dermatoses 201 39 28 antibiotics, local anesthetics, fragrances, corticosteroids
Lewis et al. 1997 Vulvar symptoms 121 58.7 49 local anesthetics, fragrances, neomycin
Lucke et al. 1998 Vulvar dermatoses 55 65 - nickel, fragrances, medicaments, dyes
Bauer et al. 2000 Anogenital symptoms 351 47 34.8 nickel, fragrances, local anesthetics
Crone et al. 2000 Vulvar dermatoses 38 47 28 fragrances, preservatives, medicaments
Virgili et al. 2003 Vulvar lichen simplex chronicus 61 47.5 26 nickel, preservatives, fragrances, medicaments
Nardelli et al. 2004 Vulvar symptoms 92 38 16 medicaments
Utas et al. 2008 Vulvar itching 50 52 16 preservatives, fragrances, medicaments
Haverhoek et al. 2008 Vulvar pruritus 43 81.4 44 preservatives, fragrances, medicaments
Warshsoaw et al. 2008 Anogenital dermatoses 570 44.1 27 medicaments, corticosteroids
Vermaat et al. 2008 Anogenital dermatoses 53 66 20 fragrances, spices
O’Gorman et al. 2013 Vulvar itching 90 69 39 preservatives, fragrances, medicaments
Al-Niaimi at al. 2014 Vulvar symptoms 282 54 49 nickel, fragrances, neomycin
Trivedi et al. 2018 Vulvar itching - 64 54 preservatives, fragrances
It is not surprising that a high level of sensitization (39–78%) is found testing patients affected by different vulvar disorders (vulvar symptoms, vulvar dermatoses, or anogenital symptoms). In selected conditions as well, like lichen simplex chronicus [20], similar percentages can be found. The reported incidence of clinically relevant patch test results for patients presenting with vulvar complaints are likewise high, ranging from 16% to 54% [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19].
Fragrances, preservatives, and topical medicaments (especially corticosteroids, neomycin, and topical anesthetics) are the relevant allergens usually found. Although some authors consider nickel a relevant positivity for the disease, in the majority of cases it is considered a non-relevant allergen that simply reflects the high level of sensitization in the general population [9][15][20].


  1. Bains, S.N.; Nash, P. Irritant Contact Dermatitis. Clin. Rev. Allergy Immunol. 2019, 56, 99–109.
  2. Nosbaum, A.; Vocanson, M.; Rozieres, A.; Hennino, A.; Nicolas, J.F. Allergic and irritant contact dermatitis. Eur. J. Dermatol. EJD 2009, 19, 325–332.
  3. Farage, M.A. Vulvar susceptibility to contact irritants and allergens: A review. Arch. Gynecol. Obstet. 2005, 272, 167–172.
  4. Davis, M.D.P. Unusual patterns in contact dermatitis: Medicaments. Dermatol. Clin. 2009, 27, 289–297.
  5. Marren, P.; Wojnarowska, F.; Powell, S. Allergic contact dermatitis and vulvar dermatoses. Br. J. Dermatol. 1992, 126, 52–56.
  6. Brenan, J.A.; Dennerstein, G.J.; Sfameni, S.F.; Drinkwater, P.; Marin, G.; Scurry, J.P. Evaluation of patch testing in patients with chronic vulvar symptoms. Australas. J. Dermatol. 1996, 37, 40–43.
  7. Goldsmith, P.C.; Rycroft, R.J.G.; White, I.R.; Ridley, C.M.; Neill, S.M.; McFadden, J.P. Contact sensitivity in women with anogenital dermatoses. Contact Dermat. 1997, 36, 174–175.
  8. Lewis, F.M.; Harrington, C.I.; Gawkrodger, D.J. Contact sensitivity in pruritus vulvae: A common and manageable problem. Contact Dermat. 1994, 31, 264–265.
  9. Lucke, T.W.; Fleming, C.J.; McHenry, P.; Lever, R. Patch testing in vulval dermatoses: How relevant is nickel? Contact Dermat. 1998, 38, 111–112.
  10. Bauer, A.; Geier, J.; Elsner, P. Allergic contact dermatitis in patients with anogenital complaints. J. Reprod. Med. 2000, 45, 649–654.
  11. Crone, A.M.; Stewart, E.; Wojnarowska, F.; Powell, S.M. Aetiological factors in vulvar dermatitis. J. Eur. Acad. Dermatol. Venereol. JEADV 2000, 14, 181–186.
  12. Utaş, S.; Ferahbaş, A.; Yildiz, S. Patients with vulval pruritus: Patch test results. Contact Dermat. 2008, 58, 296–298.
  13. Vermaat, H.; Van Meurs, T.; Rustemeyer, T.; Bruynzeel, D.P.; Kirtschig, G. Vulval allergic contact dermatitis due to peppermint oil in herbal tea. Contact Dermat. 2008, 58, 364–365.
  14. O’Gorman, S.M.; Torgerson, R.R. Allergic contact dermatitis of the vulva. Dermat. Contact Atopic Occup. Drug 2013, 24, 64–72.
  15. Al-Niaimi, F.; Felton, S.; Williams, J. Patch testing for vulval symptoms: Our experience with 282 patients. Clin. Exp. Dermatol. 2014, 39, 439–442.
  16. Trivedi, M.K.; Woodruff, C.M.; Kornik, R.; Botto, N. Patch Testing in Vulvar Allergic Contact Dermatitis. Dermat. Contact Atopic Occup. Drug 2018, 29, 95–96.
  17. Nardelli, A.; Degreef, H.; Goossens, A. Contact allergic reactions of the vulva: A 14-year review. Dermat. Contact Atopic Occup. Drug 2004, 15, 131–136.
  18. Warshaw, E.M.; Furda, L.M.; Maibach, H.I.; Rietschel, R.L.; Fowler, J.F., Jr.; Belsito, D.V.; Zug, K.A.; DeLeo, V.A.; Marks, J.G., Jr.; Toby Mathias, C.G.; et al. Anogenital dermatitis in patients referred for patch testing: Retrospective analysis of cross-sectional data from the North American Contact Dermatitis Group, 1994–2004. Arch. Dermatol. 2008, 144, 749–755.
  19. Haverhoek, E.; Reid, C.; Gordon, L.; Marshman, G.; Wood, J.; Selva-Nayagam, P. Prospective study of patch testing in patients with vulval pruritus. Australas. J. Dermatol. 2008, 49, 80–85.
  20. Virgili, A.; Bacilieri, S.; Corazza, M. Evaluation of contact sensitization in vulvar lichen simplex chronicus. A proposal for a battery of selected allergens. J. Reprod. Med. 2003, 48, 33–36.
Subjects: Allergy
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