This extremely common dermatitis is a frequent secondary factor in patients with genital symptoms, often associated with overwashing, use of topical medications, and chronic moisture from incontinence or sweat.

Chronic irritant contact dermatitis is usually manifested by symptoms of irritation, soreness, or rawness. If the patient is atopic, the irritant can precipitate itching and can initiate an itch-scratch cycle. Morphologically, the area affected depends on where the contact occurred. Generally, this is manifested by a poorly demarcate
erythematous or dusky plaque with scale that may be subtle (Fig. 6-5). Patients who have experienced itching frequently have superimposed excoriations or lichenification. In these patients, the morphology is indistinguishable from that of atopic dermatitis, and indeed the irritant can be viewed simply as a precipitating factor for atopic dermatitis or eczema. Acute irritant dermatitis is essentially a chemical burn. The rapid appearance of erythema, edema, and blistering is typical. Poorly keratinized skin such as the modified mucous membranes of the vulva, the glans penis, and the inner aspect of the prepuce is very fragile, and blister roofs are shed quickly, forming erosions.

Irritant contact dermatitis can be caused either by repeated exposure to a weak irritant or by one or few exposures to a very strong irritant. Common irritants are listed in Table 6-1. A diaper rash is a typical example of chronic irritant contact dermatitis, although in this case superimposed candidiasis is sometimes a complicating factor. Because repeated exposure is often necessary for the development of irritant contact dermatitis and the symptoms and signs occur gradually, the patient is frequently unaware that the substance is irritating and is playing a role in symptoms.

Acute irritant contact dermatitis, however, is produced by one or a few exposures to a very strong irritant, and this exposure is often accompanied by immediate burning and stinging. The patient usually is aware of the cause of the symptom and frequently misinterprets this as allergy. The most common causes of acute irritant contact dermatitis include treatment for external genital warts, such as trichloroacetic and bichloroacetic acids, podophyllum resin, and cantharidin. Some patients with very sensitive skin can experience acute irritant contact dermatitis to alcohol-containing creams, most often antifungal medications used in a setting of pre-existing inflamed skin.

The diagnosis of irritant contact dermatitis is made by correlation of the symptoms and physical findings with a history of possible contactants. The diagnosis is confirmed when the contactants are eliminated and the eruption and symptoms resolve. Dermatoses with similar morphology include eczema/lichen simplex chronicus and allergic contact dermatitis. Psoriasis, vulvar/penile/anal intraepithelial neoplasia (Bowen disease) and Paget disease can also resemble irritant contact dermatitis. Acute irritant dermatitis can be confused with other blistering or ulcerative conditions, including acute allergic contact dermatitis, herpes simplex virus infection, a fixed drug eruption, or candidiasis. Autoimmune blistering diseases are slower in onset and are less likely to produce diagnostic confusion.

The most important aspects of therapy are the identification and elimination of all irritants. A midpotency topical corticosteroid ointment, such as triamcinolone 0.1% twice a day is often useful. The pain and burning of acute irritant contact dermatitis are minimized by cool or tepid tap water sitz baths several times a day for the first few days, followed by the application of petrolatum on open erosions. Nighttime sedation provides comfort and sleep to those with pain and itching and minimizes ongoing irritation from nighttime scratching.

Allergic contact dermatitis occurs as a result of contact of an allergen to the skin of a patient who has specifically developed a hypersensitivity to that allergen.

Chronic allergic contact dermatitis is characterized by itching as well as by a poorly demarcated erythematous, scaling plaque that often shows linear erosion from scratching and lichenification. Often, chronic allergic contact dermatitis cannot be distinguished clinically from irritant contact dermatitis and atopic dermatitis and its variants. Acute allergic dermatitis, however, presents with cutaneous edema that produces tiny, monotonous, closely set vesicles in the areas of the contact (Fig. 6-6). Often, there are linear or irregular plaques in which the contactant was spread on the skin, such as by fingers for medication or brushed on by the leaves of a plant.

The allergen is rarely recognized by the patient, because symptoms follow exposure by one or several days. Allergic contact dermatitis has been found by European clinicians to play a significant role in chronic vulvovaginal symptoms, whereas American physicians have not found allergy to be a common factor (5). More common allergens are listed in Table 6-2.

The diagnosis of allergic contact dermatitis is made by correlation of symptoms and physical findings with a history of a likely contactant. The diagnosis is confirmed when the contactant is eliminated and the eruption and symptoms resolve. Sometimes, allergic contact dermatitis is suspected when atopic dermatitis does not respond to therapy, but an allergen is not identified. In these cases, patch testing by a dermatologist is warranted to identify any offending allergens.

The differential diagnosis of chronic allergic contact dermatitis includes irritant contact dermatitis, atopic dermatitis/lichen simplex chronicus, psoriasis, secondarily rubbed or scratched tinea cruris, candidiasis, seborrheic dermatitis, vulvar/penile/anal intraepithelial neoplasia (Bowen disease), and Paget disease. Acute allergic contact dermatitis can be confused with other blistering or erosive diseases, especially acute irritant contact dermatitis, candidiasis, and herpes simplex virus infection.

Most important in the treatment of contact dermatitis is the elimination of the contactant. Sometimes, the contactant cannot be identified, and the patient is counseled to avoid all topical agents other than clear water and petrolatum (petroleum jelly). After the elimination of the contactant, acute, blistering, or exudative contact dermatitis can be improved with cool soaks or sitz baths for the first few days. Oral prednisone for severe disease and topical corticosteroids for less erosive dermatitis are useful as well. Topical corticosteroids should be continued until symptoms are clear and the skin is normal. Nighttime sedation and control of secondary infection are important to minimize symptoms while the skin heals.

Seborrheic dermatitis of the scalp is a common disease, occurring at all ages. However, seborrheic dermatitis is most common in newborns and after puberty. In addition, this condition is most severe in those who cannot shampoo regularly, such as the homeless and those with neurologic disease or other infirmities that interfere with activities of daily living. Finally, patients of African background cannot shampoo daily because of the excessive dryness of their hair with frequent washing.

Seborrheic dermatitis generally affects the scalp first and most remarkably. Erythematous plaques at the hairline exhibit yellowish scale with a slightly greasy texture, hence the term seborrhea. As the disease worsens, the entire scalp becomes involved, and erythema and scale spread to other areas, preferentially affecting the ears, posterior auricular folds, eyebrows, and the nasolabial folds. Most often, seborrheic dermatitis does not extend beyond these areas. Occasionally, however, severe seborrheic dermatitis can involve the entire face, and the eruption can spread to the chest and to skin folds including the axillae, umbilicus, and genital skin (Fig. 6-7).

Seborrheic dermatitis of the genital area is accentuated within the skin folds. A classic but not unique characteristic of genital seborrheic dermatitis is a glazed, shiny texture to the affected skin.

Infants often develop seborrhea of the scalp, also called cradle cap. Spread of the eruption to the face, trunk, and genitalia is much more common in infants than in adults.

The diagnosis of seborrheic dermatitis can generally be made by the pattern of red, scaling plaques that include the scalp, central face, and other skin folds and by the absence of negative culture or skin scrapings for candidiasis. A biopsy is generally not required to make this diagnosis, but histology is characterized by varying degrees of acanthosis and elongation of the rete ridges, with hyperkeratosis and spongiosis. There is an underlying perivascular lymphocytic infiltrate, with some migration into the epidermis. Neutrophils can be seen in the stratum corneum. The diagnosis of seborrheic dermatitis is confirmed by the rapid and complete response to therapy.

Most causes of generalized red patches and plaques of the genitalia are in the differential diagnosis. This includes atopic dermatitis and its variants, allergic and irritant contact dermatitis, fungal infection, and psoriasis. The accentuation of disease in the skin folds especially mimics cutaneous candidiasis. Generally, these diseases can be differentiated by their pattern of involvement on other parts of the body, as well as by the characteristic yellowish, greasy scale on the scalp and face seen in seborrhea. Psoriasis, however, frequently exhibits the same distribution, but the thicker nature of the plaque, the more discrete rather than generalized scalp plaques, the psoriatic nail changes, and the typical lesions of psoriasis of other skin surfaces usually differentiate these two diseases.

The cause of seborrheic dermatitis is not known. Some evidence suggests that Malassezia yeasts, the causative organism of pityriasis (tinea) versicolor, play a role in the development of seborrheic dermatitis. Unencapsulated yeast forms stimulate cytokine production by keratinocytes (6). This yeast has been identified in the scalp of patients with seborrhea, and the antifungal cream ketoconazole topically is effective for the treatment of pityriasis versicolor and scalp seborrheic dermatitis. However, this organism is a frequent colonizer, and other equally effective antifungal medications have not been reported to be beneficial for the treatment of seborrhea; both of these facts suggest an alternate or additional etiology. Other clinicians believe that seborrhea is an inflammatory response to perspiration, heat, and sebum trapped under normal stratum corneum that is not normally shed from skin folds and hairy areas because of anchoring hair shafts. This theory is also used to explain the distribution of seborrhea, which includes the scalp, eyebrows, beard area, nasolabial and retroauricular folds on the head and neck, and other skin folds such as the axillae and groin (Fig. 6-7). Inflammation from heat, sweat and scale held against the skin by scale result in increased epidermal turnover and the production of even more scale.

The treatment of anogenital seborrheic dermatitis requires the control of disease on the scalp and other areas as well. This involves the removal of scale from the scalp and any other affected hairy areas, as well as administration of topical corticosteroids. Vigorous and irritating
means of scale removal is not indicated in the much more sensitive skin folds and genital regions.

Brisk shampooing of the adult scalp with antiseborrheic shampoos containing antiproliferative agents such as tar zinc pyrithione or selenium sulfide or keratolytic substances such as salicylic acid aids in the debridement of scale from the scalp. Medication is scrubbed into the scalp and is allowed to stay on the skin for 5 to 10 minutes before it is rinsed. Generally, use of these shampoos in the genital area is not recommended because of their irritant properties and because they are not required for clearing. Again, because of the irritant properties of these shampoos, infant seborrhea is not treated with these agents. The scalp scale is softened with baby oil or mineral oil and is then removed with a soft brush or gentle use of fingernails.

Otherwise, topical corticosteroids are primary therapy for seborrhea, both on the scalp and on genital skin. Patients with mild disease and infants are easily treated with a lowpotency medication such as hydrocortisone 1% or 2.5%. For more severe disease, a midpotency topical corticosteroid such as triamcinolone 0.1% cream generally produces marked improvement quickly. An inexpensive, cosmetically pleasing, and effective corticosteroid for use in the scalp is betamethasone valerate 0.01% lotion, but this alcohol-based therapy should not be used on easily irritated genital skin.

For those patients who do not improve adequately with this safe and relatively inexpensive therapy, ketoconazole (Nizoral) cream or shampoo can be a beneficial treatment. The cream is applied twice a day, and the shampoo is used daily on the scalp.

The treatment of seborrheic dermatitis in patients of African descent must be modified because of the tendency for the hair of these patients to dry excessively and to break with overwashing. Twice-weekly vigorous shampooing of the scalp initially with careful attention to moisturizing the hair afterward is usually a reasonable compromise. However, moisturizers should be applied to the hair only, with the patient’s taking care to avoid application to the scalp itself because this can exacerbate retention of scale and occlusion.

Scalp seborrheic dermatitis is a chronic skin condition with a tendency to wax and wane in severity. Usually, the regular and proper use of an antiseborrhic shampoo controls scalp disease, although some patients require intermittent application of a corticosteroid solution to the scalp. Because the groin generally is the last area involved with severe seborrhea, control of scalp disease usually prevents the recurrence of anogenital seborrheic dermatitis.

Psoriasis is a very common skin condition, occurring in 2% to 3% of people. Males and females are affected equally, and persons of African ancestry are less often affected than white individuals. This condition occurs at all ages but begins most often in young adults. There is a familial predisposition, with one in three patients reporting a family history of psoriasis.

Classic psoriasis vulgaris (common psoriasis) exhibits well-demarcated thickened, red plaques with dense, silvery scale (Figs. 6-8, 6-9 and 6-10). Often, patients report severe itching, but this is not universal. Plaques typically occur on the scalp, elbows, knees, umbilicus, and gluteal cleft. Genital involvement is common, and plaques are more generalized in patients with more severe disease. The face is usually relatively spared.

About 20% of patients exhibit Koebner phenomenon, in which psoriasis is precipitated in skin by irritation or injury. This partially explains the distribution of lesions, including the elbows and knees, as well as the frequent involvement of the genitalia, an area subject to friction and occlusion.

A variant of psoriasis that presents with prominent genital involvement is inverse psoriasis (Figs. 6-11, 6-12 and 6-13, 6-15, 6-17, 6-18 and 6-19). Inverse psoriasis involves skin folds preferentially and often spares the classic dry, keratinized knees, elbows, and scalps. The axillae, inframammary skin, umbilicus, gluteal cleft, crural creases, and genitalia are affected. Psoriasis occurring in skin folds exhibits very subtle scale as well as plaques that are far
thinner than psoriasis on other skin surfaces (Figs. 6-14, 6-15, 6-16 and 6-17). In addition, the borders frequently are less well demarcated (Fig. 6-18). Not uncommonly, yeast or dermatophyte infection may coexist with or may mimic intertriginous psoriasis (Fig. 6-19). Psoriasis predominantly affects the hairbearing vulva of women, mostly sparing the modified mucous membranes and vagina. However, psoriasis often is located on the glans penis in addition to the penile shaft, scrotum, and groin.

Psoriasis sometimes can become generalized, so that confluent erythema, scale, and sometimes exudation are indistinguishable from generalized eczema or generalized seborrhea. A final form of psoriasis, pustular psoriasis, is characterized by plaques of pustules or crusting. This variant is discussed in Chapter 8.

Psoriasis produces nail abnormalities in addition to inflammatory skin lesions (Fig. 6-20). Most common are small nail pits, not to be confused with simple irregularity or rippling of the surface. Also fairly specific are “oil-drop spots.” These are brownish-red discolorations of the nail plate. A third form of nail psoriasis, onycholysis, is much
less specific. Onycholysis refers to lifting of the nail from the underlying surface, in this case from psoriasis of the nail bed. The scale and keratin debris collect under the nail, with the final picture nearly identical to that of a fungal nail infection.

The primary extracutaneous manifestation of psoriasis is arthritis. A significant minority of patients experience joint disease that ranges from pain with minimal inflammation to severe, deforming, and mutilating arthritis.

There are also several comorbidities associated with psoriasis, suggesting that psoriasis is actually a complex constellation of systemic conditions. Patients with psoriasis are more likely to be obese, and alcoholism and depression are recognized as common occurrences. Cardiovascular disease, inflammatory bowel disease, and even osteoporosis have been reported more recently to occur more often (7,8). Autoimmune diseases also are increased in this group (9).

Psoriasis of the genitalia can be diagnosed with confidence when morphologically consistent plaques in this area are associated with typical psoriasis of the elbows and knees, scalp, and nails. If the distribution and morphology are atypical, the diagnosis can often be confirmed on biopsy, but a nondiagnostic biopsy does not rule out psoriasis as a cause of the eruption.

The classic but nonspecific histologic picture of psoriasis includes marked thickening of the epidermis with regular elongation of the rete pegs and suprapapillary thinning. Hyperkeratosis and parakeratosis are prominent, and there is an absence of the granular layer. More specific histologic findings are collections of neutrophils just under the stratum corneum of the thinned suprapapillary epidermis (spongiform pustules of Kogoj) and in the overlying parakeratotic layer (Munro microabscesses). A biopsy of an older lesion is often nonspecific and may be interpreted as psoriasiform dermatitis.

Tinea cruris is the most common disease confused with psoriasis, and they often coexist. However, in immunocompetent patients, tinea cruris usually spares the scrotum and penis, whereas these structures are often prominently affected with psoriasis. In addition, tinea
cruris is uncommon in women. Cutaneous candidiasis frequently shows satellite pustules or erosions but can also resemble and coexist with psoriasis. Lichen simplex chronicus, Bowen disease (also called squamous cell carcinoma in situ, as well as erythroplasia of Queyrat in men and vulvar intraepithelial neoplasia on the vulva), and Paget disease are all red, scaling diseases that can be confused with psoriasis, and lichen planus on the glans penis is sometimes indistinguishable from smaller papules of psoriasis of this area. Seborrheic dermatitis, especially in infants, can appear very similar to psoriasis and shows the same pattern of distribution as inverse psoriasis.