Eczema of the Nipples and Areolae

Benjamin Barankin, MD, FRCPC
Alexander K.C. Leung, MD, MBBS, FRCPC, FRCP
Volume 57 - Issue 2 - February 2017

A gravida 4, para 3, 36-year-old woman presented with a 3-month history of a bilateral pruritic eruption on her nipples and areolae. She had an 8-month-old infant whom she had breastfed. The infant had been started on solid food at 5 months of age.

The patient had had atopic dermatitis since childhood. She had outgrown childhood asthma and allergic rhinitis.

Eczema of the Nipples and Areolae Figure

Physical examination. The patient’s nipples and areolae were observed to be erythematous, scaly, hyperkeratotic, and lichenified. She also had eczematous lesions on both hands. The rest of the physical examination findings were unremarkable.

Diagnosis and treatment. Based on the clinical appearance, a diagnosis of nipple and areola eczema was made. The patient was treated with fluocinonide ointment, twice a day for 1 week and then once a day at bedtime until the condition resolved, followed by twice daily application of petrolatum ointment. At 2 weeks’ follow-up, the eczema had completely resolved.

Discussion. Nipple and areola eczema is a dermatosis characterized by various clinical manifestations such as erythema, vesicles, erosions, scaling, crusting, fissures, and lichenification, alone or in combination.1 The exact incidence is not known, given that the literature on this condition is limited to case reports. Adolescent girls and lactating mothers are most commonly affected.1 Cases occurring as early as in infancy2 and in males have also rarely been reported.3

Eczema is a general term encompassing several types of dermatitis, the most common being atopic dermatitis.4 The pathogenesis of atopic dermatitis involves complex interactions between susceptible genes, immunologic factors, skin-barrier defects, infections, neuroendocrine factors, and environmental factors.5 Patients may exhibit immunoglobulin E-mediated sensitization due to external antigens, or intrinsic sensitization without immunoglobulin E-mediated sensitization.5 Nipple and areola eczema is the most common manifestation of atopic dermatitis of the breast.1 It is included as minor criteria for atopic dermatitis, as defined by Hanifin and Rajka6 and subsequently validated by other investigators.2,7 Approximately 50% of breastfeeding mothers with nipple and areola eczema have a history of atopic dermatitis.8

Other types of eczema include irritant contact dermatitis and allergic contact dermatitis.4,8,9 Immunologic reactions are not involved in irritant contact dermatitis, and the dermatitis can occur without prior sensitization of the patient. Rather, irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage, resulting in the release of inflammatory mediators and cytokines, predominately from epidermal cells. This type of eczema occurs as a result of exposure of the areola and nipple to irritant agents such as friction, water, soaps, or washing detergents.

Allergic contact dermatitis is a type IV-delayed hypersensitivity reaction caused by a T-cell–mediated immune response to skin sensitizers. Contact allergens require prior exposure for sensitization. Allergic contact dermatitis may occur with an offending topical agent used on the nipple and areola. Offending agents can include nonpurified lanolin, chamomile ointment, and perfumes, among others.

Histologic findings include intracellular and intercellular edema of the epidermis (spongiosis) and eosinophils in acute skin lesions.5 There is marked perivascular infiltration of type 2 helper T cells in the dermis. Chronic atopic lesions are characterized by a hyperplastic and hyperkeratotic epidermis with minimal spongiosis and increased inflammatory dendritic epidermal cells.5

Nipple and areola eczema most commonly affects the areola and affects the nipple to a lesser extent. It tends to spare the area of the areola immediately adjacent to the nipple.8 Acute lesions are intensely pruritic and typically present as erythematous papules, papulovesicles, weeping lesions, crusting, or erosions.5 Subacute lesions are erythematous scaling papules or plaques. Chronic lesions are characterized by prominent scaling, excoriations, and lichenification. The condition is usually bilateral and symmetric,1 although unilateral cases have been reported.2 Nipple and areola eczema can cause considerable discomfort, itchiness, a burning sensation, and pain, especially while a woman is breastfeeding.2 It can be severe enough to force a lactating mother to curtail breastfeeding.9

The diagnosis is mainly clinical, based on the characteristic features. If there is scale and an active edge to the rash, or maceration in the nipple/areola area, a potassium hydroxide wet-mount examination of skin scrapings and a fungal culture should be performed to rule out tinea corporis.8 Patch testing can be performed to determine the contactant causing allergic contact dermatitis. The differential diagnosis includes bacterial infection of the breast such as cellulitis, impetigo, and mastitis; mammary candidiasis; jogger’s nipples; psoriasis, Bowen disease, and Paget disease.8,10,11

Prevention of nipple and areola eczema consists of identifying and eliminating offending allergens and irritants.

Hydration of the skin is of paramount importance in both the prevention and management of eczema.5 Liberal use of moisturizers should be strongly encouraged. Topical corticosteroids are the mainstay of therapy. Low-potency topical corticosteroids should be used as the first line of treatment.5 More potent topical corticosteroids should be reserved for more severe cases.8 Topical calcineurin inhibitors such as tacrolimus ointment and pimecrolimus cream are also good options for use on sensitive thin skin such as that of the nipple and areola.5 Sequential applications of topical immunomodulators with tapering of topical corticosteroids may limit the long-term use and adverse effects of topical corticosteroids while maintaining clinical control of eczema and improving quality of life.5 Nursing mothers should be instructed to wipe the cream/ointment off the nipple and areola before feeding the infant and to apply the cream/ointment soon after the infant has been fed.

Scratching to relieve the itch may cause excoriation of the skin and possible secondary infection. Also, the first scratch initiates the second, and this can become a vicious cycle. As such, it is important to minimize scratching. To avoid injury to the skin from scratching, fingernails should be kept short, smooth, and clean. 

Although pruritus in eczema does not appear to be mediated by histamine release, oral antihistamines can provide symptomatic relief at bedtime because of their sedative properties and may be effective for intense pruritus that is refractory to moisturizers and conservative measures. Breaking the itch-scratch cycle is essential for prolonged periods of eczema control.5 Of the H1-receptor antagonist antihistamines, hydroxyzine is more effective than diphenhydramine.5

Antibiotic therapy is indicated for secondary bacterial infections that may exacerbate and complicate an acute flare.5 Skin cultures and sensitivities should be considered before treatment, since methicillin-resistant Staphylococcus aureus may be an important pathogen in some patients. Cloxacillin, clindamycin, first- or second-generation cephalosporins, or macrolides are most effective against S aureus.5 Maintenance systemic antibiotic therapy should be avoided, because methicillin-resistant organisms may develop with their use. Topical antibiotics, such as mupirocin, fusidic acid, and retapamulin are often useful on impetiginized lesions. Because topical use of antibiotics may induce bacterial resistance and contact allergy, topical antibiotics should be used with caution.

The prognosis of nipple and areola eczema is good, as the lesions tend to regress with proper treatment.

REFERENCES:

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