Nummular eczema

INTRODUCTION — Nummular eczema, also called discoid eczema or nummular dermatitis, is a chronic, inflammatory skin disease characterized by multiple pruritic, coin-shaped, eczematous lesions involving the extremities and, less commonly, the trunk (picture 1A) [1]. Nummular eczema is regarded as a distinctive form of endogenous (idiopathic) eczema, although some experts suggest that it should be reclassified as a subtype of atopic dermatitis [2]. The author applies the American Academy of Dermatology criteria for atopic dermatitis [3] and, if met in a given patient, considers atopic dermatitis to be the underlying diagnosis that is presenting with nummular lesions. If the criteria are not met, the author considers it to be idiopathic nummular eczema.

This topic will discuss the clinical features, diagnosis, and treatment of idiopathic nummular eczema. Atopic dermatitis, allergic contact dermatitis, and other types of eczematous dermatitis are discussed separately.

●(See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

●(See "Treatment of atopic dermatitis (eczema)".)

●(See "Clinical features and diagnosis of allergic contact dermatitis".)

●(See "Irritant contact dermatitis in adults".)

●(See "Stasis dermatitis".)

●(See "Urticarial dermatitis".)

EPIDEMIOLOGY — Nummular eczema affects men more frequently than women. Most patients are over the age of 50, although individuals of any age can be affected [4].

PATHOGENESIS — The pathogenesis of idiopathic nummular eczema is incompletely understood. Numerous factors have been implicated as causal, including xerosis and decreased cutaneous lipid production, Staphylococcus aureus colonization, contact allergy to metals, alcohol consumption, nonceliac gluten sensitivity, and sensitization to environmental aeroallergens such as Candida albicans or house dust mites [1,5-12]. Nummular eczema has been reported in patients treated with isotretinoin and in patients with hepatitis C infection treated with interferon-alpha-2b and ribavirin [13-15]. In a study of 1662 patients undergoing breast reconstruction, approximately 3 percent developed nummular eczema in the area of reconstruction [16]. In nearly two-thirds of cases, nummular eczema developed after the implantation of tissue expanders or silicone implants, suggesting that stretching or tension applied to the skin may be a trigger for this type of dermatitis. A report of nummular eczema developing after initiating the interleukin (IL) 23 inhibitor guselkumab for psoriasis treatment suggests that the balance of Th1 and Th2 cytokines may play a role in the pathogenesis of some cases [17].

PATHOLOGY — The pathologic features of nummular eczema are indistinguishable from other forms of eczema, showing primarily spongiosis, superficial perivascular lymphocytic infiltrates, with some eosinophils and occasional neutrophils and plasma cells (picture 2) [18]. Mild papillary edema and vascular dilation may be present.

CLINICAL MANIFESTATIONS — Nummular eczema typically presents with highly pruritic, round, coin-shaped patches of eczematous dermatitis ranging in diameter from 1 to 10 cm (picture 1A-C). In the acute phase, lesions are dull red, exudative, and crusted. Over time, they become drier and scalier, occasionally with central clearing leading to annular lesions.

The legs and the upper extremities are the sites most frequently involved. Involvement of the trunk is less common, but when present, the lower trunk is more likely to be involved than the upper trunk. If the face or neck is involved, alternative diagnoses should be considered.

Nummular eczema is a chronic and relapsing disease. Days to months after resolution, apparently dormant lesions may become active again or new lesions may occur in adjacent areas.

DIAGNOSIS — The diagnosis of nummular eczema is usually clinical, based upon the typical finding of round, coin-shaped, and highly pruritic lesions in a patient with diffusely dry skin. Biopsy or laboratory tests are generally not necessary for diagnosis. However, a skin swab for bacterial culture may be performed in patients with exudative or crusted lesions, initiating appropriate antibacterial therapy based on the results of the culture. Patch testing may be helpful in patients with recalcitrant disease and/or a history suggesting allergic contact dermatitis [8,19]. (See "Patch testing".)

Differential diagnosis — The differential diagnosis of nummular eczema includes:

●Atopic dermatitis – Nummular lesions may be an atypical clinical presentation of atopic dermatitis in both adults and children, and distinguishing idiopathic nummular eczema from atopic dermatitis with primarily nummular lesions requires application of validated diagnostic criteria. The author prefers to use the American Academy of Dermatology criteria for this purpose [20,21]. For example, in one report, 13 percent of older, White patients with atopic dermatitis presented with primarily nummular lesions [22]. A history of atopic disease, including reactions to aeroallergens, asthma, and atopic dermatitis in typical flexural locations, supports the diagnosis of atopic dermatitis. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

●Allergic contact dermatitis – Allergic contact dermatitis may rarely present with lesions indistinguishable from nummular eczema. Comprehensive patch testing to contact sensitizers based upon the patient's history of exposure can clarify the diagnosis. In a large population of patients referred for patch testing due to eczematous lesions with a nummular morphology, nearly 25 percent had a positive patch test to a potentially relevant allergen (primarily those in personal care products), although there was no follow-up data to confirm that these patients improved with allergen avoidance [23]. (See "Clinical features and diagnosis of allergic contact dermatitis" and "Patch testing".)

●Tinea corporis – Early lesions of tinea corporis may mimic nummular eczema (picture 3A-B). A potassium hydroxide (KOH) preparation will show the segmented hyphae and arthrospores characteristic of all dermatophyte infections. (See "Dermatophyte (tinea) infections".)

●Stasis dermatitis – Early lesions of stasis dermatitis may present as erythematous, scaly, and itchy patches (picture 4). A history of venous insufficiency and/or the presence of other signs of chronic venous insufficiency such as varicosities, pitting edema, and hyperpigmentation support the diagnosis of stasis dermatitis. (See "Stasis dermatitis".)

●Psoriasis – Psoriatic lesions are usually dry, with more prominent scaling, and asymptomatic, although some patients may complain of pruritus. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)

●Prodromal bullous pemphigoid – Bullous pemphigoid can present with nonspecific, pruritic, eczematous lesions for a prolonged period prior to the appearance of classic blisters. In one case report, lesions typical of nummular eczema developed into classic, immunopathologically confirmed bullous pemphigoid [24]. (See "Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid".)

MANAGEMENT — The management of nummular eczema involves general measures aimed at reducing skin dryness and exposure to irritants and treatment of skin inflammation.

General measures — General measures to reduce skin dryness and exposure to skin irritants may include:

●Limit bathing to once daily with lukewarm water using mild, nonsoap cleansers.

●Apply a moisturizer at least once, preferably twice, daily and immediately after bathing. The author prefers cream preparations over lotions due to the increased lipid content of creams compared with lotions. In addition, evidence has shown that a cream containing a mixture of ceramides is more effective at reducing water loss through the skin than traditional moisturizers [25].

●Use laundry detergents that are based primarily on nonionic surfactants (laundry detergents for sensitive skin), which have the lowest potential for skin irritancy, and/or double rinse the laundry to minimize residual laundry detergent in clothing [26].

●Consider obtaining a whole house humidifier or a room humidifier for the bedroom.

Oral supplementation with L-histidine 2000 mg/day in patients with idiopathic nummular eczema has been shown to increase filaggrin levels in keratinocytes and improve xerosis [27].

First-line therapy — High- or ultra-high potency topical corticosteroids (groups 1 to 3 (table 1)) are first-line therapy for nummular eczema. Topical corticosteroids are applied once or twice daily for two to four weeks or until resolution of the lesions. The use of occlusive dressings may enhance the corticosteroid penetration into the skin and may lead to a more rapid response. 

For isolated recalcitrant lesions, intralesional triamcinolone may be a treatment option. The author injects 0.5 to 1 mL of 4 to 5 mg/mL triamcinolone per lesion. Patients should be warned about the possibility of temporary atrophy or dyspigmentation.

The efficacy of topical corticosteroids for the treatment of nummular eczema has not been evaluated in randomized trials. Their use is based upon indirect evidence of efficacy in other eczematous skin diseases (eg, atopic dermatitis, allergic contact dermatitis) and clinical experience.

Severe or refractory disease

Phototherapy — Patients with extensive disease that does not respond to topical corticosteroids may be treated with narrowband ultraviolet B (NBUVB) therapy. Typically, 10 to 30 treatments given two to three times per week are necessary before a response is noted. If a response is not noted after 30 treatments, the therapy is discontinued. In patients who respond, the author reduces the frequency once all lesions are cleared to once weekly for a month, then to every other week for two months, as needed and tolerated. (See "UVB phototherapy (broadband and narrowband)".)

If NBUVB therapy is not available or not possible for logistic reasons, commercial tanning beds or natural sunlight during the summer may be alternative options. If natural sunlight is utilized, patients should be instructed to start by obtaining 10 minutes of direct, unprotected sunlight between 10 AM and 2 PM and increasing the duration by several minutes daily, up to a maximum of 30 minutes daily. Lightly pigmented patients and those with red or blond hair may need to start with 5 minutes and limit the exposure time to a maximum of 20 minutes. Unaffected areas of the skin should be covered to limit unnecessary solar exposure.

If commercial tanning beds are the only option, the author suggests that the patient find a convenient, local tanning salon. Because there is great variability in the output of different beds and bulbs, there is no standard recommendation for a starting exposure time or progressive increases. If there is no improvement in one month of going three times a week, treatment should be discontinued. If there is improvement, treatment can be reduced to once weekly for a month and then to every other week as needed.

For all patients undergoing phototherapy, the potential increased risk of skin cancer should be weighed against the benefits of avoiding the use of systemic immunosuppressants in the individual patient.

Systemic therapies — For patients with recalcitrant disease for whom phototherapy is not feasible, treatment options include systemic immunosuppressants (eg, systemic corticosteroids, methotrexate, cyclosporine) and biologic immunomodulators:

●Systemic immunosuppressants:

•Systemic corticosteroids – The author's preference is to use intramuscular triamcinolone at a dose of 40 mg given up to once every three months. For clinicians who prefer oral corticosteroids, prednisone can be initiated at 40 mg per day, with the dose reduced by 10 mg every five days and then discontinued.

•Methotrexate – Methotrexate 10 to 15 mg per week is an alternative therapy for patients in whom systemic corticosteroids are contraindicated or in whom the disease recurs shortly after corticosteroid discontinuation. The author initiates methotrexate therapy with 10 mg weekly for six weeks. If the response is inadequate and laboratory monitoring has not shown any abnormalities, the dose is increased to 15 mg weekly for another four to six weeks. Once an adequate response is achieved, the dose is maintained for three to six months, then tapered by 2.5 mg every three months, and then stopped. In case of relapse, the prior dose that was effective is resumed.

•Cyclosporine – Cyclosporine 3 to 5 mg/kg per day is an additional alternative to systemic corticosteroids. The author initiates cyclosporine at a dose of 4 mg/kg per day (based upon ideal body weight). This dose is maintained until the disease is controlled (typically in two to six weeks). The dose is then reduced by 100 mg/day every one to two months until discontinuation.

Systemic corticosteroids, methotrexate, or cyclosporine for the treatment of nummular eczema have not been evaluated in clinical trials. Their use is based upon evidence of efficacy in the treatment of other forms of severe dermatitis. The use of methotrexate for nummular eczema has been reported in two series of 25 and 28 pediatric patients [28,29]. Complete clearance was observed in 16 and 10 children, respectively, after an average treatment time of 10.5 months.

●Biologic immunomodulators:

•Dupilumab – Dupilumab, an interleukin (IL) 4 and IL-13 inhibitor approved for the treatment of moderate to severe atopic dermatitis, has been reported as effective in several small series of patients with nummular eczema, although it was not clearly defined if the patients included in these reports met the American Academy of Dermatology criteria for atopic dermatitis or were better classified as having idiopathic nummular eczema [30-32]. However, the author has used dupilumab in several patients with idiopathic nummular eczema refractory to multiple treatments (including systemic corticosteroids, methotrexate, and cyclosporine) with disappointing results.

In patients with recalcitrant nummular lesions who meet the American Academy of Dermatology criteria for the diagnosis of atopic dermatitis, dupilumab may be the first-line systemic agent.

PROGNOSIS — Prognosis is excellent in the author's experience, with disease control achieved in nearly all patients who are treated with systemic therapies (see 'Systemic therapies' above). Eventual long-term remission that allows discontinuation of therapy occurs in most patients, although relapses are possible.

SUMMARY AND RECOMMENDATIONS

●Definition – Nummular eczema, also called discoid eczema, is a chronic, inflammatory skin disease characterized by multiple coin-shaped, eczematous lesions (picture 1A). It can be idiopathic or a manifestation of atopic dermatitis. (See 'Introduction' above.)

●Clinical presentation – Nummular eczema typically presents with highly pruritic, round, coin-shaped patches of eczematous dermatitis ranging in diameter from 1 to 10 cm (picture 1B-C). The legs and the upper extremities are the sites most frequently involved. (See 'Clinical manifestations' above.)

●Diagnosis – The diagnosis of nummular eczema is clinical. Patch testing may be helpful in patients with recalcitrant disease and/or a history suggesting allergic contact dermatitis. (See 'Diagnosis' above.)

●Treatment:

•We suggest high- or ultra-high potency topical corticosteroids (groups 1 to 3 (table 1)) as the first-line therapy for nummular eczema (Grade 2C). Topical corticosteroids are applied twice daily for two to four weeks or until resolution of the lesions. (See 'First-line therapy' above.)

•For patients with extensive or recalcitrant disease that does not respond to topical corticosteroids, narrowband ultraviolet B (NBUVB) phototherapy, systemic immunosuppressants, and dupilumab are alternative treatments. (See 'Severe or refractory disease' above.)

●Prognosis – Disease control and eventual cessation of the need for therapy are expected in most patients but may take several years to achieve. Relapses may occur. (See 'Prognosis' above.)