Nummular dermatitis


Nummular or discoid dermatitis or eczema.

Also known as discoid eczema or nummular dermatitis.

An inflammatory skin disorder characterized by multiple, pruritic, well-demarcated, coin-shaped or oval plaques with a well-defined border.

The reported prevalence varies widely from 0.1% to 9%.

The condition is rare in the first year of life, and thereafter the incidence increases with age.

The age at onset peaks between 15 and 25 years, and again between 55 and 65 years.

The condition is slightly more common in males than in females.

There is no racial predilection.

Pathogenesis is likely multifactorial.

The neuropeptides substance P, calcitonin gene-related peptide, and mast cells are more frequent in the epidermis and papillary dermis in patients with nummular eczema.

The increase in the neuropeptides substance P and calcitonin gene-related peptide, might stimulate keratinocytes to release cytokines, which enhance inflammation.

Infections, in particular Staphylococcus aureus infection, might play a role through a hypersensitivity mechanism.

Helicobacter pylori infection has also been implicated in the pathogenesis in some cases.

More frequent in persons with atopy and can develop after contact with nickel, chromate, cobalt, fragrances, wool, soaps, rubber, thimerosal, formaldehyde, or topical medications.

It is exacerbated by conditions that promote xerotic skin:frequent bathing, low humidity, windy environments, and the winter season.

Xerotic skin allows permeation of the epidermis with environmental allergens that may induce an allergic or irritant response.

Medications such as isotretinoin, streptomycin, isoniazid, interferon, ribavirin, tumor necrosis factor inhibitors, and methyldopa have also been implicated in the pathogenesis.

A potential complication of breast reconstruction with tissue expanders and silicone implants.

Emotional stress can precipitate or exacerbate the process.

Other predisposing factors include alcohol or tobacco, local trauma, venous stasis, and edema of the lower limbs.

It may be a sign of an internal pathologic condition such as pernicious anemia or diabetes mellitus.

Acute stage histologic changes include intercellular edema, intraepidermal vesicles, and perivascular lymphocytic infiltration.

Chronic changes include hyperkeratosis, acanthosis, an increase in the granular cell layer, and hyperplasia of the epidermis.

Characterized by sharply defined, coin-shaped to oval, erythematous, eczematous plaques.

The initial lesions are uniform groups of erythematous papules and vesicles.

Over time and with scratching, become inflamed and might weep.

The lesions enlarge to form the discrete, round or oval, erythematous, scaly, lichenified, hyperkeratotic, and hyperpigmented plaques that are typical of chronic nummular eczema.

The size of the lesion varies from 1 to 10 cm in diameter.

The lesions are usually symmetric and pruritic.

Sites of predilection include the lower extremities, followed by the upper extremities, although the lesion may also occur on the trunk, neck, and face.

The diagnosis is mainly clinical based on the characteristic features

Biopsy or laboratory tests are generally not necessary for diagnosis.

Must be distinguished from tinea corporis, impetigo, plaque psoriasis, granuloma annulare, allergic contact dermatitis, atopic dermatitis, and stasis dermatitis.

Crusting surface, lack of central clearing, typical locations of the lesions, and past history of atopic dermatitis help distinguish lesions from tinea corporis.

Impetigo is characterized by a thick, golden-yellow crust.

The scales in nummular eczema are thin and sparse

Negative impact on health-related quality of life is due to pruritus, discomfort, esthetic concerns, social embarrassment, lower esteem, impairment of performance.

Secondary bacterial infection, especially with S aureus, may occur.

Patients are at increased risk of developing allergic contact dermatitis.

Chronic lesions that are scratched may develop lichen simplex chronicus.

An inflammatory skin disorder characterized by multiple, pruritic, well demarcated, coin shaped or oval plaques with a well-defined borders.

Prevalence varies widely from 0.1-9%.

The process is slightly more common in males and is without racial predilection.

The next highest incidence is in girls and women aged 10 to 30, in whom it is frequently associated with atopic dermatitis.

The condition often flares in the fall and winter when the ambient temperature and humidity level drop.

Chronic relapsing inflammatory skin disorder of unknown ideology.

Typically occurs on the lower leg.

Lesions are typically highly pruritic, coin shaped, and often characterized by an erythematous exudative plaque with crust and dry plaque in later stages with thin scale.

Can affect any part of the body.

Patches appear and may persist for weeks or months.

Worse in winter months.

Can occur at any age, with the highest incidence in young adulthood and older adults.

Aggravated by alcohol, aeroallergens, and emotional stress.

The skin between the patches is often xerotic and marked by fine scale.

Most patches or plaques range from a few millimeters to several centimeters in diameter.

Most lesions are round or oval, and are typically pink, red, or brown in color.

Lesions are purplish in color in dark skinned people.

Lesions are usually well defined.

The skin surface of the may be dry, cracked, eroded, blistered, and crusted.

Initially, vesicles occur on the surface of the patches.

Lesions can be highly pruritic.

Lesions often resolve completely, but in darker skinned individuals postinflammatory hyperpigmentation or hypopigmentation may persist for months.

Diagnosis is a clinical one.

Differential diagnosis includes: tinea corporis, psoriasis, contact dermatitis, cancer, pityriasis rosea, asteatotic eczema and atopic dermatitis.

Can be treated and cleared successfully over a few weeks.

The course can be chronic and characterized by relapses and remissions in some cases.

Avoidance of precipitating factors, and underlying condition, if identified, should be treated.

Hydration of the skin improved the dryness, pruritus and restores the disturbed skin’s barrier function.

Daily baths in lukewarm water, followed by gently patting rather than rubbing the skin dry, are helpful.

A quality moisturizer, emollient, or barrier cream should be used to keep the skin soft and well hydrated and to prevent transepidermal water loss.

Topical corticosteroids are the mainstay of therapy.

Topical immunomodulators such as tacrolimus and pimecrolimus are not as fast or effective as potent topical corticosteroids.

Patients with generalized severe or refractory disease may require treatment with narrowband UV-B phototherapy, systemic corticosteroids, systemic methotrexate, or systemic cyclosporine

Although pruritus in nummular eczema does not appear to be mediated by histamine release, oral antihistamines can provide symptomatic relief to some patients because of their sedative properties and may be effective for intense pruritus that is refractory to moisturizers and conservative measures.

Of the H1 antihistamines, hydroxyzine is more effective than diphenhydramine and cyproheptadine

Treatment involves keeping the skin moist.

A home humidifier may be and helpful, and patients should apply moisturizer to damp skin after showering.

Treatment of nummular dermatitis is primarily with emollients and topical corticosteroids.

Emollients include bath oils, soap substitutes, and moisturizing creams applied to the affected area to relieve itching, scaling, and dryness.

Topical corticosteroids help relieve inflammation.

Oral corticosteroids and UV light phototherapy are reserved for severe cases.

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