Nummular eczema

<p>Review of the causes, clinical findings, and treatment of nummular eczema.</p>

Review of the causes, clinical findings, and treatment of nummular eczema.

Nummular eczema (dermatitis) is characterized by pruritic round erythematous plaques most commonly on the legs.  It is usually accompanied by xerosis; impaired skin continuity apparently leads to eczematous changes via irritants and allergens leading to inflammation and eczematization. 

Early lesions, particularly vesicular ones, often become colonized by staphylococci, producing a yellow-brown crust and serosanguineous exudate. The most common organism cultured is Staphylococcus aureus.  Secondary infection may occur, leading to cellulitis.

The prevalence is 2 cases per 1000 persons.  It is more common in males than in females and has a bimodal age distribution.  Males in the sixth to seventh decade and a lesser incidence in females in the second to third decade.  It is rare in children.

Nummular eczema is often recurrent.  Avoidance of exacerbating factors and diligent skin moisturizing may help reduce the frequency of recurrence.

Patients usually present with weeks to years of persistent waxing and waning plaques.  Exacerbations are often noted in winter (cold and dry climates).  It may improve with sun or humidity exposure.  Lesions often recur in the same locations as before.  Associated conditions include eczema, atopic dermatitis, and sensitive skin.

Physical exam
Frequently symmetrical, characteristic round-to-oval erythematous plaques may have figurate crusts within the plaques.  Nummular eczema occurs most commonly on the legs, but may occur on the arms, trunk, hands, and feet.  It does not involve the face and scalp. 

Lesions begin as erythematous-to-violaceous papules or vesicles, which coalesce to form confluent plaques. They may have overlying erosions due to excoriation. Within a few days, plaques become dry, scaling, and more violaceous, particularly when located below the knee.

The lesions then flatten to patches, usually with brown post-inflammatory hyperpigmentation that gradually lightens.  The pigment may not completely fade, particularly in darker patients and when located below the knee.

Differential diagnosis

Distinguishing between forms of dermatitis (eg, asteatotic eczema, atopic dermatitis, nummular dermatitis) may be difficult, but is not necessary to make treatment decisions.

  • Contact dermatitis may have a pattern that approximates the way the offending agent came into contact with the skin, such as a linear pattern.  It may become chronic in the setting of repeated exposure, such as with chromates and formaldehyde. The patient may recall contact with an allergen, such as poison ivy.
  • Cutaneous T cell lymphoma occurs most often on “double covered” areas of the body.  Biopsy may be necessary to rule out CTCL, and will show Pagetoid spread of lymphocytes.
  • Fixed drug eruption does not exhibit infection, exudates, or vesicles.  It is typically blue-gray, and occurring on the trunk.
  • Lichen simplex chronicus often occurs on the lower legs, the neck, the scalp, or the scrotum; it is lichenified (thickened by chronic scratching), more violaceous, and has no clear border.
  • Stasis dermatitis may occur simultaneously on the lower extremities, and is wideapread and accompanied by edema.
  • Psoriasis plaques are often found on the extensor surfaces, especially at the elbows and knees.  The scalp is often involved.  Psoriasis scale is usually silver,  thick, micaceous, and the underlying skin bleeds when scale is removed (Auspitz sign).
  • Tinea corporis plaques may show central clearing, making clinical differentiation difficult.  Tinea corporis usually has few vesicles, a raised, well-defined rolled border, and leading scale (ie, scale on the exterior of the plaque).

Nummular eczema is idiopathic and likely multifactorial.  Most patients have xerosis.  Local trauma (abrasions, arthropod bites, chemical contact) may precede an outbreak. Contact dermatitis (allergic or irritant) may play a role.  In a recent study, the most frequent sensitizers were colophony, nitrofurazone, neomycin sulfate, and nickel sulfate.  Sensitivity to cobalt and chromates has been reported.  Cases of nummular eczema–like eruptions have been caused by ethyl cyanoacrylate–containing glue, thimerosal, mercury-containing dental amalgams, and depilating creams containing potassium thioglycolate.

Venous insufficiency (and varicosities), stasis dermatitis, and edema may be related to involvement of the affected lower extremities.  Autoeczematization may partly account for cases of multiple plaques.

Laboratory Studies
Tinea corporis can be excluded by scraping scale from the lesion and microscopically examining a potassium hydroxide preparation.  A swab culture may be helpful in cases suggestive of impetiginization.  As methicillin-resistant Staphylococcus aureus becomes more common, appropriate antibiotics should be chosen for therapy of secondarily infected lesions.

A skin biopsy (4 mm punch) may be performed, but is usually not necessary.  Findings are nonspecific, but may help differentiate nummular dermatitis from fixed drug eruption, cutaneous T-cell lymphoma, tinea corporis, and psoriasis.

Patch testing may be helpful; up to 50% of patients with nummular eczema may have positive patch test reactions.

Histologic Findings

Biopsy findings reflect lesion evolution.  In early stages, a nonspecific infiltrate is present with spongiosis, vesicles, and a predominant lymphocytic infiltrate.  Eosinophils may be found in the papillary dermis.  Chronic lesions demonstrate epidermal hyperplasia, hyperkeratosis, and a pronounced granular cell layer.  The papillary dermis may be fibrotic, with a perivascular infiltrate of lymphocytes and monocytes.

Lymphocytes are predominately CD8+ in the epidermis and CD4+ in the dermis. Mast cell–derived interleukin 4 appears to be involved in activation of the T lymphocytes.

Medical Care
Treatment is aimed at re-hydration of the skin, treatment of infection, and reduction of inflammation.  Application of topical preparations to damp skin allows more effective penetration and faster healing.  Ointments are usually more effective than creams because they are more occlusive, forming a barrier between the skin and the environment, and more effectively hold moisture in the skin.

Lukewarm or cool baths or showers reduce itching and help re-hydrate the skin. Patients should be instructed to bathe, then while their skin is still moist, apply moisturizers or medicated topicals.  The "soak-and-smear" therapeutic regimen is a 20-minute plain water soak each night followed by application of steroid ointment to moist skin.  Soap should be used for cleansing only on the axillae and groin. 

Topical steroids are effective when applied 2-3 times daily.  They are most effective when used in ointment form and applied to damp skin.

Less erythematous, less pruritic lesions may be treated with low-potency (class III-VI) steroids. Severely inflamed lesions with intense erythema, vesicles, and pruritus require high-potency (class I-II) preparations.  Penetration of the medication is enhanced by occlusion or presoaking in a tub of plain water followed immediately (without drying) by application of the steroid-containing ointment.  Once lesions improve, a lower-potency steroid or moisturizer should be prescribed to avoid skin atrophy.

Severe or generalized flares may be treated with tap water–moistened dressings on top of the steroid ointment.  Oral or intramuscular steroids may be required in cases of severe eruptions.
Use of sedating antihistamines at night helps reduce itching and improve sleep.
If the patient has an overt infection, a combination of a topical antibiotic and a steroid ointment applied twice daily is usually effective. This therapy decreases inflammation and colonization by staphylococci.  Oral antibiotics, such as cephalexin, dicloxacillin, or erythromycin should be used in cases of secondary infection (cellulites).

Oral antihistamines or sedatives may help reduce itching and improve sleep.

Tar preparations are helpful to decrease inflammation, particularly in older, thickened, scaly plaques.  Patients should be advised that tar can stain clothing.

Once the eruption has resolved, ongoing aggressive hydration may decrease the frequency of flares, particularly in dry climates.  Heavy moisturizers (preferably a sensitive-skin formulation) or petroleum jelly applied to damp skin after showering may be helpful.

Activities that heat or dry the skin worsen the pruritus and the eruption.
Sunlight or phototherapy may be beneficial, particularly in chronic cases. Ultraviolet radiation helps reduce the inflammatory activity within the skin. The risk of heat worsening the pruritus and of ultraviolet light inducing cutaneous malignancies must be weighed against the potential benefits.

Aggressive hydration of the skin may decrease the frequency between eruptions.
Hot water bathing should be avoided.  Patients should use mild, nondrying cleansers.  Emollients should be used immediately after bathing. The skin may be patted dry, and the emollient should be applied before the skin is completely dry. Clothing should be loose to avoid overheating, and irritating fibers, such as wool, should be avoided.  A room humidifier is useful, particularly when a heater or air conditioning is used.

Lesions may become secondarily infected.  Heavily excoriated or infected lesions may leave permanent scars.  Lesions on the lower extremities may be slow to resolve and may leave permanent brown patches, especially in darker pigmented skin (Fitzpatrick III-VI).

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