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Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Discoid eczema comprises relatively well-defined, usually multiple, coin-sized plaques. In the acute stages they often weep or ooze; in the chronic phase lesions are discrete, hyperkeratotic, or lichenified. Itching is usual. It primarily affects the limbs (especially the legs), sometimes the trunk, and rarely the face or flexures.
Discoid eczema (nummular dermatitis) has many causes. It is usually idiopathic in older patients, but similar lesions may occur due to contact allergic reactions, as a pattern of hand and foot eczema, in atopic dermatitis (AD), as an ‘id’ eruption related to venous eczema, or locally (e.g., after trauma, insect bite reactions, ‘halo eczema’ around melanocytic nevi, and after breast reconstruction). Discoid eczema has been reported as a manifestation of drug reaction to gold, tumor necrosis factor antagonists, interferon, and retinoids. Comparisons among studies may be limited if the site(s) and etiology are not stated or represent a mixed spectrum.
There are few publications on the pathophysiology of discoid eczema to inform treatment. An association with dry skin (xerosis) is documented, and discoid lesions may appear during treatment with isotretinoin (which reduces sebum secretion). However, dry skin is not consistently present, and the morphology of discoid eczema differs from that of xerosis or asteatotic eczema.
One study suggested that patients with discoid eczema have a degree of xerosis similar to that of age-matched controls but have stronger delayed hypersensitivity to allergens that permeate the skin as a result of scratching. A link with atopy has been proposed, but serum IgE levels are generally normal.
Occult infections (e.g., dental abscess) and infections causing dry skin (e.g., leprosy) have rarely been linked with discoid eczema. Helicobacter pylori has been implicated, but the evidence is weak.
It is difficult to provide specific therapeutic strategies because of the various different causes and the paucity of pertinent publications; most reports are retrospective from individual departments or are anecdotal, rather than formal, trials. The main therapeutic issues are:
Other disorders may need to be excluded, especially mycoses, psoriasis, Bowen disease, mycosis fungoides, and sarcoidosis
A medication and alcohol history should be taken
Patch testing may be useful; metals and medicaments (such as fusidic acid, lanolin, neomycin, and cetostearyl alcohol) are most implicated
The management of discoid eczema is generally similar to that of other eczemas; emollients appear to be helpful due to the link with dry skin
The mainstay of treatment is topical corticosteroids. Severe itch in discoid eczema usually dictates that strong agents are applied; this is safe because the individual lesions are small, rarely affect thin skin sites such as the face or flexures, and usually respond to this approach. Chronic lichenified lesions may respond better to steroid-impregnated tapes or by using a potent steroid with hydrocolloid dressing or paste bandage occlusion
Calcineurin antagonists have been used successfully both as monotherapy and in combination with topical steroids, but trials specifically looking at efficacy in discoid eczema exclusively, rather than atopic eczema generally, are lacking
If weeping is present, the use of soaks (with, e.g., 1 in 10,000 potassium permanganate solution) will help dry lesions up and prevent lesions from sticking to clothes or dressings
Secondary impetiginization, particularly in the exudative phase, is common, and combining with a topical antibiotic or antiseptic , or the use of an oral antistaphylococcal antibiotic , helps
Tar -based treatments and impregnated bandages to minimize the effects of scratching may help
Sedating antihistamines before retiring will help nocturnal scratching and minimize excoriation
Phototherapy and systemic immunosuppressive therapies are usually not required, but there is a literature relating to ultraviolet B (UVB) and methotrexate
Newer drugs such as biological agents (dupilumab) and small molecules such as apremilast and topical PDE 4 antagonists, and Janus kinase (JAK) inhibitors show efficacy in atopic eczema, but specific reports relating to discoid eczema are lacking to date.
Wilkinson SM, Smith AG, Davis MJ, et al. Ann Rheum Dis 1992; 51: 881–4.
Discoid eczematous lesions occur in up to 30% of patients on gold therapy and may be dose related.
Moore MM, Elpern J, Carter DJ. Arch Dermatol 2004; 140: 215–7.
Bruno MC, Vilela MA, Oliveira CA. An Bras Dermatol 2013; 8: 368–75.
Discoid eczema, along with psoriasis, pellagra, and pigmented purpuric eruptions, were felt to be potential indicators of alcoholism.
Iwahira Y, Nagasao T, Shimizu Y, et al. Plast Surg Int 2015, Article ID 209458, 6 pages, 2015. https://doi.org/10.1155/2015/209458.
Almost 3% of postmastectomy reconstructions resulted in peri-wound or breast discoid eczema.
Fleming C, Parry E, Forsyth A, et al. Contact Dermatitis 1997; 36: 261–4.
Retrospective study of persistent and severe discoid eczema; 24 of 48 cases were positive (16 relevant) to rubber chemicals, formaldehyde, neomycin, chromate, and nickel.
Bonamonte D, Foti C, Vestita M, et al. Dermatitis 2012; 23: 153–7.
Nickel, cobalt, and chromate allergy was found in 32% of discoid eczema patients. Irritants may also be relevant as perpetuating factors.
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