Nummular (meaning round or “coin shaped”) dermatitis or eczema (NE) is an inflammatory skin condition characterized by the presence of well-demarcated round-to-oval erythematous plaques. The term nummular dermatitis has been used both as an independent disease and as a description of lesion morphology that can be found in many different diseases, including atopic dermatitis, contact dermatitis, and asteatotic eczema. This discussion focuses on the disease entity that has been described in the literature. Other names have included discoid eczema or orbicular eczema.
Nummular eczema was first described by Deverigie in 1857  as coin-shaped lesions on the upper extremities. Since then, it has been reported in all age groups and in all body areas but is most commonly found on the upper and lower extremities.  Lesions usually start as papules, which coalesce into plaques. They are usually scaly. Early lesions may be studded with vesicles containing serous exudate. Nummular eczema is usually very pruritic. Many precipitating factors have been reported, including dry skin, contact allergies, weather (particularly winter), nutritional issues, and emotional stress.
Nummular dermatitis is a condition confined to the skin.
Little is known about the pathophysiology of nummular eczema, but it is frequently accompanied by xerosis. Like most other forms of dermatitis, the cause is likely to be a combination of epidermal lipid barrier dysfunction and an immunologic response. Dryness of the skin results in leaking of the epidermal lipid barrier; this allows environmental allergens to penetrate the skin and induce an allergic or irritant response. [3, 4] This is supported by one study that showed that elderly patients with nummular dermatitis had increased sensitivity to environmental aeroallergens compared with age-matched controls. This impaired cutaneous barrier in the setting of nummular dermatitis may also lead to increased susceptibility to allergic contact dermatitis to materials such as metals, soaps, and chemicals. 
Nummular eczema has been associated with medications. Any medication that induces dryness of the skin can theoretically initiate nummular eczema, particularly diuretics and statins. Onset of severe, generalized nummular lesions has been reported in association with interferon and ribavirin therapy for hepatitis C. [6, 7] Association with use of inhibitors of tumor necrosis factor has also been reported. 
Onset has also been described in association with mercury in dental amalgams. Hypersensitivity to the metals in the mouth is posulated to be sufficient to drive an immune response that results in cutaneous nummular plaques.
Because of the intense pruritus associated with nummular eczema, the potential role of mast cells in the disease process has been investigated. Increased numbers of mast cells have been observed in lesional compared with nonlesional samples in persons with nummular dermatitis.
One study identified neurogenic contributors to inflammation in both nummular eczema and atopic dermatitis by investigating the association between mast cells and sensory nerves and identifying the distribution of neuropeptides in the epidermis and upper dermis of patients with nummular eczema. Researchers hypothesized that release of histamine and other inflammatory mediators from mast cells may initiate pruritus by interacting with neural C-fibers. The research showed that dermal contacts between mast cells and nerves were increased in number in both lesional and nonlesional samples of nummular eczema compared with normal controls. In addition, substance P and calcitonin gene-related peptide fibers were prominently increased in lesional samples compared with nonlesional samples from patients with nummular eczema. These neuropeptides may stimulate release of other cytokines and promote inflammation. [9, 10, 11]
Other research has demonstrated that mast cells present in the dermis of patients with nummular eczema may have decreased chymase activity, imparting reduced ability to degrade neuropeptides and protein. This dysregulation could lead to decreased capability of the enzyme to suppress inflammation.
Colonization of with Staphylococcus aureus has been described both on lesional skin and in the nares of patients and their close contacts.  Whether this is important in the precipitation of disease has yet to be determined.
The etiology of nummular dermatitis is unknown and likely multifactorial. Most patients with nummular eczema also have very dry (xerotic) skin. Local trauma, such as arthropod bites, contact with chemicals, or abrasions, may precede an outbreak.
Contact dermatitis may play a role in some cases. Contact dermatitis may be irritant or allergic in nature. Sensitivity to nickel, cobalt, or chromates has been reported in patients with nummular dermatitis. In one study, the most frequent sensitizers were colophony, nitrofurazone, neomycin sulfate, and nickel sulfate. In the past, 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 (ie, lesional spread from the initial focal site) may account for the presence of multiple plaques.
Onset of severe, generalized nummular lesions has been reported in association with interferon therapy for hepatitis C as well as exposure to mercury. 
Various types of eczematous eruptions, including nummular eczema, have been observed following tumor necrosis factor-alpha–blocking therapy. 
Nummular eczema has been found in association with infection in rare cases. Giardiasis has been reported.  One study reported that in patients with Helicobacter pylori infection and nummular dermatitis, eradication of H pylori caused clearance of the skin lesions in 54% of the patients.  Another case report noted nummular eczema in association with a dental infection that cleared after the treatment of the infection. 
No racial predilection has been observed.
Nummular eczema is more common in males than in females (see Age below).
Nummular eczema has two peaks of age distribution. The most common is in the sixth to seventh decade of life. This is most often seen in males. A smaller peak occurs in the second to third decade of life, which is most often seen in association with atopic dermatitis. This is more often seen in females, by two thirds in one study.  It is uncommon in children. 
Nummular eczema tends to be a chronic condition that remits and relapses. Patients need to be informed that once nummular dermatitis develops, it is often recurrent. Avoidance of exacerbating factors and close attention to moisturizing the skin may help reduce the frequency.
Pruritus, often worst at night, may cause irritability, insomnia, or both.
Secondary infection may result in lesions that ooze serosanguineous exudate. The most common organism revealed by culture is Staphylococcus aureus.
Generalized flares may require systemic antibiotics and/or systemic steroids.
Increased contact sensitivity to environmental antigens (especially metals) could limit ability to tolerate those antigens, especially clothing, metal snaps, jewelry, dental amalgams or occupational exposure.
Patients must be educated about the most important predisposing condition to nummular eczema—dry skin. Use of gentle soaps and copious application of moisturizers, especially while the skin is still damp after bathing, is imperative. Once the lesions develop, use of topical steroids or calcineurin inhibitors helps with the itch and hastens resolution.
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Jami L Miller, MD Assistant Professor, Division of Dermatology, Department of Internal Medicine, Vanderbilt University Medical School; Director of Phototherapy Unit, Vanderbilt University Medical Center; Consulting Attending Physician, Nashville Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Disclosure: Nothing to disclose.
Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine
Disclosure: Nothing to disclose.
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
John D Wilkinson, MD, MBBS, MRCS, FRCP Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK
Disclosure: Nothing to disclose.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Khristina Collins, MD, and Lloyd King, MD, to the development and writing of this article.
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