Nummular (ie, round or coin-shaped) dermatitis (nummular eczema) is an inflammatory skin condition characterized by the presence of well-demarcated round-to-oval erythematous plaques. Since its first description by Deverigie in 1857, it has been reported in all age groups and in all body areas, but it is most commonly found on the upper and lower extremities.[1]
The term nummular dermatitis has been used both as a label for 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 independent disease entity described in the literature. Other names that have been used for this condition include diskoid eczema and orbicular eczema.
Signs and symptoms
The lesions most often start as papules, which coalesce into plaques; they are usually scaly. Early lesions may be studded with vesicles containing serous exudate. Nummular eczema usually is highly pruritic. Many precipitating factors have been reported, including dry skin, contact allergies, weather (particularly winter), nutritional issues, and emotional stress.
Workup
Tinea corporis should be excluded by scraping and microscopically analyzing a potassium hydroxide preparation of a lesion.
For lesions that have erythema spreading away from the lesions, suggesting cellulitis, swab culture of the exudate may be helpful. First-generation cephalosporins are still usually effective first-line treatment. As methicillin-resistant Staphylococcus aureus (MRSA) becomes more common in a community, the culture results help in the choice of appropriate antibiotic therapy for treatment-resistant cases of documented secondarily infected lesions.
If the history is suggestive of infection, a workup for infection (eg, with Helicobacter pylori or Giardia) should be considered.
Management
Treatment includes moisturizers and topical steroids. If there is an overt infection, a combination of a topical antibiotic and a steroid ointment may be used. Nighttime use of antihistamines can help with sleep. Severe or generalized flares may be treated with dressings on top of the steroid ointment. Oral or parenteral steroids may be used in severe flares, followed by topical therapy. Oral antibiotics, such as dicloxacillin, cephalexin, or erythromycin, should be used in cases of secondary infection.
Little is known about the pathophysiology of nummular eczema, but as with most other forms of dermatitis, the cause is likely to be a combination of epidermal lipid barrier dysfunction and an immunologic response.
Nummular eczema is known to be frequently accompanied or preceded by xerosis. Dryness of the skin results in "leaking" of the epidermal lipid barrier; this allows environmental allergens and bacteria to penetrate the skin and induce an allergic or irritant immune response.[2] A study by Aoyama et al showed that elderly patients with nummular dermatitis were more sensitive to environmental aeroallergens than age-matched control subjects were.[3] This impaired cutaneous barrier in the setting of nummular eczema may also lead to increased susceptibility to allergic contact dermatitis to materials such as metals, soaps, and chemicals.[1]
Nummular eczema has been associated with medications. Theoretically, it can be initiated by any medication that induces dryness of the skin, particularly diuretics and statins. the onset of severe, generalized nummular lesions has been reported in association with interferon and ribavirin therapy for hepatitis C.[4, 5] Other medications that influence immune response may also induce nummular eczema, including tumor necrosis factor (TNF) inhibitors[6] and guselkumab.[7]
Nummular eczema can occur after surgery. A review of 1662 Japanese women found that nummular eczema developed in almost 3% of patients undergoing breast reconstruction, presumably due to surgical cleansers or bandage tape.[8] Kost et al reported two cases of nummular eczema developing as a postoperative complication of total knee arthroplasty in elderly women.[9]
The onset of nummular dermatitis 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 samples as 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.[10] Researchers hypothesized that release of histamine and other inflammatory mediators from mast cells might initiate pruritus by interacting with neural C-fibers. The number of dermal contacts between mast cells and nerves was increased in both lesional and nonlesional samples from patients with nummular eczema as compared with normal control subjects.
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.[10] These neuropeptides may stimulate release of other cytokines and promote inflammation.
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.[11] This dysregulation could lead to decreased capability of the enzyme to suppress inflammation.
Colonization of the skin with S aureus has been described both on lesional skin and in the nares of patients and their close contacts.[12] Whether this is important in the precipitation of disease remains to be determined.
The etiology of nummular eczema is unknown and likely multifactorial. Most patients with nummular eczema also have very dry (xerotic) skin. Local trauma (eg, from 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,[13] and depilating creams containing potassium thioglycolate.[14]
Venous insufficiency (and varicosities), stasis dermatitis, and edema may be related to the development of nummular eczema on the affected lower extremities.
Autoeczematization (ie, lesional spread from the initial focal site) may account for the presence of multiple plaques.
The onset of severe, generalized nummular lesions has been reported in association with interferon therapy for hepatitis C, as well as exposure to mercury.[4, 5] Various types of eczematous eruptions, including nummular eczema, have been observed following TNF-α–blocking therapy,[6] and nummular dermatitis has also been reported after treatment of psoriasis with guselkumab.[15]
Nummular eczema of the breast has reported in breast cancer patients undergoing mastectomy with subsequent breast reconstruction.[16, 17] In the majority of these patients, this condition developed after the insertion of tissue expanders or breast implants, which suggested that stretching of the skin might play a role in causing it.
In rare cases, nummular eczema has been found in association with infection. It has been reported as a manifestation of giardiasis.[18] In a study that included patients with H pylori infection and nummular eczema, eradication of H pylori led to clearance of the skin lesions in 54% of cases.[19] A case report by Tanaka et al described nummular eczema occurring in association with a dental infection that cleared after the treatment of the infection.[20]
In children, nummular eczema occurs most frequency in association with atopic dermatitis.[21]
The prevalence of nummular eczema is two cases per 1000 people. Dermatitis in general (eg, atopic, asteatotic, dyshidrotic, nummular, hand) is one of the most common of dermatologic conditions.
Nummular eczema has two peaks of age distribution. The larger peak is in the sixth and seventh decades of life, more often involving males. A smaller peak is in the second and third decades, usually in association with atopic dermatitis and more often involving females (by two thirds, in one study).[22] Although nummular eczema can also occur in children, this is uncommon.[23]
Overall, nummular eczema is more common in males than in females.
No racial predilection has been established; however, in children, nummular dermatitis appears to be more common in those with skin of color.[21]
Nummular eczema tends to be a chronic condition that remits and relapses.
Pruritus, often worst at night, may cause irritability, insomnia, or both. Secondary infection may result in lesions that ooze serosanguineous exudate; the organism most commonly revealed by culture is S aureus. Generalized flares may require treatment with systemic antibiotics, systemic steroids, or both.
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 should be informed that once nummular eczema develops, it is often recurrent. Avoidance of exacerbating factors and close attention to moisturizing the skin may help reduce the frequency of recurrences.
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.
For patient education resources, visit the Skin Conditions and Beauty Center. Also, see the patient education article Eczema.
Patients with nummular dermatitis (nummular eczema) present with days to months, or even years, of a pruritic eruption, which usually starts on the legs; the eruption may also burn or sting.
Nummular eczema often waxes and wanes with winter; cold or dry climates or swings in temperature may be exacerbating factors. It may improve with sun or humidity exposure or with moisturizer use. Occasionally, it may worsen with heat or humidity.
Recurrent nummular eczema lesions often occur in the same locations as previous lesions.
The patient's medical history may be positive for eczema, atopic dermatitis, or dry and sensitive skin.
The diagnosis of nummular eczema is made on the basis of observing the characteristic round-to-oval erythematous plaques (see the image below). These plaques are most commonly located on the extremities (particularly the legs) but may occur anywhere on the trunk, hands, or feet[24] ; nummular eczema does not usually involve the face or scalp. Lesions are often symmetrically distributed. Plaques may be several centimeters in diameter.
View Image
Dry, scaling plaque of nummular dermatitis (size, 3 X 5 cm) on shin.
The lesions begin as erythematous-to-violaceous papules or vesicles, which then coalesce to form confluent plaques. They may have overlying erosions due to excoriation.
Early lesions, particularly vesicular ones, often become colonized by staphylococci, which produces a yellowish crust. Secondary overt infection may occur, with cellulitis surrounding the plaques, requiring oral antibiotics.
Within a few days, plaques become dry, scaly, and more violaceous, particularly when located below the knee.
The lesions then flatten to macules, usually with brown postinflammatory hyperpigmentation that gradually lightens. The pigment may never completely fade, particularly when located below the knee.
Lesions may demonstrate the yellow crusting of secondary impetiginization. Older plaques typically show scale that trails the lesional border.
Plaques may show central clearing, making it difficult to differentiate them from tinea corporis on the basis of clinical findings. Tinea corporis usually has few vesicles, a raised narrow border, and leading scale (ie, scale on the outside of the plaque).
Distinguishing the various forms of dermatitis (eg, asteatotic eczema, atopic dermatitis, nummular eczema) from each other may be difficult, but fortunately, this is not necessary for making proper treatment decisions.[25] Contact dermatitis may have a pattern that approximates the manner in which the offending agent came into contact with the skin (eg, a linear pattern). It may become chronic in the setting of repeated exposure (eg, with chromates and formaldehyde). The patient may recall contact with an allergen, such as poison ivy.
Longstanding lesions that have been aggressively scratched may develop lichen simplex chronicus. This often occurs on the lower legs, neck, scalp, or scrotum. The typical erythema of nummular eczema becomes violaceous and thickened. Although the border of lichenified lesions remains well demarcated, it may become less so in some areas, particularly on the genitalia. Postinflammatory hyperpigmentation may occur, especially with involvement of the lower leg.
Stasis dermatitis may occur simultaneously on the lower extremities, and venous stasis may lead to the concomitant development of both conditions.
Nummular eczema lesions may become secondarily infected. Heavily excoriated or infected lesions may leave permanent scars. Lesions on the lower extremities take a long time to heal and may leave permanent brown macules. Cellulitis may occur but is rare. Particularly pruritic cases may result in difficulty sleeping and concentrating.
A skin biopsy may be performed. The findings are nonspecific, but they may help differentiate nummular dermatitis (nummular eczema) from tinea corporis, psoriasis, a fixed drug eruption, or cutaneous T-cell lymphoma.
Some studies have recommended patch testing in patients with refractory nummular dermatitis. One study found that 50% of 56 patients with nummular eczema showed positive reactions on patch testing,[26] and other research identified positive patch testing in 23 of 50 patients with nummular dermatitis.[27] A 2012 study strongly recommended patch testing in nummular dermatitis, finding that 332 (32.5%) of 1022 patients with nummular dermatitis had positive patch test results for one or more allergens.[1]
Biopsy findings mirror the evolution of the lesion. In the early stages, a nonspecific infiltrate is present with spongiosis, vesicles, and a predominant lymphocytic infiltrate. Eosinophils may be observed in the papillary dermis. Chronic lesions demonstrate epidermal hyperplasia, hyperkeratosis, and a pronounced granular cell layer. The papillary dermis may be fibrotic, with a perivenular infiltrate of lymphocytes and monocytes.
Lymphocytes are predominately CD8+ in the epidermis and CD4+ in the dermis. Mast cell–derived interleukin (IL)-4 appears to be involved in activation of the T lymphocytes.
Treatment of nummular dermatitis (nummular eczema) is aimed at rehydration of the skin, repair of the epidermal lipid barrier, reduction of inflammation and treatment of any infection.
Hydration of the skin is the most important factor in treating nummular eczema.
To reduce inflammation, a topical steroid is applied to the affected areas several times daily. Once lesions improve, a lower-potency steroid or moisturizer should be prescribed to avoid skin atrophy.
Severe or generalized flares may be treated with tapwater-moistened dressings on top of the steroid ointment. Oral or parenteral steroids may be used in severe flares, followed by topical therapy.
If the patient has an overt infection, a combination of a topical antibiotic and a steroid ointment should be applied twice daily. In cases of secondary infection, oral antibiotics should be used .
Mindfulness-based therapies, including meditation and hypnotherapy, have also been reported to be helpful.[28]
Use of sedating antihistamines at night helps with sleep.
Use of hypoallergenic, fragrance-free creams, lotions, or ointments is the first step in therapy. The medications and emollients employed for this purpose are best absorbed by dampening the skin first.
Lukewarm or cool baths or showers reduce itching and help rehydrate the skin; a gentle soap or liquid cleanser may be used. Skin should be patted dry and then moisturizers are applied to still-damp skin. The "soak-and-smear" therapeutic regimen includes a 20-minute plain water soak each night followed by application of steroid ointment or petrolatum to wet skin, along with alteration of cleansing habits so that soap is applied only to the axilla and groin. One study showed greater than 90% response in 27 of 28 patients with refractory chronic pruritic eruptions when the regimen was followed as directed.[29]
Wet wrap treatments are often helpful. This involves dampening the skin with lukewarm water until it is well hydrated (usually 10 min). Then, petrolatum or steroid ointment is applied liberally, followed by occlusion for 1 hour with damp pajamas or a nonbreathable sauna suit. For small areas of involvement, plastic wrap may be used to occlude the area. This process may be repeated five or six times a day with petrolatum. Caution must be used when prescription steroid medications are used; overuse of these medications can cause striae, thinning of the skin, and, rarely, enough systemic absorption of steroid to affect the hypothalamic-pituitary-adrenal axis.
Topical application of steroids is the therapy most commonly used to reduce inflammation. 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.
Ointments are usually more effective than creams because they are more occlusive, form a barrier between the skin and the environment, and more effectively hold water into the skin. However, patients may be more likely to use a cream formulation; education and discussion is key to patient compliance.
In cases of severe, generalized eruptions, oral, intramuscular, or parenteral steroids may be required.
Tar preparations are helpful for decreasing inflammation, particularly in older, thickened, scaly plaques.
Topical immune modulators (tacrolimus and pimecrolimus) also reduce inflammation.[30] These are often initiated a few days after the topical steroid to decrease the risk of a burning sensation that may occur when applied to extremely irritated skin.
Other topical treatments that are currently approved for atopic dermatitis may be helpful, including crisaborole and topical ruxolitanib, though data specifically for nummular eczema are lacking.
When eruptions are generalized and prolonged, more aggressive therapy is warranted. Systemic steroids have long been a mainstay for the treatment of dermatitis, including nummular eczema, though they should be used only in short courses and only when topical treatment has been insufficient. Cyclosporine A has been used as an alternative to systemic steroids; however, its use requires monitoring of blood pressure and renal function.
Phototherapy (generally with ultraviolet [UV] B) may be helpful.[31] Broadband or narrowband UVB is most commonly used, though psoralen plus UVA (PUVA) may be used in severe cases.
Oral immunosuppressive agents may help to attenuate the immune response; methotrexate has been used successfully in children with nummular eczema.[32, 33] Data are lacking for other immunosuppressants such as azathioprine and mycophenolate mofetil in the treatment of nummular eczema, though these medications have been used in other forms of dermatitis.
Dupilumab, a monoclonal antibody targeting interleukin (IL)-4 and IL-13, has also been successfully used to treat nummular eczema.[34, 35] The phosphodiesterase-4 (PDE4) inhibitor roflumilast has been used off label to treat this condition as well.[36, 37] Treatment with Janus kinase (JAK) inhibitors has not been reported, but given the success of these medications in cases of atopic dermatitis, it is reasonable to think that they may prove to have a role in treating extremely refractory cases of nummular eczema.
Oral antihistamines or sedatives may help reduce itching and improve sleep. Topical antihistamines are known to be potent topical sensitizers; therefore, preparations containing topical diphenhydramine in particular should not be used. Oral gabapentin and pregabalin, as well as opioid receptor antagonists, may be more efficacious in treating itching due to nummular eczema.[38]
Topical antibiotics (eg, mupirocin) may help with impetiginization. Neomycin- or bacitracin-containing medications are potent topical sensitizers and therefore should be avoided. Oral antibiotics (eg, dicloxacillin, cephalexin, or erythromycin) should be used in cases of secondary infection. Swab cultures of the skin guide selection of antibiotics.
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.
Disease may be severe and refractory to the above treatments. Immune-suppressive medications have been described as safe and effective in severely affected patients.
Activities that heat or dry the skin worsen the pruritus and the eruption. Resting in a cool, moist environment is therapeutic. Heat, soap, drying conditions, and irritating activities should be avoided. Extreme cold may also exacerbate nummular eczema.
Sunlight or phototherapy may be beneficial, particularly in chronic cases. UV radiation helps reduce the inflammatory activity within the skin. The risks of heat worsening the pruritus and of UV light inducing cutaneus malignancies must be weighed against the potential benefits.
Aggressive hydration of the skin may decrease the frequency of nummular dermatitis eruptions.
Bathing is permissible, but hot water should be avoided. Patients should use mild, nondrying cleansers. They should be encouraged to use nonsoap cleansers only for control of body odor and for cleanliness (eg, on the groin, axillae, and feet). Oil additives may be used in bathing water. To avoid drying of the lesions, an emollient should be used immediately after bathing. The skin may be patted and the emollient applied before the skin is completely dry. Clothing should be loose to avoid overheating, and irritating fibers (eg, wool) should be avoided.
A room humidifier is useful, particularly when a heater or air conditioning is used.
What is nummular dermatitis?How is nummular dermatitis characterized?What kind of condition is nummular dermatitis?What is the pathophysiology of nummular dermatitis?What is the relationship between nummular dermatitis and medication?What is the relationship between nummular dermatitis and the mercury in dental amalgams?What is the role of mast cells in the pathophysiology of nummular dermatitis?What is the role of neurogenic mechanisms in the pathophysiology of nummular dermatitis?What is the role of mast cell dysfunction in the pathophysiology of nummular dermatitis?What is the role of Staphylococcus aureus in the pathophysiology of nummular dermatitis?How common is nummular dermatitis?Does nummular dermatitis have a racial predilection?Does nummular dermatitis have a sexual predilection?Does nummular dermatitis have an age predilection?What is the prognosis of nummular dermatitis?How do secondary infections affect the prognosis of nummular dermatitis?How are generalized flares managed in nummular dermatitis?How does increased sensitivity to environmental antigens affect the prognosis of nummular dermatitis?What should patients know about nummular dermatitis?What causes nummular dermatitis?What is the role of contact dermatitis in the etiology of nummular dermatitis?What is the role of venous insufficiency, varicosities, stasis dermatitis, and edema in the etiology of nummular dermatitis?What is the role of autoeczematization in nummular dermatitis?What other uncommon factors may play a role in the etiology of nummular dermatitis?What are common features of a patient's medical history in nummular dermatitis?How long do pruritic eruptions last with nummular dermatitis?What factors cause the fluctuation of nummular dermatitis symptoms?Where do recurrent nummular dermatitis lesions occur?How is nummular dermatitis diagnosed?What is the clinical course of nummular dermatitis?How are older nummular dermatitis plaques characterized?How is nummular dermatitis differentiated from tinea corporis?How is nummular dermatitis distinguished from other forms of dermatitis?How can nummular dermatitis lead to lichen simplex chronicus?How does stasis dermatitis manifest in patients with nummular dermatitis?What are the possible complications of nummular dermatitis?What are the differential diagnoses for Nummular Dermatitis (Nummular Eczema)?How are lab studies used to exclude tinea corporis in the workup of nummular dermatitis?Which lab studies are indicated for lesions with spreading erythema in the workup of nummular dermatitis?When is a workup for infection indicated in nummular dermatitis?What is the role of a skin biopsy in the workup of nummular dermatitis?What is the role of patch testing in the workup of nummular dermatitis?What are the histology findings in nummular dermatitis?What is the goal of nummular dermatitis treatment?What bathing regimen is recommended for the treatment of nummular dermatitis?How are wet wrap treatments used to manage nummular dermatitis?How are topical steroids used to treat nummular dermatitis?Are ointments or creams more effective in the treatment of nummular dermatitis?When are oral, intramuscular, or parenteral steroids indicated in the treatment of nummular dermatitis?How do tar preparations treat nummular dermatitis?How do topical immune modulators treat nummular dermatitis?What treatment is indicated for generalized and prolonged eruptions in nummular dermatitis?How are oral antihistamines or sedatives used to treat nummular dermatitis?How do topical antibiotics treat nummular dermatitis?When are oral antibiotics indicated in the treatment of nummular dermatitis?What is the role of aggressive hydration in the treatment of nummular dermatitis?What is the role of immune suppressive medications in the treatment of nummular dermatitis?Which activities should people with nummular dermatitis avoid?What is the role of sunlight or phototherapy in the treatment of nummular dermatitis?How does aggressive hydration therapy help prevent nummular dermatitis?What bathing precautions should patients with nummular dermatitis take?What measures can be taken at home to help treat nummular dermatitis?What specialist consultations are indicated in the treatment of nummular dermatitis?How are potent steroids used in the treatment of nummular dermatitis?Which medications used to treat an overt infection associated with nummular dermatitis?What is the role of sedating antihistamines in the treatment of nummular dermatitis?How are generalized or severe flares treated in nummular dermatitis?Which oral antibiotics are used to treat secondary infection in nummular dermatitis?Which medications in the drug class Cephalosporins, 1st Generation are used in the treatment of Nummular Dermatitis (Nummular Eczema)?Which medications in the drug class Calcineurin Inhibitors are used in the treatment of Nummular Dermatitis (Nummular Eczema)?Which medications in the drug class Antihistamines, 1st Generation are used in the treatment of Nummular Dermatitis (Nummular Eczema)?Which medications in the drug class Antibiotics, Combos are used in the treatment of Nummular Dermatitis (Nummular Eczema)?
Jami L Miller, MD, Associate Professor, Department of Dermatology, Vanderbilt University Medical School; Vice Chair for Education, Director of Phototherapy Unit, Medical Director of Dermatology Clinic at 100 Oaks, Vanderbilt University Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
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.
Chief Editor
William D James, MD, Emeritus Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier<br/>Served as a speaker for various universities, dermatology societies, and dermatology departments.
Acknowledgements
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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