Nummular Dermatitis (Nummular Eczema) 

Updated: Aug 16, 2019
Author: Jami L Miller, MD; Chief Editor: William D James, MD 

Overview

Background

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[1] 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.[2] 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.

Pathophysiology

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.[5]

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.[8]

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.[12] Whether this is important in the precipitation of disease has yet to be determined.

Etiology Nummular Dermatitis

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,[13] mercury-containing dental amalgams,[14] and depilating creams containing potassium thioglycolate.[15]

Venous insufficiency (and varicosities), stasis dermatitis, and edema may be related to involvement of the affected lower extremities.[16]

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.[17]

Various types of eczematous eruptions, including nummular eczema, have been observed following tumor necrosis factor-alpha–blocking therapy.[8]

Nummular eczema of the breast has reported in breast cancer patients undergoing mastectomy with subsequent breast reconstruction.[18, 19]

Nummular eczema has been found in association with infection in rare cases. Giardiasis has been reported.[20] 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.[21] Another case report noted nummular eczema in association with a dental infection that cleared after the treatment of the infection.[22]

Epidemiology

Frequency

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.

Race

No racial predilection has been observed.

Sex

Nummular eczema is more common in males than in females (see Age below).

Age

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.[23] It is uncommon in children.[24]

Prognosis

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.

Patient Education

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.

 

Presentation

History

Patients present with days to months of a pruritic eruption, which usually starts on the legs. It 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.

New nummular dermatitis lesions often recur in the same locations as old lesions.

The patient's medical history may be positive for eczema, atopic dermatitis, or dry and sensitive skin.

Physical Examination

The diagnosis of nummular eczema is made on the basis of observing the characteristic round-to-oval erythematous plaques. They are most commonly located on the extremities, particularly the legs, but they may occur anywhere on the trunk, hands, or feet.[25] Nummular eczema does not involve the face and scalp. Lesions are often symmetrically distributed. Plaques may be several centimeters.

See the image below.

Dry, scaling plaque of nummular dermatitis (size, Dry, scaling plaque of nummular dermatitis (size, 3 X 5 cm) on the shin.

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 differentiation from tinea corporis based on clinical findings difficult. Tinea corporis usually has few vesicles, a raised narrow border, and leading scale (ie, scale on the outside of the plaque).

Distinguishing among forms of dermatitis (eg, asteatotic eczema, atopic dermatitis, nummular eczema) may be difficult, but, fortunately, this is not necessary to make proper treatment decisions.[26] Contact dermatitis may have a pattern that approximates the manner in which 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.

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, in some areas it may become less so, particularly on the genitalia.

Stasis dermatitis may occur simultaneously on the lower extremities, and venous stasis may lead to the concomitant development of both conditions.

Complications

Nummular dermatitis 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 rarely occurs. Particularly pruritic cases may result in difficulty sleeping and concentrating.

 

DDx

 

Workup

Laboratory Studies

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 becomes more common in a community, the culture results help choose appropriate antibiotics in treatment-resistant cases of documented secondarily infected lesions.

Consider a workup for infection, such as with H pylori and for giardiasis, if appropriate history is suggestive of infection.[20]

Procedures

A skin biopsy may be performed. The findings are nonspecific, but they may help differentiate nummular dermatitis 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, and other research identified positive patch testing in 23 of 50 patients with nummular dermatitis.[27, 28]  A 2012 study strongly recommended patch testing in nummular dermatitis, as it showed that 332 (32.5%) of 1022 patients with nummular dermatitis had positive patch test results for one or more allergens.[5]

Histologic Findings

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 4 appears to be involved in activation of the T lymphocytes.

 

Treatment

Medical Care

Treatment is aimed at rehydration of the skin and repair of the epidermal lipid barrier, reduction of inflammation and treatment of any infection.

Lukewarm or cool baths or showers reduce itching and help rehydrate the skin, as long as soap is not used and moisturizers are applied to wet skin. Patients should be instructed to bathe 1-2 times a day at least, followed by the application of moisturizers or medicated topical preparations, without drying off, to seal the water in the 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 and includes 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 5-6 times a day with petrolatum. Caution must be used when prescription steroid medications are used because 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.

Steroids are the most commonly used therapy to reduce inflammation.

Topical steroids are effective. 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.

Application of the medicine to damp skin allows more effective penetration and faster healing.

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.

Emollients and topical class I-III topical steroids may be used short term.

Oral, intramuscular, or parenteral steroids may be required in cases of severe, generalized eruptions.

Tar preparations are helpful to decrease 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.

When eruptions are generalized and prolonged, phototherapy (generally UVB) may be helpful.[31]  Broadband or narrow band UVB is most commonly used, although PUVA (Psoralen + UVA) may be used in severe cases.

Oral antihistamines or sedatives may help reduce itching and improve sleep. Topical antihistamines are known to be potent topical sensitizers, and, thus, preparations containing topical diphenhydramine in particular should not be used.

Topical antibiotics such as mupirocin may help impetiginization; as neomycin-containing medications are potent topical sensitizers, these should be avoided.

Oral antibiotics, such as 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 between 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 such as methotrexate have been described to be safe and effective in these severely affected patients.[32, 33]

Consultations

Because lesions are persistent and may be difficult to treat, consultation with a dermatologist in an outpatient setting may be advisable.

Activity

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. Ultraviolet radiation helps reduce the inflammatory activity within the skin. The risk of heat worsening the pruritus and of ultraviolet light inducing cutaneus malignancies must be weighed against the potential benefits.

Prevention

Aggressive hydration of the skin may decrease the frequency between nummular dermatitis eruptions.

Bathing is permissible, but hot water should be avoided. Patients should use mild, nondrying cleansers. Patients should be encouraged to use nonsoap cleansers only for control of body odor and 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, such as wool, should be avoided.

A room humidifier is useful, particularly when a heater or air conditioning is used.

 

Medication

Medication Summary

A potent-to-intermediate potency steroid may be applied 2-4 times daily to the affected areas. They are most effective when used in ointment form (rather than cream) and applied to damp skin. Once lesions improve, a lower-potency steroid or moisturizer should be prescribed to avoid skin atrophy.

If the patient has an overt infection, a combination of a topical antibiotic and a steroid ointment applied twice daily is usually very effective. This therapy decreases inflammation and colonization by staphylococci.

Use of sedating antihistamines at night helps with sleep.

Severe or generalized flares may be treated with tap water–moistened 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.

Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, they modify the body's immune response to diverse stimuli.

Triamcinolone topical (Aristocort) Cream or Ointment

Triamcinolone topical is used for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. It is a good choice once lesions stabilize and the threat of secondary infection has passed. Use 0.025-0.1% strength.

Prednisone (Deltasone, Meticorten, Orasone)

Prednisone is for severe generalized flares. It may decrease inflammation by reversing increased capillary permeability and suppressing PMN leukocyte activity.

Clobetasol (Clarelux, Clobex, Clobex Spray)

Clobetasol propionate is a class I superpotent topical steroid; it suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Clobetasol propionate decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN and mast cell degranulation.

Immune modulators

Class Summary

Immune modulators reduce inflammation.

Pimecrolimus 1% cream (Elidel)

Pimecrolimus is the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. It is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus. Pimecrolimus selectively inhibits production and release of inflammatory cytokines from activated T-cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. Pimecrolimus is indicated only after other treatment options have failed.

Tacrolimus 0.03% or 0.1% ointment (Protopic)

The mechanism of action of tacrolimus in atopic dermatitis is not known. It reduces itching and inflammation by suppressing the release of cytokines from T cells. It also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, tacrolimus may inhibit the release of preformed mediators from skin mast cells and basophils, and down-regulate expression of FCeRI on Langerhans cells. It can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. Tacrolimus is available as an ointment in concentrations of 0.03 and 0.1%. It is indicated only after other treatment options have failed.

Antihistamines

Class Summary

Antihistamines used to help with sleep. Caution must be used because even the traditionally nonsedating classes may cause somnolence.

Hydroxyzine (Atarax, Vistaril, Vistazine)

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the CNS. Hydroxyzine is a piperazine type of antihistamine that has fewer sedating effects compared with diphenhydramine and is effective. It is usually well tolerated in most individuals.

Antibiotics

Class Summary

Antibiotics are used for severe exudative flares with infection. Empiric antimicrobial therapy should cover S aureus and other likely pathogens in the context of the clinical setting.

Sulfamethoxazole and trimethoprim (Bactrim)

Sulfamethoxazole and trimethoprim combination agent inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. It is also used for MRSA infections.

Dicloxacillin (Dynapen, Pathocil, Dycill)

Dicloxacillin binds to one or more penicillin-binding proteins, which, in turn, inhibits the synthesis of bacterial cell walls. Dicloxacillin is used for the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when staphylococcal infection is suspected.

Erythromycin (E.E.S., E-Mycin, Eryc)

Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal and streptococcal infections.

In children, age, weight, and severity of infection determine proper dosage. When twice-daily dosing is desired, half the total daily dose may be taken every 12 hours. For more severe infections, double the dose.

Cephalexin (Biocef, Keflex, Keftab)

Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting the synthesis of bacterial cell walls. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora. Cephalexin is used for skin infections or prophylaxis in minor procedures.

 

Questions & Answers

Overview

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?

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?

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?

Presentation

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 new 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?

DDX

What are the differential diagnoses for Nummular Dermatitis (Nummular Eczema)?

Workup

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?

Treatment

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?

What is the role of emollients and class I-III topical steroids 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?

What specialist consultations are indicated 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?

Medications

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 Antibiotics are used in the treatment of Nummular Dermatitis (Nummular Eczema)?

Which medications in the drug class Antihistamines are used in the treatment of Nummular Dermatitis (Nummular Eczema)?

Which medications in the drug class Immune modulators are used in the treatment of Nummular Dermatitis (Nummular Eczema)?

Which medications in the drug class Corticosteroids are used in the treatment of Nummular Dermatitis (Nummular Eczema)?