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Dermatology > REACTIVE AND INFLAMMATORY DERMATOSES
Nummular Dermatitis
Article Last Updated: Mar 14, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Jami L Miller, MD, Assistant Professor, Department of Medicine, Division of Dermatology, Vanderbilt University Medical School
Jami L Miller is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association
Coauthor(s):
Kristina Collins, BS, Vanderbilt University School of Medicine;
Lloyd King, MD, Chairman, Professor, Department of Internal Medicine, Division of Dermatology, Vanderbilt University Medical Center
Editors: John D Wilkinson, MD, MBBS, MRCS, FRCP, Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK; Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA; Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
Author and Editor Disclosure
Synonyms and related keywords:
discoid eczema, nummular eczema, nummular eczema, coin-shaped eczema, coin-shaped dermatitis, nummular pruritus, Staphylococcus aureus, S aureus, staphylococcal skin infection, staphylococcal dermatitis
Background
Nummular (meaning "coin-shaped") dermatitis is a form of eczema. It is characterized by round-to-oval erythematous plaques most commonly found on the arms and legs. Lesions start as papules, which then coalesce into plaques. Early lesions may be studded with vesicles containing serous exudate. They are usually very pruritic.
Pathophysiology
Nummular dermatitis is a condition confined to the skin. Little is known about the pathophysiology of the disease, but it is frequently accompanied by xerosis. The cracking and fissuring of the skin surface that occurs in the setting of xerotic and pruritic skin may allow permeation of environmental allergens and induce eczematous changes. One study showed that elderly patients with nummular dermatitis had increased sensitivity to environmental aeroallergens compared to 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. Onset of severe, generalized nummular lesions has been reported in association with interferon and ribavirin therapy for hepatitis C.
Because of the intense pruritus associated with nummular dermatitis, 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 dermatitis 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.
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.
Frequency
United States
The prevalence of nummular dermatitis is 2 cases per 1000 people. Dermatitis (eg, atopic, asteatotic, dyshidrotic, nummular, hand) is one of the most common dermatologic conditions.
Mortality/Morbidity
- 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 bed rest, oral antibiotics, a cool environment, systemic antibiotics, and/or systemic steroids.
Race
No racial predilection has been observed.
Sex
Nummular dermatitis is more common in males than in females.
Age
Nummular dermatitis has 2 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. It is rare in children.
History
Patients present with a days-to-months' history of a pruritic eruption. It may also burn or sting.
- It often waxes and wanes with winter; cold or dry climates 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 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
The diagnosis 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. It does not involve the face and scalp. Lesions are often symmetrically distributed.
- 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.
- 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 between forms of dermatitis (eg, asteatotic eczema, atopic dermatitis, nummular dermatitis) may be difficult, but, fortunately, this is not necessary to make proper treatment decisions. 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.
- 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, often, has no clear border.
- Stasis dermatitis may occur simultaneously on the lower extremities, and venous stasis may lead to the concomitant development of both conditions.
- Psoriasis plaques are often found on the extensor surfaces, especially at the elbows and knees, in addition to other areas. The scalp is often involved. Psoriasis scale is usually thick and silver and bleeds when removed (Auspitz sign).
Causes
The etiology is unknown and likely multifactorial.
- Most patients with nummular dermatitis 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 a recent study, the most frequent sensitizers were colophony, nitrofurazone, neomycin sulfate, and nickel sulfate. In the past, cases of nummular eczem–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 dermatitis, have been observed following tumor necrosis factor-alpha blocking therapy
- Nummular eczema has been found in association with giardiasis in rare cases. 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.
Asteatotic Eczema
Atopic Dermatitis
Contact Dermatitis, Allergic
Contact Dermatitis, Irritant
Cutaneous T-Cell Lymphoma
Lichen Simplex Chronicus
Pityriasis Rosea
Psoriasis, Plaque
Tinea Corporis
Other Problems to be Considered
Fixed drug eruption
Lab Studies
- Tinea corporis should be excluded by scraping and microscopically analyzing a potassium hydroxide preparation of a lesion.
- For lesions that are vesicular or have yellow crusting suggestive of impetiginization, swab culture may be helpful. As methicillin-resistant Staphylococcus aureus becomes more common in the community, appropriate antibiotics must be chosen for therapy of secondarily infected lesions.
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 more recent research identified positive patch testing in 23 of 50 patients with nummular dermatitis.
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.
Medical Care
Treatment is aimed at rehydration of the skin, treatment of any infection, and reduction of inflammation.
- Lukewarm or cool baths or showers reduce itching and help rehydrate the skin. Patients should be instructed to bathe 1-2 times a day at least, followed by the application of moisturizers or medicated topical preparations 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 to wet skin and includes alteration of cleansing habits so that soap is applied only to the axilla and groin. A recent study showed greater than 90% response in 27 of 28 patients with refractory chronic pruritic eruptions when the regimen was followed as directed.
- 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.
- Oral, intramuscular, or parenteral steroids may be required in cases of severe, generalized eruptions.
- 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.
- Oral antihistamines or sedatives may help reduce itching and improve sleep.
- Oral antibiotics, such as dicloxacillin, cephalexin, or erythromycin, should be used in cases of secondary infection.
- Tar preparations are helpful to decrease inflammation, particularly in older, thickened, scaly plaques.
- 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.
Consultations
Because lesions are persistent and 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, drying conditions, and irritating activities should be avoided.
- 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.
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.
Drug Category: Corticosteroids
Have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, modify the body's immune response to diverse stimuli.
| Drug Name | Triamcinolone (Aristocort) |
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| Description | For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. A good choice once lesions stabilize and the threat of secondary infection has passed. Use 0.025-0.1% strength. |
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| Adult Dose | Apply thin film to affected area bid |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; fungal, viral, or bacterial skin infections |
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| Interactions | None reported |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Prolonged use may induce skin atrophy; avoid use in sensitive areas (eg, groin, axillae, face); prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria |
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| Drug Name | Prednisone (Deltasone, Meticorten, Orasone) |
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| Description | For severe generalized flares. May decrease inflammation by reversing increased capillary permeability and suppressing PMN leukocyte activity. |
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| Adult Dose | 40-60 mg PO qd with rapid taper |
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| Pediatric Dose | 0.14 mg/kg or 4-6 mg/m2 PO in divided doses |
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| Contraindications | Documented hypersensitivity; viral, fungal, tubercular skin, or connective-tissue infections; peptic ulcer disease; hepatic dysfunction |
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| Interactions | May decrease oral anticoagulant effectiveness; increases metabolism of isoniazid and salicylates; coadministration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur; adjust dose in persons with hypoglycemia and in those on insulin |
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| Drug Name | Clobetasol propionate (Clobex, Cormax) |
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| Description | Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN and mast cell degranulation. |
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| Adult Dose | Apply bid for up to 2 wk; not to exceed 50 g/wk |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; viral or fungal skin infections |
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| Interactions | None reported |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | May suppress adrenal function in prolonged therapy |
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Drug Category: Antibiotics
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.
| Drug Name | Dicloxacillin (Dynapen, Pathocil, Dycill) |
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| Description | Binds to 1 or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected. |
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| Adult Dose | 125-500 mg PO qid for 7-10 d |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity |
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| Interactions | May decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment |
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| Drug Name | Erythromycin (E.E.S., E-Mycin, Eryc) |
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| Description | Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose. |
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| Adult Dose | 500 mg PO bid for 7-10 d |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; hepatic impairment |
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| Interactions | Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, or abdominal colic occurs |
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| Drug Name | Cephalexin (Biocef, Keflex, Keftab) |
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| Description | First-generation cephalosporin arrests bacterial growth by inhibiting synthesis of bacterial cell walls. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora. Used for skin infections or prophylaxis in minor procedures. |
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| Adult Dose | 250-500 mg PO qid for 7-10 d |
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| Pediatric Dose | 25-50 mg/kg/d PO divided qid (125 or 250 mg/5 mL) |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Probenecid may increase effect of cephalosporins; tetracyclines may decrease effect of cephalosporins with concurrent use |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Caution in impaired renal function |
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Drug Category: Antihistamines
To help with sleep. Caution must be used because even the traditionally nonsedating classes may cause somnolence.
| Drug Name | Hydroxyzine (Atarax, Vistaril, Vistazine) |
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| Description | Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Piperazine type of antihistamine that has fewer sedating effects compared with diphenhydramine and is effective. Usually well tolerated in most individuals. |
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| Adult Dose | 25-100 mg PO qd/qid |
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| Pediatric Dose | 2 mg/kg/d PO; 0.6 mg/kg/dose PO q6h |
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| Contraindications | Documented hypersensitivity |
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| Interactions | CNS depression may increase with alcohol or other CNS depressants |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T-waves) may occur; may cause drowsiness |
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Deterrence/Prevention
- Aggressive hydration of the skin may decrease the frequency between 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 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.
Complications
- 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.
Prognosis
- 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.
Patient Education
Medical/Legal Pitfalls
- Few medicolegal pitfalls apply to this condition. Aggressive hydration, early treatment of secondary infection, and counseling regarding somnolence (due to medications or lack of sleep due to itching) are important to minimize the eruption and scarring and help avoid danger to the patient.
| Media file 1:
Dry, scaling plaque of nummular dermatitis (size, 3 X 5 cm) on the shin. |
 |  View Full Size Image | |
Media type: Photo
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Nummular Dermatitis excerpt Article Last Updated: Mar 14, 2007
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