Updated: Aug 17, 2009
Dyshidrotic eczema is a recurrent or chronic relapsing form of vesicular palmoplantar dermatitis of unknown etiology. Dyshidrotic eczema also is termed pompholyx, which derives from cheiropompholyx, which means "hand and bubble" in Greek.
The etiology of dyshidrotic eczema is unresolved and is believed to be multifactorial. Dyshidrotic eczema is considered a reaction pattern caused by various endogenous conditions and exogenous factors.
Several hypotheses have been proposed for the pathophysiology of dyshidrotic eczema. The original hypothesis of sweat gland dysfunction has been disputed because vesicular lesions are not associated with sweat ducts. However, hyperhidrosis is an aggravating factor in 40% of patients with dyshidrotic eczema. Improvement in pruritus, erythema, vesicles, and hand dermatitis with fewer or no signs of relapse has been obtained after botulinum toxin A injection.[1 ]
Dyshidrotic eczema may be associated with atopy and familial atopy. Of patients with dyshidrosis, 50% have atopic dermatitis.
Exogenous factors (eg, contact dermatitis to nickel, balsam, cobalt; sensitivity to ingested metals; dermatophyte infection; bacterial infection) may trigger episodes. These antigens may act as haptens with a specific affinity for palmoplantar proteins of the stratum lucidum of the epidermis. The binding of these haptens to tissue receptor sites may initiate pompholyx.
Evidence shows that the ingestion of metal ions such as cobalt can induce both type I and type IV hypersensitivity reactions, and, in addition, they can also act as atypical haptens activating T lymphocytes through human leucocyte antigen–independent pathways, causing systemic allergic dermatitis in the form of dyshidrotic eczema.[2,3 ]
Emotional stress and environmental factors (eg, seasonal changes, hot or cold temperatures, humidity) reportedly exacerbate dyshidrosis.
Dyshidroticlike eczematous eruptions with the use of intravenous immunoglobulin infusions have been reported.
In some patients, a distant fungal infection can cause palmar pompholyx as an id reaction. In one study, one third of pompholyx occurrences on the palms resolved after treatment for tinea pedis.
Dyshidrotic eczema occurs in 5-20% of patients with hand eczema and more commonly occurs in warmer climates and during spring and summer months (seasonal or summer pompholyx).
Dyshidrotic eczema comprised 1% of initial consultations in a 1-year Swedish study. In a study of 107,206 Swedish individuals, 51 (0.05%) were diagnosed with dyshidrosis. Of all hand dermatitis cases in that population, 3% had dyshidrosis.[4 ]
In a retrospective study reviewing records of 714 Portuguese patients during a 6-year period, Magina et al found dyshidrotic eczema to be the third most common type of hand dermatitis (20.3%).[5 ]
Dyshidrotic eczema can be severe, resulting in occupational disability and time away from work; however, disability compensation usually is not provided for this condition.
The male-to-female ratio for dyshidrotic eczema is 1:1.
Dyshidrotic eczema affects individuals aged 4-76 years; the mean age is 38 years. After middle age, the frequency of dyshidrotic eczema episodes tends to decrease.
Patients report pruritus of hands and feet with a sudden onset of vesicles. Burning pain or pruritus occasionally may be experienced before vesicles appear. Dyshidrotic eczema episodes vary in frequency from once per month to once per year. Patients with dyshidrotic eczema may report a variety of factors that possibly are related to eruptions, as follows:
Symmetric crops of clear vesicles and/or bullae on the palms and lateral aspects of fingers characterize dyshidrotic eczema (Media Files 1-2, Media Files 5-7, and Media File 9). Feet, soles, and the lateral aspects of toes also may be affected.
The cause of dyshidrotic eczema is unknown. The condition often appears related to other skin diseases (eg, atopic dermatitis, contact dermatitis, allergy to ingested metals, dermatophyte infection, bacterial infection, environmental or emotional stress). Several factors may participate in causing dyshidrotic eczema.
| Acropustulosis of Infancy | Juvenile plantar dermatosis |
| Bullous Pemphigoid | Linear IgA-disease with (hemorrhagic)
pompholyx |
| Contact Dermatitis, Allergic | Pemphigoid Gestationis |
| Contact Dermatitis, Irritant | Pemphigus Vulgaris |
| Epidermolysis Bullosa | Pityriasis Rubra Pilaris |
| Erythema Multiforme | Subcorneal Pustular Dermatosis |
| Fixed Drug Eruptions | Urticaria, Contact Syndrome |
| Friction Blisters | Vesicular mycosis fungoides |
| Herpes Simplex | |
| Impetigo, bullous |
Dyshidrosiform pemphigoid
Inflammatory tinea pedis or tinea manus
Palmoplantar pustular psoriasis
Pustular bacterid
Some mildly affected patients experience spontaneous resolution within 2-3 weeks. Biofeedback therapy for stress reduction has succeeded in some patients. Outpatient care is multifaceted.
For nickel-sensitive patients, consider a low-nickel diet for 3-4 weeks. The diet regimen is only rarely successful and is difficult for patients to follow. The diet requires avoiding foods rich in nickel, such as canned foods, foods cooked using nickel-plated utensils, herring, oysters, asparagus, beans, mushrooms, onions, corn, spinach, tomatoes, peas, whole grain flour, pears, rhubarb, tea, cocoa, chocolate, and baking powder. A list of additional nickel-containing foods has been reported by Lofgren and Warshaw.[4 ]
For cobalt-sensitive patients, consider a low-cobalt diet that avoids apricots, beans, beer, beets, cabbage, cloves, cocoa, chocolate, coffee, liver, nuts, scallops, tea, and whole grain flour. A point-based low-cobalt diet has been described by Stuckert and Nedorost.[2 ]
Bedrest may be necessary if bullae develop on the feet. Additionally, if palmar bullae develop, patients may not be able to work or perform the activities of daily living.
The goals of pharmacotherapy for dyshidrotic eczema are to reduce morbidity and prevent complications.
Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Topical ointments are more potent but greasier than creams.
For severe episodes. Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.
Apply cream or ointment bid to severely affected areas for up to 2 wk; not to exceed 50 g/wk
Not established
None reported
Documented hypersensitivity; viral or fungal skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May suppress adrenal function and result in thinning of skin in prolonged therapy
Ointment is a class II, cream is a class III steroid. High-potency; like all topical steroids, has anti-inflammatory, antipruritic, and vasoconstrictive properties.
Apply cream or ointment sparingly bid as severity warrants
Apply as in adults
None reported
Documented hypersensitivity; herpes simplex infection, fungal, viral, or tubercular skin lesions
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause adverse systemic effects if used over large areas, denuded areas, on occlusive dressings, or during prolonged treatment periods; prolonged use may result in thinning of skin
Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation
by reversing increased capillary permeability and suppressing PMN activity.
0.5-1 mg/kg/d PO qam; taper over 2 wk
Administer as in adults
Ketoconazole, erythromycin, clarithromycin, estrogens, and birth control pills increase levels
Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels
Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
For severe acute episodes. Rapid onset (within 1 h) with 72-h duration. For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability.
5-9 mg IM as single dose
Not advised
Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels
Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Increases risk of multiple complications, including severe infections; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications
If given by injection, bruising, infection, cold abscess, temporary depression in skin, and temporary discoloration of skin (usually lightened) may occur at injection site
For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. Long duration, 4-6 wk.
40-60 mg IM as single dose
2.5-15 mg (10 mg/mL or 40 mg/mL solutions) IM single dose; repeat prn
Aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
Levels of potassium-depleting diuretics (due to potentiation of potassium loss and digitalis toxicity) and cyclosporine may increase; levels of isoniazid, insulin (resistance is induced), and salicylates may decrease; monitor anticoagulant therapy and theophylline levels
Absolute: Systemic fungal infection, herpes simplex keratitis, hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, and pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Multiple complications may occur (eg, severe infections, hyperglycemia, myopathy, peptic ulcer disease, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression)
If given by injection, bruising, infection, cold abscess, temporary depression in skin, and temporary discoloration of skin (usually lightened) may occur at injection site
For severe acute episodes.[25,26,27 ]
For short-term treatment or intermittent long-term treatment in unresponsive or intolerant cases. Inhibits T-lymphocyte activation. Some patients may benefit from topical tacrolimus or pimecrolimus. Primary author follows several patients in her practice who are controlled with topical calcineurin inhibitors alone. Available at 0.03% and 0.1% ointment.
Apply bid to affected areas; continue for 1 wk after clearing
<2 years: Not established
>2-15 years: Apply 0.03% ointment bid to affected areas; continue for 1 wk after clearing
>15 years: Apply as in adults
None reported
Documented hypersensitivity; local infection at treatment site; Netherton syndrome; children <2 y; immunodeficiency syndromes; caution in herpes simplex or varicella-zoster virus infections, eczema herpeticum, or erythroderma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Serious adverse reactions include varicella-zoster virus infection and eczema herpeticum; common adverse reactions include skin burning, pruritus, flulike symptoms, headache, erythema, allergic reaction, skin tingling, hyperesthesia, acne, folliculitis, rash, and urticaria; do not use with occlusive dressings; limit use to affected skin.
Product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment indicated for use in children aged 2-15 y
For short-term treatment or intermittent long-term treatment in unresponsive or intolerant cases. Inhibits T-lymphocyte activation. Available at 1% cream
Apply bid to affected areas; discontinue after clearing
<2 years: Not indicated
>2 years: Administer as in adults
None reported
Documented hypersensitivity; local infection at treatment site; Netherton syndrome; children <2 y; immunodeficiency syndromes; caution in herpes simplex or varicella-zoster virus infection, eczema herpeticum, and erythroderma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Serious adverse reactions include varicella-zoster or herpes simplex virus infection, eczema herpeticum, angioneurotic edema, and anaphylaxis; common adverse reactions include skin burning, flulike symptoms, headache, nasopharyngitis, cough, pyrexia, erythema, hypersensitivity reaction, skin infection, herpes simplex, skin papilloma, erythema, and pruritus
Do not use with occlusive dressings; limit use to affected skin; avoid continuous long-term use; reevaluate if symptoms persist >6 wk.
product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment indicated for use in children aged 2-15 y
Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Antimetabolite that inhibits DNA synthesis and cell reproduction in malignant cells; may suppress immune system. Satisfactory response seen within 3-6 wk following administration. Adjust dose gradually to attain satisfactory response.
Administer 1. 5- to 10-mg test dose; check CBC count in 1 wk; if results are normal, continue weekly 1-time 7.5-mg doses (may split if GI upset, ie, 8 am, 8 pm, 8 am dosing); increase dose by 2.5 mg/wk each month (may taper by 2.5 mg/wk each month when decreasing dose to lowest possibility)
Not recommended
Salicylates, NSAIDs, dipyridamole, probenecid, retinoids, ethanol, triamterene, pyrimethamine, sulfonamides, tetracycline, chloramphenicol, penicillin or other broad-spectrum antibiotics, trimethoprim, dapsone, theophylline, phenytoin, phenothiazines, barbiturates, and nitrofurantoin (impair folic acid absorption), ascorbic acid, phenylbutazone, cyclosporin, aminoglycosides
Absolute: Pregnancy or desire to get pregnant, active peptic ulcer, alcoholism, primary/secondary immunodeficiency, blood dyscrasias, active hepatitis, cirrhosis, chronic renal failure, and active infections
Relative: History of excessive ethanol intake or substance abuse, increased LFT results, recent hepatitis, diabetes mellitus, obesity, history of heritable liver disease, unreliable patient, CrCl <50 mL/min, males contemplating conception (must discontinue for 3 mo)
X - Contraindicated; benefit does not outweigh risk
Monitor CBC counts, differentials, renal panel, urinalysis, and LFT results monthly; CrCl baseline recommended for patients >50 y; monitor more frequently during initial dosing, dose adjustments, or if risk of elevated methotrexate levels (eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood cell counts occurs; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs including salicylates not tested yet)
Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.
100-150 mg/d PO initially; then 50-100 mg/d PO maintenance after improvement occurs; more accurate dosing possible with measurement of thiopurine methyltransferase level
Not established
Allopurinol increases risk of pancytopenia; captopril/ACE inhibitors may increase risk of anemia and leukopenia; increased dose of warfarin may be necessary; may need increased dose of pancuronium for adequate paralysis; live-virus vaccines, co-trimoxazole (increased risk of hematologic toxicity); rifampicin (transplants possibly rejected); clozapine (increased risk of agranulocytosis)
Absolute: Documented hypersensitivity, pregnancy or attempting pregnancy, and clinically significant active infection
Relative: Concurrent use of allopurinol; prior treatment with alkylating agents (cyclophosphamide, chlorambucil, melphalan, others) (high risk of neoplasia)
Pediatric: Safety and efficacy not established
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
TPMT testing is not entirely reliable; it involves testing the activity of TPMT activity in RBCs, which correlates with systemic TPMT activity; functional enzyme test has been shown to have variability between test sites, and kits may contain varying amounts of enzyme inhibitor; starting at low doses, monitoring for pancytopenia, and then increasing dose is alternative; if clinical response is not good, patient may be a homozygote for high activity and may need an increased dose
Possible increased risk of lymphoproliferative disorders with long-term therapy; increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur
Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs. For children and adults, base dosing on ideal body weight.
3-5 mg/kg/d PO
Not established
Increase levels: Erythromycin, clarithromycin, azithromycin, norfloxacin ciprofloxacin, cephalosporins, doxycycline, ketoconazole, itraconazole, fluconazole, ritonavir, indinavir, saquinavir, nelfinavir, diltiazem, verapamil, nicardipine, cimetidine, methylprednisolone, dexamethasone, thiazides, furosemide, allopurinol, bromocriptine, danazol, amphotericin B, metoclopramide, oral contraceptive pills, warfarin, and grapefruit juice.
Decrease levels: Rifampin, rifabutin, nafcillin, carbamazepine, phenobarbital, phenytoin, valproate, octreotide, and ticlopidine.
Potentiate renal toxicity: Tobramycin, gentamicin, ketoconazole, azapropazone, TMP-SMZ, vancomycin, sulindac, amphotericin B, indomethacin, naproxen, cimetidine, ranitidine, diclofenac, tacrolimus, and melphalan.
Decreased renal clearance may lead to digitalis toxicity; atorvastatin renal clearance may be decreased, leading to myositis; methylprednisolone or prednisolone renal clearance may be decreased, leading to convulsions; concurrent ACE inhibitors, potassium supplements, and potassium-sparing diuretics may increase risk of hyperkalemia
Absolute: Significantly decreased renal function, uncontrolled hypertension, documented hypersensitivity, and clinically cured or persistent malignancy (except nonmelanoma skin cancer)
Relative: Age <18 or >64 y (transplant recipients as young as 1 y have been treated with no unusual effects; however safety in patients <18 y has not been established); controlled hypertension; planning to receive a live attenuated vaccine; active infection or evidence of immunodeficiency; concurrent phototherapy, coal tar, methotrexate, or other immunosuppressive agents; pregnancy or lactation; unreliable patient; and severe hepatic dysfunction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO
For dyshidrosis with secondary impetiginization.
Binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected
250-500 mg PO qid for 7-10 d
25-50 mg/kg/d PO divided qid for 7-10 d
May decrease effects of anticoagulants; probenecid and disulfiram may increase levels; with concurrent use, tetracyclines may decrease effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment
First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections or prophylaxis in minor procedures.
250-500 mg PO qid for 7-10 d
25-50 mg/kg/d PO divided bid for 7-10 d (125 and 250 mg/5 mL)
Coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
Age, weight, and severity of infection determine proper dosage in children. When bid dosing is desired, one half of total daily dose may be taken q12h. Double the dose for more severe infections.
250-500 mg PO qid for 7-10 d
25-50 mg/kg/d PO divided qid
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
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (administer pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
To treat pruritus associated with dyshidrosis. Desloratadine (Clarinex) is a long-acting tricyclic histamine antagonist selective for H1 receptor. Is a major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine. The dose for adults and children >12 y is 5 mg PO daily. Decrease dose in hepatic impairment. Data limited regarding drug interactions; however, erythromycin and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma concentrations, but no increase in clinically relevant adverse effects, including QTc, was observed. Adverse effects were similar to placebo, and it rarely causes pharyngitis or dry mouth.
Nonsedating; selectively inhibits peripheral histamine H1 receptors.
10 mg PO, usually in morning
<6 years: Not established
6-11 years: 10 mg Redi-Tab or 10 mL syr daily (1 mg/mL)
Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Initiate therapy at lower dose in liver impairment
Antagonizes H1 receptors in periphery. Sedating; may suppress histamine activity in subcortical region of CNS.
10-50 mg PO q4-6h, often at bedtime
0.5 mg/kg PO q4-6h or 10 mg/5 mL
CNS depression may increase with alcohol or other CNS depressants when coadministered
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness
Topical antihistamine and mild anti-inflammatory. Blocks nerve conduction and impulses by inhibiting depolarization of neurons. Available alone or as 1% or 2.5% cream or ointment. Available OTC as Prax.
Topically apply cream or ointment bid/tid to affected area
Apply as in adults
<12 years: Not indicated
None reported
Documented hypersensitivity; do not apply over large areas and avoid contact with eyes and nose
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Serious adverse reactions include anaphylactic reactions and skin sloughing (rare); common adverse reactions include contact dermatitis, edema, burning, stinging, and tenderness; caution in patients with trauma in area to be treated
Minimize effects of nickel in eczema.
Thiuram derivative that interferes with aldehyde dehydrogenase. For patients highly allergic to nickel with severe vesicular hand dermatitis. Chelating effect of disulfiram helps reduce the body's nickel burden in individuals allergic to nickel. Do not administer if patient has ingested alcohol within last 12 h. Supplied as a 250-mg tab.
250-500 mg/d PO (range 125-500 mg); not to exceed 500 mg/d
Not established
Increases effects of diazepam and chlordiazepoxide; metronidazole, isoniazid, and phenytoin may increase toxicity of disulfiram; coadministration with warfarin may increase PT; coadministration with alcohol may cause disulfiram reaction
Documented hypersensitivity; severe myocardial disease and coronary occlusion
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hypothyroidism, hepatic cirrhosis, hepatic disease or insufficiency, seizure disorders, diabetes mellitus, cerebral damage, and nephritis
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dyshidrotic eczema, pompholyx, vesicular palmoplantar eczema, atopic dermatitis, contact dermatitis, hand eczema, atopic diathesis, asthma, hay fever, allergic sinusitis, contact allergens, intravenous immunoglobulin therapy, interdigital maceration, desquamation of interdigital spaces
cellulitis, lymphangitis, Dyshidrotic Eczema Area and Severity Index, allergy to ingested metals, dermatophyte infection, emotional stress, nickel sensitivity, id reaction, tinea pedis infection, pompholyx dermatophytid, palmar pompholyx reaction, implanted metals.
Sadegh Amini, MD, Senior Clinical Research Fellow, Skin Research Group, Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami
Sadegh Amini, MD is a member of the following medical societies: American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, and International Society of Dermatology
Disclosure: Nothing to disclose.
Anne E Burdick, MD, MPH, Professor of Dermatology, Director of Leprosy Program, Associate Dean for TeleHealth and Clinical Outreach, University of Miami Miller School of Medicine
Anne E Burdick, MD, MPH is a member of the following medical societies: Washington State Medical Association
Disclosure: Nothing to disclose.
John D Wilkinson, MD, MBBS, MRCS, FRCP, Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK
John D Wilkinson, MD, MBBS, MRCS, FRCP is a member of the following medical societies: American Academy of Dermatology and Royal College of Physicians
Disclosure: Nothing to disclose.
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire Consulting
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.