eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses
Vesicular Palmoplantar Eczema: Treatment & Medication
Updated: Oct 30, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Several modalities of therapy are available for the treatment and control of vesicular palmoplantar eczema. Therapy should be chosen according to the type and severity of the condition. Whenever possible, eliminate known triggers. If pruritus is a problem, antihistamines (eg. hydroxyzine) can relieve some symptoms.
Preventative measures
Regular use of hand emollients and avoidance of frequent contact with irritants are important means to prevent flare-ups of vesicular palmoplantar eczema. Contact allergy has been noted in one study to be responsible for 67.5% of pompholyx eczema, and all patients should be considered for patch testing to identify relevant allergens.
Topical therapy
Topical therapy for vesicular palmoplantar eczema includes high-potency glucocorticoids, Burow solution (aluminum acetate 1% or potassium permanganate solution [1:8000 dilution]), tacrolimus, and/or psoralen plus UVA (PUVA).
- Topical high-potency glucocorticoids, such as betamethasone valerate and clobetasol propionate, are first-line therapies. Application of these medications under plastic and vinyl occlusion enhances their efficacy. However, this method may predispose the patient to secondary bacterial or fungal infection and to both local and systemic adverse effects of corticosteroids. Therefore, it should be used only intermittently and should never be used in the presence of coexisting infection.
- Patients with mild vesicular palmoplantar eczema may be controlled with the use of less potent corticosteroids.
- Acute, severe episodes of pompholyx benefit from rest, and bland applications with wet soaks and compresses and with drying agents such as Burow solution. Occasionally, large blisters may need to be aspirated.
- Newer agents, such as topical tacrolimus and pimecrolimus, have been shown to be as effective as mometasone furoate in the treatment of chronic relapsing eczema of the hands.10 These topical immunomodulators may be used as steroid-sparing agents to treat resistant palmar eczema, with minimal systemic absorption or systemic effect.11 Use of other agents should be considered when plantar eczema is being treated because this therapy is less effective on the soles of the feet than on the hands. The use of occlusion with these agents has also been shown to increase their efficacy.
- A small open-label study demonstrated efficacy of topical vitamin D-3 derivatives (ie, calcipotriol, maxacalcitol) for the control of hyperkeratotic palmoplantar eczema.12
Systemic therapy includes steroids, immunosuppressive agents (eg, azathioprine,13 cyclosporine), retinoids (eg, acitretin), and PUVA.
- Consider the use of systemic glucocorticoids or intralesional steroids in acute episodes of vesicular palmoplantar eczema when local therapy fails. These agents are not helpful for long-term treatment because of a potential for severe adverse effects.
- Cyclosporine, mycophenolate mofetil, and methotrexate either alone or in combination with steroids may be used for severe, recalcitrant cases of vesicular palmoplantar eczema.14,15 These therapies have also been tried as steroid-sparing agents in chronic relapsing eczema.
- For hyperkeratotic eczema, consider the use of aromatic retinoids, such as acitretin, which help control hyperkeratosis. These agents are best used in relatively low doses because of adverse effects. Therapy may need to be continued indefinitely in cases of hyperkeratotic eczema and is often accompanied by topical occlusive therapy, with combined or alternating steroids and keratolytics (5-20% salicylic acid) or tar preparations.
- The use of etanercept in a case study achieved a 4-month remission of vesicular palmoplantar eczema, which was followed by relapse.16
- Photochemotherapy has been shown to be effective in dyshidrotic eczema, in particular PUVA. However, the use of psoralen has been associated with carcinogenic risk of the skin. Although conventionally used with psoralen for its photosensitizing effects, UVA-1 alone has also shown success in treating palmoplantar eczema, with the advantage that it does not require psoralen.17,18 PUVA can be administered orally or topically. In a study comparing the effectiveness of the 2 modalities, dyshidrotic eczema responded well to both oral and topical (bath) treatment, while hyperkeratotic eczema cleared significantly better with oral therapy than with topical (bath) PUVA.19
Other therapies20
Other treatment options for vesicular palmoplantar eczema that have been reported include treatment with intradermal injections of botulinum toxin A, x-ray therapy, disulfiram for nickel-induced disease, and, in patients with obstructive sleep apnea, continuous positive airway pressure (CPAP).
- Botulinum toxin A is a potent neurotoxin that blocks the autonomic cholinergic fibers.21,22 It has been shown to improve symptoms of itching and vesicular formation in a controlled left-right hand comparison study with 8 subjects.23 This therapy may be used alone or in combination with topical steroids. However, the mechanism of action in reducing the severity of palmoplantar eczema is disputed. Some proposed mechanisms are a disruption of the afferent nerve supply of the skin, which may reduce sweating, because sweat is known to exacerbate the condition. Another mechanism is the possible effect of the toxin on afferent nerve fibers. Blockade of the inflammatory process and inhibition of neuropeptides such as substance P via toxic effects may explain the reduction of pruritus in treated patients.
- The inflammatory cells functioning in eczema are highly radiosensitive, and, therefore, x-ray irradiation has been used in some patients with resistant chronic eczema of the hand when other treatments have not been successful.
- Grenz rays and superficial radiotherapy were popular treatments for chronic severe hand eczema in the 1980s; however, they have currently decreased in popularity, mostly because of a lack of availability than because of the risk for potential carcinogenesis. Superficial radiation therapy appears to have a higher success rate than grenz ray therapy because of its deeper penetration into the skin.24
- One study revealed excellent results with the use of superficial radiation for palmoplantar eczema, while others have not.25,26 However, the potential risk of irradiation for a benign non–life-threatening disease must be recognized, and care must be taken not to exceed the maximum safe cumulative lifetime dose by using dosimetry. External-beam megavoltage radiation therapy was reportedly successful in treatment of this condition in one patient.
- Disulfiram may be administered as a nickel-chelating agent in patients with known nickel sensitivity, but this should not be used in thiuram-sensitive patients.
- One case report describes a patient with obstructive sleep apnea and dyshidrotic palmar eczema whose dermatitis resolved after being placed on a CPAP machine. The authors speculated the resolution of the eczema may reflect the effects of increased tissue oxygenation and decreased circulating inflammatory factors associated with better sleep quality.27
- Id reactions tend to resolve with treatment of the primary infection. Consider systemic antibiotics if secondary infection is suspected, and culture suspicious lesions.
Consultations
- Refer patients to a dermatologist because vesicular palmoplantar eczema is likely to be a lifelong disease (albeit intermittent in some patients).
Diet
- Maintaining a low-cobalt diet has been suggested to decrease the number of dyshidrotic eczema flares.28
- Patients with established nickel sensitivity may benefit from nickel-free diets.
Medication
The goals of pharmacotherapy for vesicular palmoplantar eczema are to reduce morbidity and to prevent complications.
The dyshidrotic eczema severity index (DASI), a standardized severity scale for palmoplantar eczema, has made it easier to compare the efficacy of various therapies in controlled clinical trials.29
Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the immune response of the body to diverse stimuli.
Betamethasone (Diprolene)
For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.
Adult
Apply thin film qd/bid, not to exceed 2 wk
Pediatric
Administer as in adults
None reported
Documented hypersensitivity; paronychia, cellulitis, impetigo, angular cheilitis, erythrasma, erysipelas, rosacea, perioral dermatitis, acne
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
Precautions
Do not use in skin with decreased circulation; can cause atrophy of groin, face, and axillae; may cause striae distensae, rosacea-like eruption; may increase skin fragility; may suppress HPA axis (rare); if infection develops and is not responsive to antibiotics, discontinue until infection is controlled; do not use as monotherapy for widespread plaque psoriasis; topical fluorinated steroids should be used cautiously in children
Clobetasol (Temovate)
Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.
Adult
Apply qd/bid for up to 2 wk; not to exceed 50 g/wk
Pediatric
Not established
None reported
Documented hypersensitivity; viral or fungal skin infections
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
Precautions
Not for use on face or flexures; use no longer than 2 wk; treatment of large areas may result in significant systemic absorption and suppression of adrenal function
Prednisone (Deltasone)
Immunosuppressant to treat autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.
Adult
0.5-1 mg/kg/d PO with food; taper over 2 wk as symptoms resolve
Pediatric
Administer as in adults
Coadministration with estrogens may decrease prednisone clearance; concurrent digoxin may cause digitalis toxicity due to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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 with glucocorticoid use
Systemic immunosuppressives
These agents are used for severe acute episodes and as steroid-sparing agents in the chronic forms of the disease.
Azathioprine (Imuran)
Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, resulting in low autoimmune activity. Used in transplant recipients and some autoimmune conditions.
Adult
Initial dose: 100-150 mg/d PO
Maintenance dose: 50-100 mg/d PO
Alternatively, 1 mg/kg/d PO for 6-8 wk; increase by 0.5 mg/kg q4wk until response or dose is 2.5 mg/kg/d
Pediatric
Initial dose: 2-5 mg/kg/d PO/IV
Maintenance dose: 1-2 mg/kg/d PO/IV
Allopurinol increases toxicity; concurrent ACE inhibition may induce severe leukopenia; may increase methotrexate metabolite levels and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine
Documented hypersensitivity; low levels of serum thiopurine methyl transferase (TPMT)
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur; check TPMT level before therapy and monitor liver, renal, and hematologic function; pancreatitis rarely associated
Cyclosporine (Neoral, Sandimmune)
Calcineurin inhibitor. Potent immunosuppressant; nonmyelotoxic but markedly nephrotoxic. Widely used in organ and tissue transplantation and skin diseases (eg, psoriasis, atopic dermatitis).
Adult
2.5-5 mg/kg/d PO in divided doses
Pediatric
Not established
Grapefruit juice increases plasma-cyclosporin concentration (toxicity risk); carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase with concurrent lovastatin
Documented hypersensitivity; uncontrolled hypertension or malignancies; concomitant with PUVA or UVB in psoriasis (may increase cancer risk)
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
Precautions
Monitor kidney function (serum creatinine, urea), liver function, and blood pressure; measure blood lipids before treatment; may increase risk of infection and malignancy
Methotrexate (Rheumatrex)
Antimetabolite; inhibits enzyme dihydrofolate reductase, which is essential for purine and pyrimidine synthesis. Unknown mechanism of anti-inflammatory action. Folinic acid after MTX administration helps prevent MTX-induced mucositis or myelosuppression.
Adult
7.5 mg PO q12h for 3 doses/wk (eg, 2.5 mg PO at 6 pm, 2.5 mg PO at 6 am, then 2.5 mg PO at 6 pm the next day); not to exceed 25-30 mg/wk
Pediatric
Not recommended
Oral aminoglycosides may decrease absorption and blood levels of concurrent oral MTX; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity; folic acid or its derivatives in some vitamins may decrease response; coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity; may increase plasma thiopurines levels
Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Monitor CBC count monthly and liver and renal function q1-3mo during therapy (more frequently during initial dosing, dose adjustments, or when elevated MTX levels likely [eg, dehydration]); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if blood counts significantly decrease; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs, including salicylates, not tested)
Mycophenolate (CellCept)
Immunosuppressant to prevent acute rejection of renal or cardiac transplants. Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, inhibiting their proliferation. Inhibits antibody production.
Adult
1-1.5 g PO bid
Pediatric
Not established
May elevate acyclovir and ganciclovir levels; antacids and cholestyramine decreases absorption, reducing levels (do not administer together); probenecid may increase levels; salicylates may increase toxicity
Documented hypersensitivity; pregnancy (exclude before therapy and avoid for 6 wk after discontinuation), breastfeeding
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
CBC counts every wk for 4 wk, twice a month for 2 mo, then monthly for 1 y; risk of neutropenia; caution with older patients, GI disease, and patients susceptible to skin cancer
Retinoids
Beta-carotene derivatives have marked effects on keratinizing epithelia. Etretinate often helps control hyperkeratosis in hyperkeratotic palmar eczema. Therapy may have to be continued indefinitely. The incidence of adverse effects tends to be high.
Acitretin (Soriatane)
Retinoic acid analog, like etretinate and isotretinoin. Etretinate is main metabolite and has clinical effects similar to those of etretinate. Mechanism of action unknown.
Adult
25-50 mg/d PO as single dose with main meal; terminate when lesions resolve sufficiently
Pediatric
Not established
Increases toxicity of methotrexate (avoid concomitant use); interferes with effects of microdosed progestin minipill; coadministration with alcohol may enhance synthesis of etretinate, which has half-life longer than that of acitretin (>120 d)
Documented hypersensitivity
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Do not use in severe obesity; women of childbearing age must be able to comply with effective contraceptive; contraception should be continued for at least 3 years after treatment with acitretin is stopped; etretinate may form from acitretin, which takes about 2-3 years to clear from the body; caution in impaired renal or liver function; perform AST, ALT, and LDH tests before acitretin therapy at q1-2wk until stable, then as clinically indicated
Nickel-chelating agents
These drugs split into 2 molecules of sodium diethyldithiocarbamate after absorption, which, in turn, chelates divalent metal ions (eg, Ni++) and results in the increased urinary excretion of nickel. Effective in the treatment of vesicular palmoplantar dermatitis in nickel-hypersensitive patients whose eczema is aggravated by oral challenge with nickel.
Disulfiram (Antabuse)
Thiuram derivative that interferes with aldehyde dehydrogenase. Chelating effect helpful in reducing the nickel burden in patients allergic to nickel.
Adult
100 mg PO tid/qid
Pediatric
Not established
Alcohol; risk of psychotic reaction with metronidazole; increased risk of toxicity with phenytoin and theophylline; enhances sedative effect of benzodiazepines
Documented hypersensitivity; cardiac failure, coronary artery disease hypertension, psychosis, pregnancy, breastfeeding; alcohol ingestion in previous 12 h
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
Precautions
Caution with hepatic or renal impairment; respiratory disease, hypothyroidism, diabetes, epilepsy, drowsiness, fatigue, nausea, vomiting, urticaria, and jaundice may occur; patients should avoid alcohol for a minimum of 1 wk after therapy ends
Phototherapy
PUVA therapy is used to treat many skin conditions, including psoriasis, eczema, urticaria, mycosis fungoides, vitiligo, and palmoplantar pustular dermatoses.
The drug 8-methoxypsoralen (8-MOP) is taken 2 h before exposure to UVA irradiation. The initial UVA irradiation dose of 2.5 J/cm2 is usually increased by 0.5 J/cm2 for approximately 6 treatments, then by 1 J/cm2 per treatment for a total of 25-35 treatments.
Local bath-PUVA therapy has been successful in treating palmoplantar eczema and psoriasis. Compared with systemic PUVA, local-bath therapy has several advantages, particularly the absence of phototoxicity, severe hyperpigmentation, and protracted photosensitivity. The drug 8-MOP in a 0.15% alcoholic solution is added to tap water (37°C) at a concentration of 1 mg 8-MOP/L (0.0001%). After a 15-minute bath, the palms or soles are exposed to UVA radiation.
Methoxsalen (Oxsoralen, Meladinine, Basotherm)
Inhibits mitosis by covalently binding to pyrimidine bases in DNA when photoactivated by UV-A.
Adult
Oral: 0.6 mg/kg PO 2 h before UV-A exposure, 3 times/wk
Topical: 0.5 J/cm2 UV-A (standard) increased by 0.5 J/cm2 q3d initially; increased by increments of 0.5-1 J/cm2 until slight erythema reaction seen; approximate total of 25 treatments
Pediatric
Not established
Caution with concomitant photosensitizing drugs (eg, anthralin, coal tar, griseofulvin, phenothiazines, nalidixic acid, halogenated salicylanilides, sulfonamides, tetracyclines, thiazides) and organic dyes (eg, methylene blue, toluidine blue, rose bengal, and methyl orange)
Documented hypersensitivity; squamous cell cancer; cataract; light-sensitive diseases (eg, lupus, porphyria); ingestion of photosensitizing drugs; hepatic disease; arsenic therapy
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
Precautions
Phototoxic reactions may occur; marked erythema, pruritus, blistering, hyperpigmentation, persistent light sensitivity after treatment, cataract formation; patients must wear protective glasses for 24 h after therapy; reported adverse effects include dizziness, headache, malaise, depression, hypopigmentation, bullae, rash, herpes simplex, miliaria, urticaria, folliculitis, GI upset, skin tenderness, leg cramps, and hypotension
Topical immunosuppressives
Topical immunosuppressive agents, such as tacrolimus, have been successfully used to decrease the severity of chronic palmar eczema. These drugs may be used as steroid-sparing agents.
Tacrolimus topical (Protopic)
Reduces itching and inflammation by suppressing release of cytokines from T cells; inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha (all involved in early T-cell activation).
May inhibit release of preformed mediators from skin mast cells and basophils; may down-regulate FCeRI expression on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class more expensive than topical corticosteroids.
Adult
Apply thin layer to affected skin areas bid; rub in gently and completely; continue treatment for 1 wk after signs and symptoms clear
Pediatric
<2 years: Not established
>2 years: Apply as in adults
None reported
Documented hypersensitivity to tacrolimus or components of ointment
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
Precautions
Possible burning sensation during first few days of application; skin photosensitivity (caution patients about exposure to direct or artificial sunlight and to use sunscreen); safety and efficacy in infected atopic dermatitis not known; application under occlusion, which may promote systemic exposure, not evaluated (do not use ointment with occlusive dressings); absorption after topical applications is minimal (relative to systemic administration); excreted in human milk (base decision to stop breastfeeding or therapy on importance of maternal therapy and potential serious adverse reactions in infant)
More on Vesicular Palmoplantar Eczema |
| Overview: Vesicular Palmoplantar Eczema |
| Differential Diagnoses & Workup: Vesicular Palmoplantar Eczema |
 Treatment & Medication: Vesicular Palmoplantar Eczema |
| Follow-up: Vesicular Palmoplantar Eczema |
| Multimedia: Vesicular Palmoplantar Eczema |
| References |
| « Previous Page | Next Page » |
References
Chen JJ, Liang YH, Zhou FS, et al. The gene for a rare autosomal dominant form of pompholyx maps to chromosome 18q22.1-18q22.3. J Invest Dermatol. Feb 2006;126(2):300-4. [Medline].
Edman B. Palmar eczema: a pathogenetic role for acetylsalicylic acid, contraceptives and smoking?. Acta Derm Venereol. 1988;68(5):402-7. [Medline].
Man I, Ibbotson SH, Ferguson J. Photoinduced pompholyx: a report of 5 cases. J Am Acad Dermatol. Jan 2004;50(1):55-60. [Medline].
Man I, Ibbotson SH, Ferguson J. Photoinduced pompholyx: a report of 5 cases. J Am Acad Dermatol. Jan 2004;50(1):55-60. [Medline].
Guillet MH, Wierzbicka E, Guillet S, Dagregorio G, Guillet G. A 3-year causative study of pompholyx in 120 patients. Arch Dermatol. Dec 2007;143(12):1504-8. [Medline].
Uyttendaele H, Obadiah J, Grossman M. Dyshidrotic-like spongiotic dermatitis after intravenous immunoglobulin therapy. J Drugs Dermatol. Jun 2003;2(3):337-41. [Medline].
Colebunders R, Zolfo M, Lynen L. Severe dyshidrosis in two patients with HIV infection shortly after starting highly active antiretroviral treatment. Dermatol Online J. Aug 1 2005;11(2):31. [Medline].
MacConnachie AA, Smith CC. Pompholyx eczema as a manifestation of HIV infection, response to antiretroviral therapy. Acta Derm Venereol. 2007;87(4):378-9. [Medline].
Kim YJ, Kim MY, Kim HO, Park YM. Dyshidrosiform bullous pemphigoid. Acta Derm Venereol. 2004;84(3):253-4. [Medline].
Schnopp C, Remling R, Mohrenschlager M, Weigl L, Ring J, Abeck D. Topical tacrolimus (FK506) and mometasone furoate in treatment of dyshidrotic palmar eczema: a randomized, observer-blinded trial. J Am Acad Dermatol. Jan 2002;46(1):73-7. [Medline].
Schurmeyer-Horst F, Luger TA, Bohm M. Long-term efficacy of occlusive therapy with topical pimecrolimus in severe dyshidrosiform hand and foot eczema. Dermatology. 2007;214(1):99-100. [Medline].
Egawa K. Topical vitamin D3 derivatives in treating hyperkeratotic palmoplantar eczema: a report of five patients. J Dermatol. May 2005;32(5):381-6. [Medline].
Scerri L. Azathioprine in dermatological practice. An overview with special emphasis on its use in non-bullous inflammatory dermatoses. Adv Exp Med Biol. 1999;455:343-8. [Medline].
Egan CA, Rallis TM, Meadows KP, Krueger GG. Low-dose oral methotrexate treatment for recalcitrant palmoplantar pompholyx. J Am Acad Dermatol. Apr 1999;40(4):612-4. [Medline].
Pickenacker A, Luger TA, Schwarz T. Dyshidrotic eczema treated with mycophenolate mofetil. Arch Dermatol. Mar 1998;134(3):378-9. [Medline].
Ogden S, Clayton TH, Goodfield MJ. Recalcitrant hand pompholyx: variable response to etanercept. Clin Exp Dermatol. Jan 2006;31(1):145-6. [Medline].
Behrens S, von Kobyletzki G, Gruss C, Reuther T, Altmeyer P, Kerscher M. PUVA-bath photochemotherapy (PUVA-soak therapy) of recalcitrant dermatoses of the palms and soles. Photodermatol Photoimmunol Photomed. Apr 1999;15(2):47-51. [Medline].
Petering H, Breuer C, Herbst R, Kapp A, Werfel T. Comparison of localized high-dose UVA1 irradiation versus topical cream psoralen-UVA for treatment of chronic vesicular dyshidrotic eczema. J Am Acad Dermatol. Jan 2004;50(1):68-72. [Medline].
Tzaneva S, Kittler H, Thallinger C, Honigsmann H, Tanew A. Oral vs. bath PUVA using 8-methoxypsoralen for chronic palmoplantar eczema. Photodermatol Photoimmunol Photomed. Apr 2009;25(2):101-5. [Medline].
Robertson L. New and existing therapeutic options for hand eczema. Skin Therapy Lett. Mar 2009;14(3):1-5. [Medline].
Swartling C, Naver H, Lindberg M, Anveden I. Treatment of dyshidrotic hand dermatitis with intradermal botulinum toxin. J Am Acad Dermatol. Nov 2002;47(5):667-71. [Medline].
Kontochristopoulos G, Gregoriou S, Agiasofitou E, Nikolakis G, Rigopoulos D, Katsambas A. Letter: regression of relapsing dyshidrotic eczema after treatment of concomitant hyperhidrosis with botulinum toxin-A. Dermatol Surg. Oct 2007;33(10):1289-90. [Medline].
Wollina U, Karamfilov T. Adjuvant botulinum toxin A in dyshidrotic hand eczema: a controlled prospective pilot study with left-right comparison. J Eur Acad Dermatol Venereol. Jan 2002;16(1):40-2. [Medline].
Fairris GM, Jones DH, Mack DP, Rowell NR. Conventional superficial X-ray versus Grenz ray therapy in the treatment of constitutional eczema of the hands. Br J Dermatol. Mar 1985;112(3):339-41. [Medline].
Cartwright PH, Rowell NR. Comparison of Grenz rays versus placebo in the treatment of chronic hand eczema. Br J Dermatol. Jul 1987;117(1):73-6. [Medline].
Lindelof B, Wrangsjo K, Liden S. A double-blind study of Grenz ray therapy in chronic eczema of the hands. Br J Dermatol. Jul 1987;117(1):77-80. [Medline].
Matin A, Bliwise DL, Wellman JJ, Ewing HA, Rasmuson P. Resolution of dyshidrotic dermatitis of the hand after treatment with continuous positive airway pressure for obstructive sleep apnea. South Med J. Feb 2002;95(2):253-4. [Medline].
Stuckert J, Nedorost S. Low-cobalt diet for dyshidrotic eczema patients. Contact Dermatitis. Dec 2008;59(6):361-5. [Medline].
Vocks E, Plotz SG, Ring J. The Dyshidrotic Eczema Area and Severity Index - A score developed for the assessment of dyshidrotic eczema. Dermatology. 1999;198(3):265-9. [Medline].
Burton JL, Holden CA. Morphological types of hand eczema, pompholyx. Eczema, lichenification and prurigo. In: Champion RH, Wilkinson DS, Ebling FJG, eds. Rook, Wilkinson, Ebling Textbook of Dermatology. 6th ed. Blackwell Science: 1998:650-2.
Douwes KE, Karrer S, Abels C, Landthaler M, Szeimies RM. Does smoking influence the efficacy of bath-PUVA therapy in chronic palmoplantar eczema?. Photodermatol Photoimmunol Photomed. Feb 2000;16(1):25-9. [Medline].
Kimball A. Vesicular palmoplantar eczema. In: Fitzpatrick's Dermatology in General Medicine. 2003.
Odia S, Vocks E, Rakoski J, Ring J. Successful treatment of dyshidrotic hand eczema using tap water iontophoresis with pulsed direct current. Acta Derm Venereol. Nov 1996;76(6):472-4. [Medline].
Schmidt T, Abeck D, Boeck K, Mempel M, Ring J. UVA1 irradiation is effective in treatment of chronic vesicular dyshidrotic hand eczema. Acta Derm Venereol. Jul 1998;78(4):318-9. [Medline].
Storrs FJ. Acute and recurrent vesicular hand dermatitis not pompholyx or dyshidrosis. Arch Dermatol. Dec 2007;143(12):1578-80. [Medline].
Sugimura C, Katsuura J, Moriue T, Matsuoka Y, Kubota Y. Dyshidrosiform pemphigoid: report of a case. J Dermatol. Jul 2003;30(7):525-9. [Medline].
Wilkinson JD. Vesicular palmoplantar eczema. In: Freedberg IM, Elsen AZ, Wolff K, eds. Fitzpatrick's Dermatology in General Medicine. 5th ed. McGraw-Hill; 1999:1489-94.
Further Reading
Keywords
vesicular palmoplantar eczema, pompholyx, dyshidrotic eczema, vesicobullous dermatitis, dyshidrosis, subacute vesiculosquamous eczema, chronic relapsing vesiculosquamous eczema, hand eczema
