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Vesicular Palmoplantar Eczema Treatment & Management

  • Author: Elaine Dupuis, MD, MBA; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Jun 21, 2016
 

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.[12]

Topical therapy

Topical therapy for vesicular palmoplantar eczema includes high-potency glucocorticoids, topical calcineurin inhibitors, adjunctive keratolytics, and/or topical retinoids.

Topical high-potency glucocorticoids, such as betamethasone dipropionate and clobetasol propionate, are first-line therapies. Ointment preparations are less irritating and can enhance drug delivery. As well, application of these medications under plastic and vinyl occlusion enhances their efficacy. However, this method may predispose the patient to secondary 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 such as betamethasone valerate, triamcinolone, or mometasone cream or ointment.

In the hyperkeratotic form of hand eczema, topical keratolytic agents like salicylic acid and tar agents may be useful adjunctive therapies.

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.

Topical calcineurin inhibitors, such as topical tacrolimus 0.1% ointment and pimecrolimus, have been shown to be as effective as mometasone furoate in the treatment of chronic relapsing eczema of the hands.[28] These topical immunomodulators may be used as steroid-sparing agents to treat resistant palmar eczema, with minimal systemic absorption or systemic effect.[29] 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.[30]

Systemic therapy

Systemic therapy includes steroids, immunosuppressive agents (eg, azathioprine,[31] cyclosporine), retinoids (eg, acitretin, alitretinoin), 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.[32, 33] 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.

Increasingly, the retinoid alitretinoin has been shown to be a favorable option for severe hand eczema. Oral alitretinoin has been shown to be an effective and well-tolerated therapy for treatment of severe hand eczema.[34, 35] One randomized, double-blind, placebo-controlled multicenter trial examining severe chronic hand eczema found alitretinoin superior to placebo, with 48% of patients achieving full or almost full resolution of signs and symptoms.[36] A 2012 observational study noted alitretinoin improved vesicular eczema in 47.9% of patients.[37] An open-label study showed significant improvement with alitretinoin at doses starting at 10 mg daily (increased to 30 mg daily as tolerated).[38]

The use of etanercept in a case study achieved a 4-month remission of vesicular palmoplantar eczema, which was followed by relapse.[39]

Phototherapy, in particular PUVA, has been shown to be effective in dyshidrotic eczema for disease control and maintaining remission.[40] 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.[41, 42] 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.[43]  

Narrowband UVB therapy has been shown to be equally efficacious as PUVA therapy for dyshidrotic and "dry" types of hand eczema and can be used as an alternative to PUVA, with fewer adverse effects.[44] As UV radiation has an immunosuppressive effect, one case noted resolution of dyshidrotic eczema symptoms with repeated sunlight exposures (although recurrences were not reduced).[45] Only a few reports describe the role of narrowband UVB therapy in hyperkeratotic hand eczema. However, narrowband UVB has been used with some success in other hyperkeratotic disorders like palmoplantar psoriasis. One study comparing PUVA therapy with narrowband UVB for palmoplantar psoriasis demonstrated significant improvement with both modalities. However, PUVA was superior to narrowband UVB in reducing clinical severity scores.[46] PUVA may be superior to UVB modalities for hyperkeratotic hand eczema because of the deeper penetration of UVA rays into the skin.

Other therapies

Other treatment options[47] 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.[48, 49] It has been shown to improve symptoms of itching and vesicular formation in a controlled left-right hand comparison study with 8 subjects.[50] 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. One case report showed improvement of relapsing dyshidrotic eczema with treatment of coexisting hyperhidrosis with the anticholinergic oxybutynin.[51]

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.[52] One study revealed excellent results with the use of superficial radiation for palmoplantar eczema, while others have not.[53, 54] 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.[55]

Id reactions tend to resolve with treatment of the primary infection. Consider systemic antibiotics if secondary infection is suspected, and culture suspicious lesions.

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Consultations

Refer patients to a dermatologist because vesicular palmoplantar eczema is likely to be a lifelong disease (albeit intermittent in some patients).

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Diet

Maintaining a low-cobalt diet has been suggested to decrease the number of dyshidrotic eczema flares.[56]

Patients with established nickel sensitivity may benefit from nickel-free diets.

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Prevention

Elimination of known exacerbating factors, although often difficult to accomplish, is crucial in preventing relapses of vesicular palmoplantar eczema.

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Contributor Information and Disclosures
Author

Elaine Dupuis, MD, MBA Resident Physician, Section of Dermatology, Department of Medicine, University of Calgary Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Wingfield Rehmus, MD, MPH Dermatologist, BC Children's Hospital, Vancouver, British Columbia

Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie; Valeant Canada<br/> Received honoraria from Valeant Canada for advisory board; Received honoraria from Pierre Fabre for advisory board; Received honoraria from Mustella for advisory board; Received honoraria from Abbvie for advisory board.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Steven R Feldman, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, North Carolina Medical Society, Society for Investigative Dermatology

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Arash Taheri, MD Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Carol E Cheng, MD Attending Physician, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, (1) Spiros Gramvussakis, MD; (2) John D Wilkinson, MBBS, MRCS, FRCP; and (3) Raeesa W Mirza, MD, MBBS, to the development and writing of this article.

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