Background
Dyshidrotic eczema is a type of eczema (dermatitis) that is characterized by a pruritic vesicular eruption (bullae, or blisters) on the fingers, palms, and soles; typically these intensely itchy blisters develop on the edges of the fingers, toes, palms, and soles of the feet. (See the image below.) This skin condition affects teenagers and adults and may be acute, recurrent, or chronic. A more appropriate term for this vesicular eruption is pompholyx, which means bubble. Some have suggested that the terms pompholyx and dyshidrosis are both obsolete and that acute and recurrent vesicular hand dermatitis is a better term for this condition.
The etiology of dyshidrotic eczema is unresolved and is believed to be multifactorial. Dyshidrotic eczema is considered to be a reaction pattern caused by various endogenous conditions and exogenous factors.
The clinical course of dyshidrotic eczema can range from self-limited to chronic, severe, or debilitating. The skin condition's unresponsiveness to treatment can be frustrating for the patient and physician.
Signs and symptoms
Signs and symptoms of dyshidrotic eczema include the following:
-
Symmetric crops of clear vesicles and/or bullae (blisters)
-
Intensely pruritus (itchiness)
-
Typically present on the palms and soles, as well as the lateral aspects of fingers and toes
-
Deep-seated vesicles with a tapiocalike appearance
-
May become large, form bullae, and become confluent
-
In chronic disease, fingernails may reveal dystrophic changes
-
Vesicles typically resolve without rupturing, followed by desquamation
Diagnosis
Diagnosis of dyshidrotic eczema includes the following:
-
Typically a clinical diagnosis
-
Bacterial culture and sensitivity can rule out secondary infection
-
Patch testing to exclude allergic contact dermatitis
-
Recalcitrant cases warrant systemic evaluation
-
Potassium hydroxide (KOH) wet mount to exclude dermatophyte infection
-
Punch biopsy for direct immunofluorescence to exclude bullous pemphigoid
Treatment
Treatments for dyshidrotic eczema include the following:
-
First-line treatment - High-strength topical steroids and cold compresses; systemic steroids are also used
-
Treatment for bullae (blisters) - Compresses with Burow solution or 1:10.000 solution of potassium permanganate; drainage of large bullae with a sterile syringe, with the roof left intact; systemic antibiotic therapy covering Staphylococcus aureus and group A streptococci
-
Ultraviolet A (UVA) or UVA-1 light therapy, alone or with oral or topical psoralen (PUVA); UVB therapy has also shown utility
-
Topical calcineurin inhibitors
-
OnabotulinumtoxinA injections
-
For severe refractory pompholyx - Azathioprine, methotrexate, mycophenolate mofetil, cyclosporine, or etanercept
-
Nickel chelators (eg, disulfiram) occasionally used in nickel-sensitive patients
-
Alitretinoin (9-cis retinoic acid)
-
Dietary avoidance of nickel and cobalt for nickel- and cobalt-sensitive patients
Etiology
The hypothesis of sweat gland dysfunction as the cause of dyshidrotic eczema was refuted on the grounds that vesicles have not been shown to be associated with sweat ducts. A 2009 case report provided clear histopathologic evidence that sweat glands do not play a role in dyshidrosis. [1] 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 onabotulinumtoxinA injection. [2]
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 type I and type IV hypersensitivity reactions. In addition, they can also act as atypical haptens, activating T lymphocytes through human leukocyte antigen (HLA)-independent pathways, causing systemic allergic dermatitis in the form of dyshidrotic eczema. [3, 4]
Emotional stress [5] and environmental factors (eg, seasonal changes, hot or cold temperatures, and humidity) have been reproted to exacerbate dyshidrosis.
Dyshidrosislike eczematous eruptions with the use of intravenous (IV) immunoglobulin (IVIG) infusions have been reported. [6] A 2011 search of the literature identified pompholyx as one of the most important cutaneous adverse effects of IVIG, being present in 62.5% of the patients reported, of whom 75% developed the lesions after just one IVIG treatment. [7] The eruption tends to be mild and to wane over time. It usually responds very well to topical steroids, [8, 9, 10] but it may become recurrent and more aggressive after repeated doses of IVIG.
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. The factors believed to be associated with dyshidrotic eczema are discussed in more detail below.
Genetic factors
Monozygotic twins have been affected simultaneously by dyshidrotic eczema. The pompholyx gene has been mapped to band 18q22.1-18q22.3 in the autosomal dominant form of familial pompholyx. [11]
Mutations on the filaggrin gene leading to loss of filaggrin, a structural protein of the stratum corneum involved in the barrier function of the skin, cause dyskeratinization, increased transepidermal water loss, and an increase in the transepidermal antigen transfer. Combined, these features have been associated with the development of ichthyosis and atopic dermatitis, and they may be involved in the development of irritant and allergic contact dermatitis, which are well-known skin conditions associated with dyshidrotic eczema.
Chronic hand dermatitis, including dyshidrotic eczema, has also been associated with defects in the skin barrier, and in a few cases, it has also been associated with mutations in the filaggrin gene; however, these have not reached statistical significance. [12]
Aquaporins are known to be expressed in patients with atopic dermatitis, and such expression may also be related to exacerbation and chronicity of pompholyx. Aquaporins are channel proteins located on cell membranes that increase their permeability. Particular examples include the aquaglyceroporins, which can transport water and glycerol. Aquaporin-3 and aquaporin-10 are normally expressed in the basal layer of the epidermis, and immunohistochemical staining has demonstrated their presence in all epidermal layers in patients with pompholyx. These channels may participate in the increase of transepidermal water loss seen in atopic dermatitis and possibly in pompholyx.
Owing to osmotic gradients, among other factors, the direction of water and glycerol through aquaporins is from the skin to the environment, possibly contributing to skin dehydration, even immediately after hand washing. Hypothetically, topical or systemic inhibition of the expression of aquaporins in the epidermis could contribute with the preservation of water and glycerol, decreasing the frequency and severity of pompholyx exacerbations. [13]
Atopy
As many as 50% of patients with dyshidrotic eczema have reportedly had personal or familial atopic diathesis (eg, eczema, asthma, hay fever, or allergic sinusitis). The serum immunoglobulin E (IgE) level frequently is increased, even in patients who do not report a personal or familial history of atopy. Occasionally, dyshidrotic eczema is the first manifestation of an atopic diathesis.
Nickel sensitivity
Nickel sensitivity may be a significant factor in dyshidrotic eczema. It was reported to be low in some studies of dyshidrosis patients but significantly elevated in others. Increased nickel excretion in the urine has been reported during exacerbations of pompholyx. Ingested metals have been found to provoke exacerbations of pompholyx in some patients.
Low-nickel diets have reportedly decreased the frequency and severity of pompholyx flares. A high palmoplantar perspiration rate has been suggested to result in a local concentration of metal salts that may provoke the vesicular reaction. Contact allergy has been documented in 30% of patients with dyshidrotic eczema.
Cobalt sensitivity
Oral ingestion of cobalt manifests systemic allergic dermatitis as dyshidrotic eczema less frequently than oral ingestion of nickel does. Much more common is the simultaneous occurrence of nickel and cobalt allergy seen in 25% of nickel-sensitive patients developing pompholyx. In these cases, the eczema is usually more severe. When suspected as the cause of the dyshidrotic eczema, high oral ingestion of cobalt should be taken into consideration, regardless of the patch test results. [3]
A point-based low-cobalt diet has been proposed to help patients limit cobalt ingestion and to keep the serum level below the threshold for developing flares (approximately < 12 μg/day). This diet has demonstrated higher compliance than an avoidance diet list. In addition, this diet reduces the amount of nickel consumed. [3]
Exposure to other sensitizing chemicals or metals
Dyshidrotic eczema outbreaks are sometimes associated with exposure to other sensitizing chemicals or metals (eg, chromium, carba mix, fragrance mix, diaminodiphenylmethane, dichromates, benzoisothiazolones, paraphenylenediamine, perfumes, fragrances, balsam of Peru, or Primula plant).
Id reaction
Controversy has surrounded the possible existence of an id reaction, which is considered to be a distant dermatophyte infection (tinea pedis, kerion of scalp) triggering a palmar pompholyx reaction (also termed pompholyx dermatophytid).
Fungal infection
Pompholyx occasionally resolves when a tinea pedis infection is treated, then relapses when the fungal infection recurs, supporting the existence of this reaction pattern. Of patients who have a vesicular reaction to intradermal trichophytin testing, fewer than one third have experienced a resolution of pompholyx after treatment with antifungal agents.
Emotional stress
This is a possible factor in dyshidrotic eczema. Many patients report recurrences of pompholyx during stressful periods. Improvement of dyshidrotic eczema with the use of biofeedback techniques for stress reduction supports this hypothesis.
Other factors
Isolated reports have described other possible causative factors (eg, aspirin ingestion, oral contraceptive use, cigarette smoking, and the presence of implanted metals). A 3-year prospective study (N = 120) of the causes of dyshidrotic eczema found causes of pompholyx related to contact exposure (67.5%), including to cosmetic products (31.7%) and metals (16.7%); interdigital-plantar intertrigo (10%); and internal factors (6.7%); an additional 15% of patients had undiagnosed (idiopathic) causes probably related to atopic factors. [14]
Contact allergy was found in 89 (74.2%) of the 120 patients. [14] The most frequent allergens were nickel, shower gel, chromium, fragrance, shampoo, and balsam of Peru; less frequent allergens were lanolin, cobalt, thiuram, lauryl sulfate, fresh tobacco, p-phenylenediamine (PPD), formaldehyde, parabens, and octyl gallate. In 97 of 193 positive patch test results, application of the agent was correlated with pompholyx recurrence. The relevance of the analysis was confirmed in 81 (67.5%) of the 120 patients. In summary, the most frequent causes of pompholyx related to contact with substances were hygiene product intolerance (46.7%), metal allergy (25%), and others (28.3%).
Intertrigo occurred in 19 (15.8%) of the 120 patients. [14] Of those individuals, 80% presented with dermatophytosis and 20% presented with candidiasis. After 3 weeks of antifungal therapy, 13 of 19 patients remained asymptomatic of pompholyx.
With regard to internal causes, 30 patients presented with a positive patch test result for metals, but only two presented with exacerbations of the lesions after a challenge test. [14]
Of 58 patients with a history of smoking tobacco, five presented with a positive reaction on a tobacco patch test, and two of those were considered relevant. [14] Drug allergy was determined to be the causative agent in 3 patients (amoxicillin in 2 and intravenous immunoglobulin in 1). Food-related pompholyx was detected in 4 patients, and, after a challenge test, reactivation occurred in 3 of these patients (2 for paprika and 1 for orange juice).
Ultraviolet A light
In a case series, five patients with prior diagnosis of pompholyx developed lesions morphologically and histologically consistent with a vesicular dermatitis after provocation with long-wavelength UVA light. [15] Further workup ruled out contact dermatitis, polymorphous light eruption, and heat as the culprit, confirming that the reaction was due to true photosensitivity rather than to photoaggravation.
Pompholyx caused by UVA exposure may possibly be considered a variation of seasonal (summer) pompholyx. In the United States, dyshidrotic eczema is more commonly seen in warmer climates and during the spring and summer months. A study in Turkey also revealed a higher prevalence of dyshidrotic eczema in the summer months. [16]
In a case series, three patients with frequent pompholyx exacerbations, mostly during summer (ie, photoaggavated pompholyx), were subjected to photoprovocation testing, with positive development of pompholyx lesions in two. [17] Lesions occurred after exposure to solar-simulated UV radiation and broadband UVA. Treatment included photoprotective measures in addition to standard treatment and led to decreased frequency and severity of exacerbations. The authors suggested that this condition may be underdiagnosed and recommended recognition and early detection to institute sun protection as soon as possible and to avoid starting phototherapy or photochemotherapy in this subset of pompholyx patients.
It is noteworthy that UVB phototherapy and photochemotherapy are well-known, efficient treatments for pompholyx.
Epidemiology
US and international statistics
Dyshidrotic eczema occurs in 5-20% of US patients with hand eczema; it more commonly develops in warmer climates and during spring and summer months (seasonal or summer pompholyx).
In a 1-year study from Sweden, dyshidrotic eczema accounted for 1% of initial consultations. A study that included 107,206 Swedish individuals found that 51 (0.05%) were diagnosed with dyshidrosis. [18] Of all hand dermatitis cases in that population, 3% had dyshidrosis. 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%). [19]
Age- and sex-related demographics
Dyshidrotic eczema affects individuals over a broad age range (4-76 y; mean age, 38 y). The peak incidence of the skin condition occurs between the ages of 20 and 40 years. After middle age, the frequency of dyshidrotic eczema episodes tends to decrease.
The male-to-female ratio for dyshidrotic eczema has variably been reported as 1:1 or 1:2.
Prognosis
Dyshidrotic eczema follows a chronic, intermittent course, with fewer episodes occurring after middle age. Some mildly affected patients experience spontaneous resolution within 2-3 weeks. (See Treatment and Medication.)
Patient Education
Individuals with dyshidrotic eczema should be educated about the difficulty of achieving successful treatment. They should be informed that the typical first-line treatments for the blisters of this condition are high-strength topical steroids and cold compresses and that additional treatments that might be helpful include stress reduction (possibly involving consultation with a mental health professional and potentially including biofeedback therapy) and hand care measures (eg, use of moisturizers and emollients).
Bed rest may be necessary if large blisters develop on the feet. Work activities or activities of daily living (ADLs) may be hampered by blisters on the hands.
Nickel- or cobalt-sensitive dyshidrotic eczema patients should be instructed to avoid contact with these allergens; this may involve avoidance of certain activities, foods, and beverages.
For patient education information, see the Skin Conditions and Beauty Center, as well as Eczema (Atopic Dermatitis).
-
Dyshidrotic eczema (pompholyx). Tense vesicles and bullae on the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.
-
Dyshidrotic eczema (pompholyx). Close-up view of tense vesicles and bullae of the palm. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.
-
Dyshidrotic eczema (pompholyx). Discrete yellow pustules on the sole of the foot. Courtesy of Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.
-
Dyshidrotic eczema (pompholyx). Multiple tense vesicles on the palm.
-
Dyshidrotic eczema (pompholyx). Small tense vesicles on the fingers.
-
Dyshidrotic eczema (pompholyx). Small, discrete, coalesced vesicles on the dorsal hand.
-
Dyshidrotic eczema (pompholyx). Small, discrete, coalesced vesicles on the fingers.
-
Dyshidrotic eczema (pompholyx). Palms and soles of a patient with a dyshidrosis flare. The patient unroofed a large bulla on the right sole.
-
Dyshidrotic eczema (pompholyx). Small discrete vesicles of the lateral fingers.
Tables
What would you like to print?
- Overview
- Presentation
- DDx
- Workup
- Treatment
- Guidelines
- Medication
- Antihistamines, 1st Generation
- Antihistamines, 2nd Generation
- Antineoplastics, Retinoids
- Antipruritics/Non-corticosteroid Topical
- Calcineurin Inhibitors
- Cephalosporins, 1st Generation
- Corticosteroids
- Corticosteroids, Topical
- Immunosuppressants
- Interleukin Inhibitors
- Macrolides
- Penicillins, Penicillinase-Resistant
- Psychiatry Agents, Other
- Show All
- Media Gallery
- References