What is dyshidrotic eczema?

This common form of eczema causes small, intensely itchy blisters on the edges of the fingers, toes, palms,
and soles of the feet. It is is twice as common in women as it is in men.

Because of the association with seasonal allergies, the dyshidrotic eczema blisters are known to erupt more
frequently during the spring allergy season. The blisters may last up to three weeks before they begin to dry
and can sometimes be large and painful. As the blisters dry, they may turn into skin cracks or cause the skin
to feel thick and spongy, especially if you’ve been scratching the area.

Deep blisters on the sides of the feet are typical of dyshidrotic eczema

Doctors also may refer to dyshidrotic eczema as:

 Cheiropompholyx
 Dyshidrosis
 Foot-and-hand eczema
 Pompholyx
 Vesicular eczema
 Palmoplantar eczema
There is no cure for dyshidrotic eczema, but the good news is, in many cases it’s manageable. And like all
types of the condition, it isn’t contagious. You cannot “catch” dyshidrotic eczema from another person, or
give it to someone else.

What does dyshidrotic eczema look like?

All types of eczema cause itching and redness. But some, like dyshidrotic eczema, look and act slightly
different than others. It is possible to have dyshidrotic eczema and another form of eczema such as contact
dermatitis, at the same time.

Symptoms of dyshidrotic eczema include:

 Deep-set blisters on the edges of the fingers, toes, palms and soles of the feet
 Itching
 Redness
 Flaking
 Scaly, cracked skin
 Pain
Dyshidrotic eczema blisters can be hard to see on the palms and fingers because the skin is thicker here

It’s important to understand which type of eczema you may have and also your symptoms and triggers, so
that you can better treat and manage it. The only way to be sure that you have dyshidrotic eczema, is to
make an appointment with your doctor.

What causes dyshidrotic eczema?

Dyshidrotic eczema usually appears in adults ages 20 through 40 but it can also affect children. People
with contact dermatitis, atopic dermatitis or hay fever, are at higher risk of developing dyshidrotic eczema.
Dyshidrotic eczema seems to run in families, so if you have a close relative with this form of eczema, your
chance of also developing it is increased.
There are some common triggers for dyshidrotic eczema:

 Stress
 Pollen
 Moist hands and feet from excessive sweating or prolonged contact with water
 Nickel in everyday objects such as jewelry, keys, cell phones, eyeglass frames, stainless steel items,
and metal buttons, snaps and zippers
 Nickel in foods such as cocoa, chocolate, soy beans, oatmeal, nuts, almonds, fresh and dried
legumes, and canned foods
 Cobalt in everyday objects such as cobalt-blue colored dishware, paints and varnishes; certain
medical equipment; jewelry; and in metal snaps, buttons and zippers
 Cobalt in foods such as clams, fish, leafy green vegetables, liver, milk, nuts, oysters, and red meat
 Chromium salts used in the manufacturing of cement, mortar, leather, paints and anticorrosives
Treatment for dyshidrotic eczema
At-home treatment for dyshidrotic eczema includes soaking hands and feet in cool water or applying
compresses for 15 minutes to the affected area two to four times a day followed by a rich moisturizer or
a skin barrier repair cream.
For more severe cases of dyshidrotic eczema, a provider may prescribe topical steroids, TCIs
or phototherapy. Additionally, the provider may drain the blisters in-office, and/or give a dose of Botox in
the hands and feet to reduce sweating and wetness, which are known triggers for this form of eczema.
Dyshidrotic eczema has the tendency to get infected, which can delay clearing of symptoms. If you suspect
you have an infection in the area where the eczema appears, make an appointment with your provider.

Atopic dermatitis and contact dermatitis may look like dyshidrotic eczema.
Tips for managing dyshidrotic eczema
There is no surefire way to prevent dyshidrotic eczema. However, good skin care and moisturizing can help
strengthen your skin against irritation, so that it doesn’t flare up, or get worse. The most important thing to
remember is to be consistent
https://nationaleczema.org/eczema/types-of-eczema/dyshidrotic-eczema/

Dyshidrotic eczema on a patient's palm: The tiny, deep-seated

blisters are often very itchy.

What is dyshidrotic eczema?

Dyshidrotic (dis-hi-drah- tic) eczema (DE) is a common group of skin conditions in which the skin cannot
protect itself as well as it should, so the person often gets itchy, dry skin).

DE causes itchy, dry skin. People also develop small, deep-seated blisters, usually on their hands. It’s also
possible to develop blisters on your feet.

Whether on your hands, feet, of both, the blisters are often very itchy and painful.

When the blisters clear (usually in 2 or 3 weeks), the skin tends to be red, dry, and cracked.

There is no cure for DE, so people can have flares. For many people, DE flares when they’re under a lot of
stress, temperatures rise (such as in spring or summer), or their hands stay wet for long periods of time.

DE flares range from mild to debilitating. A severe flare on your feet can make walking difficult. Having
many blisters on your hands can make it difficult to work and perform everyday tasks like shampooing your
hair and washing dishes.

This common skin disease has many names, including:

 Cheiropompholyx (affects the hands)

 Dyshidrosis

 Dyshidrotic dermatitis

 Foot-and-hand eczema

 Pedopompholyx (affects the feet)

 Pompholyx

 Vesicular eczema

 Vesicular palmoplantar eczema

 Severe dyshidrotic eczema: As the blisters dry, the skin often starts
to peel.

How dyshidrotic eczema begins

This skin disease appears suddenly. For most people, the first sign is deep-seated blisters on their hands.
Some people feel an itchy or burning sensation before the blisters appear.

Signs and symptoms

If you have dyshidrotic eczema (DE), you’ll likely notice:

 Small blisters that vary in size on your palms and sides of your fingers (and/or soles)
 A rash and scaly skin where blisters appear

 Excessive sweating where you have blisters

 An tching or burning feeling on blistered skin (and sometimes before the blisters appear)

 Pain where you have blisters

The blisters usually clear in 2 to 3 weeks — or sooner with treatment. As the blisters clear, the skin is often
dry and cracked. It may peel.

If you have frequent DE flares, the skin can start to thicken, feel scaly, and develop deep, painful cracks.

Signs of infection
An infection can develop where you have DE. A staph infection is most common. Signs of a staph infection
include:

 Pain
 Swelling

 Crusting

 Pus-filled blisters

Who gets dyshidrotic eczema?

The people most likely to get dyshidrotic eczema (DE) are adults aged 20 to 40, who often have one or more
of the following:

Certain medical condition: You have a higher risk of developing DE if you have any of the following:

 Atopic dermatitis (eczema) or blood relatives who have eczema

  Contact dermatitis, especially an allergy to nickel

 Dyshidrotic eczema in your family

 Hay fever

Sweaty or moist hands: Some people have flares every spring or summer when the temperature rises.

Wet hands throughout the day or work with certain substances: DE is more common in people who:

 Immerse their hands in water frequently during the day, such as healthcare workers, hair stylists, and
florists
 Work with cement

 Work with chromium, cobalt, or nickel

Patients receiving immunoglobulin therapy may get DE

If you are receiving intravenous (IV) immunoglobulin and develop blisters on your hands or feet after an
infusion, be sure to tell your doctor. This is likely DE. A few patients develop this eczema after receiving
immunoglobulin therapy.

The eczema can worsen with each infusion, so early diagnosis is important. With treatment, most cases of
DE due to this therapy are treated successfully. This will allow you to continue receiving immunoglobulin
therapy.

Common triggers

Some people find that their DE flares at certain times, such as periods of:

 Intense stress or worrying

 Warm weather, when heat and humidity rise

 Wet work (having wet hands frequently throughout the day)

What causes dyshidrotic eczema?

While researchers have discovered that some people are more likely to get DE, the cause is still unknown.

The cause may be a complex reaction that happens in the immune system.

If you think that you might have DE, an accurate diagnosis and proper treatment are important.

How do dermatologists diagnose dyshidrotic eczema?

When dyshidrotic eczema (DE) flares, a dermatologist can diagnose it by looking at your skin.
Your dermatologist will also ask about your medical history, work, hobbies, and recent stress level.
If your dermatologist thinks that the DE could be due to an allergy, an allergy test called patch testing may
be recommended. During patch testing, small amounts of substances that you may be allergic to are placed
on your skin — often the skin on your back.
How do dermatologists treat dyshidrotic eczema?
Your treatment plan will be designed to treat your signs and symptoms. You may be responsible for doing
much of the treatment at home. It is important to carefully follow your treatment plan, which may include
several of the following:

 Soaks and cool compresses: Soaks or cool compresses that you apply 2 to 4 times a day can be very
effective for drying blisters. You apply these for 15 minutes at a time.
After each soak or cool compress, you’ll likely need to apply a medicated cream or ointment, such as
a corticosteroid.

 Corticosteroid that you apply to your skin: This can reduce the inflammation and clear the
blisters.

 Anti-itch medicine: An antihistamine pill or other anti-itch medicine can reduce scratching.
Anything you can do to reduce scratching is helpful because scratching tends to worsen DE.

 Pramoxine (pra mox’ een): A cream or lotion containing this can relieve itch and pain.

 Moisturizer or a barrier repair cream: Your dermatologist will recommend a moisturizer or barrier
repair cream. These can reduce dryness and flares of DE.
It’s important to apply the product after each shower, bath, and hand washing.

 Medicine to treat an infection: The skin with DE can get infected. Before prescribing this medicine,
your dermatologist will first determine what type of infection you have.

Infection may cause dyshidrotic eczema to linger

Having an infection can stop DE from clearing. In one study, researchers found that about 33% of patients
who had DE on their hands got rid of the DE only after treating an infection on their feet.

When treatment fails to clear DE or a patient has severe DE

If the above treatments fail to work or you have severe DE, your dermatologist may recommend one of the
following:

 Botulinum toxin: These injections, which are given in a dermatologist’s office, bring some patients
relief because botulinum toxin temporarily relaxes the muscles and stops excessive sweating.
Botulinum toxin is FDA approved to treat wrinkles and excessive sweating in the underarms — but
not DE. It’s legal to prescribe a medicine for a condition other than its FDA-approved use. This is
called “off-label” use, which can be very helpful for some patients.

 Draining large blisters in the office. Draining blisters is safe and effective when performed in a
dermatologist’s office, but you should not drain your own blisters. Attempting this at home can lead
to an infection, which can worsen DE and prevent clearing.

 Corticosteroid that works throughout the body: For a severe case, a corticosteroid pill or injection
may be prescribed.

 Light treatments: This treatment exposes the skin with DE to ultraviolet (UV) light for a prescribed
amount of time. Under a dermatologist’s care, light treatment can be a safe and effective treatment
for DE. In one study, more than 90% of patients report good to excellent results after 6 to 8 weeks of
 treatment.
It’s extremely important to get these treatments at a hospital, clinic, or your dermatologist’s office.
Trying to treat your skin by using a tanning bed is not recommended.

 Changing your diet: Sometimes, DE continues to flare despite all you do to treat it. If this happens,
your dermatologist may recommend a change to your diet.

Eliminating foods that contain nickel or cobalt helps some people.

Many foods contain nickel or cobalt. If you are allergic to either, your dermatologist can tell you how
to change your diet.

Other treatments than the ones listed here can also be helpful. Your dermatologist can tell you what
treatment may be best for you.

Outcome for people who have dyshidrotic eczema

Some people have one mild outbreak that clears without treatment. It’s much more common to have flares
throughout your life. Treatment can help control DE, which cannot be cured.

Making some simple changes to your everyday routine can help clear your skin and prevent flares.
Dermatologists recommend the following to their patients who have dyshidrotic eczema (DE):

1. Wash skin with DE gently: When washing, you’ll want to:

Remove rings: Always remove these before washing your hands. If the skin beneath your ring gets
wet and stays damp, the DE can flare.

Use lukewarm water: Using lukewarm water every time can help prevent flares.
Wash with mild, fragrance-free cleansers: Skip the antibacterial soaps, waterless hand sanitizers,
and deodorant soaps, which can cause DE to flare.

Even when the eczema clears, you'll want to continue gently washing the skin that had eczema. This
will help prevent flares.
2. Apply moisturizer frequently: You’ll want to apply moisturizer:

• After washing
• Throughout the day when your skin feels dry.

Dermatologists often recommend using a product called a barrier repair cream that contains
dimethicone. This product allows skin to breathe. It also helps relieve itch and creates a barrier to
protect you from things that can irritate your skin. If you opt to use another moisturizer, make sure it
is:
• Thick and creamy
• Fragrance free (“Fragrance free” and “unscented” are different.)
• Something you like enough to use frequently
Avoid moisturizer that is thin and runny as are many lotions. Lotions contain a lot of water, which
can worsen DE.

3. Learn to manage stress really well: Some patients find that they can clear their skin by practicing a
stress-reduction technique and treating their skin as directed.
 It can be helpful to continue finding ways to relieve your stress. Many people say that the DE returns
when they feel stressed.
4. Try to avoid scratching: Anything you can do to reduce scratching is helpful because scratching
tends to worsen DE.

5. Avoid dry environments and hot conditions that cause you to sweat a lot: Both heat and dryness
can trigger flares.

6. Ask your dermatologist if something could be triggering your DE. If the DE won’t clear, you
may:
• Have an allergy
• Be irritating your skin
Your dermatologist can ask questions to find out if something is irritating your skin. Allergy testing
can find out whether you have allergies.

7. Avoid what causes an allergic reaction and what irritates your skin. If either allergens or irritants
are the problem, avoiding them may be necessary to clear your skin — and keep it clear.

8. Wear gloves to protect your hands: Many things that touch your skin can cause DE to flare. Water,
detergents, and household cleaners are a few. To protect your hands, you’ll want to put gloves on
before you get your hands wet and before touching something that irritates your skin. Dermatologists
recommend the following:
• Wear 100% cotton gloves (hands won’t get wet)
• Wear 100% cotton gloves under waterproof gloves (wet work)

9. Remove your rings: Rings can irritate your sensitive skin. To reduce irritation, dermatologists
recommend that you remove your rings BEFORE:
• Washing your hands
• Applying moisturizer
• Going to sleep

10. Wear moisture-wicking socks: If you have dyshidrotic eczema on your feet, this will help keep
your feet dry.

https://www.aad.org/public/diseases/eczema/dyshidrotic-eczema#tips

Background
Dyshidrotic eczema is a type of eczema (dermatitis) of unknown cause that is characterized by a pruritic
vesicular eruption on the fingers, palms, and soles. The 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. The clinical course of dyshidrotic eczema can range from self-limited to chronic, severe, or
debilitating. The condition's unresponsiveness to treatment can be frustrating for the patient and physician
(see the images below).
 Tense vesicles and bullae on the palm. Courtesy of Norman Minars,
MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

Multiple tense vesicles on the palm.

Some believe the terms pompholyx and dyshidrosis are obsolete and favor a new term, such as "acute and
recurrent vesicular hand dermatitis." 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.
Etiology
The hypothesis of sweat gland dysfunction has been disputed because 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–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, humidity)
reportedly exacerbate dyshidrosis.
Dyshidrosislike eczematous eruptions with the use of intravenous immunoglobulin (IVIG) infusions have
been reported. 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, with 75% of those patients
developing the lesions after just one IVIG treatment. [6] The eruption tends to be mild and to wane over time.
It usually responds very well to topical steroids, [7, 8, 9] 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. [10]
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, causes dyskeratinization, increased transepidermal water loss,
and an increase in the transepidermal antigen transfer. Combined, these features have been associated with
the development of icthyosis and atopic dermatitis, and they may be involved in the development of irritant
and allergic contact dermatitis, which are well-known conditions associated with dyshidrotic eczema.
Chronic hand dermatitis, including dyshidrotis eczema, has also been associated with defects in the skin
barrier, and, in a few cases, it has been also associated with mutations in the filaggrin gene; however, these
have not reached statistical significance. [11]
Aquaporins have been shown to be expressed in patients with atopic dermatitis and may also be related to
exacerbation and chronicity of pompholyx. Aquaporins are channel proteins located on cell membranes that
increase their permeability, in particular aquaglyceroporins. Aquaglyceroporins can transport water and
glycerol. Aquaporin-3 and aquaporin-10 are normally expressed in the basal layer of the epidermis, and
immunohistochemical staining had 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 with skin
dehydration, even immediately after hand washing. Hypothetically, topical and/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. [12]
Atopy
As many as 50% of patients with dyshidrotic eczema have reportedly had personal or familial atopic
diathesis (eczema, asthma, hay fever, 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
This may be a significant factor in dyshidrotic eczema. Nickel sensitivity was reportedly low in some studies
of dyshidrosis patients, but significantly elevated in other studies. 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
The oral ingestion of cobalt manifests systemic allergic dermatitis as dyshidrotic eczema less frequently than
does the oral ingestion of nickel. 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 in 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, which is approximately less than 12 mcg/d. This diet
has demonstrated higher compliance than an avoidance diet list. In addition, this diet reduces the amount of
nickel consumed. [3]
Exposure to sensitizing chemicals or metals
Dyshidrotic eczema outbreaks are sometimes associated with exposure to sensitizing chemicals or metals
(eg, chromium, cobalt, carba mix, fragrance mix, diaminodiphenylmethane, dichromates,
benzoisothiazolones, paraphenylenediamine, perfumes, fragrances, balsam of Peru, Primula plant).
Id reaction
Controversy surrounds 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, less 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 using biofeedback techniques for stress reduction
supports this hypothesis.
Other factors
Isolated reports describe other possible causative factors, such as aspirin ingestion, oral contraceptives,
cigarette smoking, and implanted metals, among others. A 3-year prospective study of the causes of
dyshidrotic eczema (pompholyx) in 120 patients 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%), with an additional 15% of patients having undiagnosed (idiopathic) causes
probably related to atopic factors. [13]
Contact allergy was found in 89 (74.2%) of the 120 patients. 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, correlation existed between the application of the agent
and 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. 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 2
presented with exacerbations of the lesions after a challenge test.
Of 58 patients with a history of smoking tobacco, 5 presented with a positive reaction on a tobacco patch
test, and 2 of those were considered relevant. 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, 5 patients with prior diagnosis of pompholyx developed lesions morphologically and
histologically consistent with a vesicular dermatitis after provocation with long-wavelength ultraviolet A
(UVA) light. Further workup ruled out contact dermatitis, polymorphic light eruption, and heat as the culprit,
confirming that the reaction was due to true photosensitivity rather than to photoaggravation.[14]
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. [15]
In a case series, three patients with histories of frequent pompholyx exacerbations, mostly during summer
(ie, photoaggavated pompholyx), were subjected to photoprovocation testing, with positive development of
pompholyx lesions in two of them. Patients reported lesions after exposure to solar-simulated ultraviolet
radiation and broadband UVA. They were treated with photoprotective measures in addition to the standard
treatment for pompholyx, resulting in a decrease in the frequency and severity of the exacerbations. These
authors suggested that the 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 particular subset of pompholyx patients. [16]
Of interest, UVB phototherapy and photochemotherapy are well-known, efficient treatments for pompholyx.
Epidemiology
Occurrence in the United States
Dyshidrotic eczema occurs in 5-20% of patients with hand eczema and more commonly develops in warmer
climates and during spring and summer months (seasonal or summer pompholyx).
International occurrence
Dyshidrotic eczema accounted for 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. [17]
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%). [18]
Sex- and age-related demographics
The male-to-female ratio for dyshidrotic eczema has variably been reported as 1:1 and 1:2. Dyshidrotic
eczema affects individuals aged 4-76 years; the mean age is 38 years. The peak incidence of the condition
occurs in patients aged 20-40 years. After middle age, the frequency of dyshidrotic eczema episodes tends to
decrease.
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.
Patient Education
Instruct dyshidrotic eczema patients to avoid contact with certain allergens or irritants (eg, nickel), to follow
a hand care routine that avoids irritants, and to use emollients regularly. In addition, inform individuals with
this disorder about the difficulty of achieving successful treatment.
History
Patients report pruritus of the hands and feet with a sudden onset of vesicles. Burning pain or pruritus
occasionally may be experienced before vesicles appear. Tiny vesicles erupt first along lateral aspects of the
fingers and then on the palms or soles. Palms and soles may be red and wet with perspiration. The vesicles
usually persist for 3-4 weeks. Vesicle outbreaks may occur in waves. A photo-induced form of hand
dermatitis resembling dyshidrotic eczema has been described. [14]
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:

Emotional stress

Personal or familial atopic diathesis (eg, asthma, hay fever, sinusitis)

Certain work exposures (eg, cobalt) and/or recreational exposures

Recent exposure to contact allergens (eg, nickel, balsams, paraphenylenediamine, chromate,
sesquiterpene lactones) before condition flares

Exposure to contact irritants before condition flares

Recent exposure to costume jewelry (patients with palmar pompholyx and allergy to nickel)

Recent treatment with intravenous immunoglobulin therapy [19, 20, 6]

Human immunodeficiency virus (HIV) infection
Two cases were reported of HIV-positive patients who developed dyshidrotic eczema as an immune
reconstitution inflammatory syndrome shortly after highly active antiretroviral therapy. [21] Pompholyx has
also been described as a manifestation of symptomatic HIV infection, including in individuals who do not
respond to topical and systemic therapies and whose condition resolves only after the initiation of
combination antiretroviral therapy. [22]
One publication provides an algorithm for the diagnosis of chronic hand dermatitis, which offers an easy
way of classifying these conditions, helping in the decision making when choosing treatment modalities. [23]
Physical Examination
Symmetrical crops of clear vesicles and/or bullae on the palms and lateral aspects of the fingers characterize
dyshidrotic eczema. The feet, the soles, and the lateral aspects of toes also may be affected. (See the images
below.)

Small tense vesicles on the fingers.

Small, discrete, coalesced vesicles on the dorsal hand.

 Small, discrete, coalesced vesicles on the fingers.

In mildly affected patients, vesicles are present only on the lateral aspects of the fingers and, occasionally,
involve feet and toes. (See the image below.)

Small discrete vesicles of the lateral fingers.

Vesicles are deep seated and have a tapiocalike appearance, without surrounding erythema. They may
become large, form bullae, and become confluent. Vesicles typically resolve without rupturing, followed by
desquamation. (See the image below.)

Close-up view of tense vesicles and bullae of the palm. Courtesy of

Norman Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.

In 80% of patients, only the hands are involved, while in 10% of patients, the disease affects only the feet,
and in another 10% of patients, the hands and feet are involved together. (See the images below.)

Discrete yellow pustules on the sole of the foot. Courtesy of Norman

Minars, MD, University of Miami, Department of Dermatology & Cutaneous Surgery.
 Palms and soles of a patient with a dyshidrosis flare. The patient unroofed a large
bulla on the right sole.

With long-standing disease, patients' fingernails may reveal dystrophic changes (eg, irregular, transverse
ridging; pitting; thickening; discoloration). Interdigital maceration and desquamation of the interdigital
spaces often are present, despite the possible absence of a dermatophyte infection. Vesicles and/or bullae
may become infected secondarily, and pustular lesions may be present. Cellulitis and lymphangitis may
develop.
Severity index
The Dyshidrotic Eczema Area and Severity Index was developed based on severity grades for the number of
vesicles per square centimeter, erythema, desquamation, itch, and the extent of affected areas. [24] The index
was found to be a simple standardized method for assessing the condition and was used to assess disease
severity and treatment effectiveness in two clinical studies. Further evaluation with larger patient groups is
needed.
Complications
Secondary bacterial infection of dyshidrotic eczema vesicles or bullae can result in cellulitis, lymphangitis,
and septicemia (rare). Dystrophic nail changes may develop, with the occurrence of transverse ridging,
thickening, discoloration, and pitting. Dyshidrotic eczema has no associated mortality, although some severe
cases can become debilitating. A 2015 study determined that dyshidrosis is a risk factor in the development
of herpes zoster. [25]
Diagnostic Considerations
Conditions to consider in the differential diagnosis of dyshidrotic eczema include the following:

Dyshidrosiform pemphigoid - May have vesicles (vesicular pemphigoid) or may be evident as
erythema and swelling, with bullae on the palmoplantar areas [26](In fact, bullous pemphigoid may
closely resemble recurrent vesicular hand eczema. [27] )

Inflammatory tinea pedis or tinea manus

Palmoplantar pustular psoriasis

Pustular bacterid

Pustular psoriasis

Recurrent focal palmar peeling (previously termed keratolysis exfoliativa) [28]

Dyshidrosis-like variant of adult T-cell leukemia/lymphoma [29]

Bullous impetigo

Juvenile plantar dermatosis

Linear IgA-disease with (hemorrhagic) pompholyx

Vesicobullous mycosis fungoides/Sézary syndrome

Keratolysis exfoliativa: Intermittent air-filled blisters and centrifugal collarette of the palms and
soles; histopathologically characterized by cleavage within the stratum corneum and partial
 degradation of corneodesmosomes in the mid stratum corneum; normal expression of
corneodesmosomal components reported by immunofluorescence; no mutations in SPINK6⁄9 have
been found; no association with dyshidrotic eczema, dermatophytosis, acral peeling skin syndrome, or
localized epidermolysis bullosa simplex [28]
Differential Diagnoses
 Acropustulosis of Infancy
 Allergic Contact Dermatitis
 Bullous Pemphigoid
 Contact Urticaria Syndrome
 Dermatologic Manifestations of Herpes Simplex
 Epidermolysis Bullosa
 Erythema Multiforme
 Fixed Drug Eruptions
 Friction Blisters
 Irritant Contact Dermatitis
 Keratolysis Exfoliativa
 Pemphigoid Gestationis
 Pemphigus Vulgaris
 Pityriasis Rubra Pilaris
 Subcorneal Pustular Dermatosis
Approach Considerations
The diagnosis of dyshidrotic eczema is usually made clinically, although bacterial culture and sensitivity
tests exclude secondary infection. Blood tests are not usually ordered; however, immunoglobulin E levels
are commonly elevated.
Substances used to systemically challenge patients with possible ingested allergens may trigger
exacerbations. Vasculitis or erythema multiforme may develop during this testing.
Use patch testing to exclude allergic contact dermatitis. Measuring thiopurine methyltransferase levels
allows accurate dosing of azathioprine. Systemic evaluation is recommended in recalcitrant cases, including
serology for human T-cell lymphotrophic virus type 1 (HTLV1), which can rule out dyshidrosis-like variant
of adult T-cell leukemia/lymphoma. [30] Perform potassium hydroxide wet mount preparation to exclude
dermatophyte infection.
Punch biopsy for hematoxylin and eosin staining usually is not necessary. Punch biopsy for periodic acid-
Schiff staining may help to exclude dermatophytosis in patients with unresponsive disease. Use punch
biopsy for direct immunofluorescence to exclude bullous pemphigoid.
Histologic findings
Spongiosis with an epidermal lymphocytic infiltrate and intraepidermal vesicles or bullae are present. The
vesicles are not associated with sweat glands.
Approach Considerations
In dyshidrotic eczema, typical first-line treatment includes high-strength topical steroids and cold
compresses. Short courses of oral steroids are the second line of treatment for acute flares, and other
immunosuppressants have also been tried. Corticosteroids are cornerstones of topical therapy. Guidelines
have been established by the National Institute of Clinical Evidence. [31] Calcineurin inhibitors may also be
effective. [32]
Variable effects have been reported using oral administration of psoralen and subsequent exposure to long-
wavelength UV light (PUVA) therapy. Topical photochemotherapy with 8-methoxypsoralen is probably as
effective as systemic photochemotherapy or high-dose UVA-1 irradiation. For recalcitrant cases,
corticosteroids are combined with immunosuppressants.
An evolving treatment seems to be the intradermal injection of onabotulinumtoxinA. Probiotics have been
suggested as a potential treatment for eczema. [33] Topical khellin and natural sunlight therapy have been
suggested for patients with recalcitrant palmoplantar pompholyx. [34] Tap water iontophoresis with pulsed
direct current may be helpful as adjuvant treatment. [35]
Excellent results have been reported with the use of oxybutynin in two patients with coexistent
hyperhidrosis and dyshidrotic eczema. [36] Further studies are needed before recommending this treatment
modality.
Identification of the causes of stress and the use of stress management techniques as adjuncts may be helpful
in some patients. Biofeedback therapy for stress reduction has succeeded in some individuals.
Treatment for bullae
The following treatment is appropriate if bullae are present:
 Use compresses with Burow solution (10% aluminum acetate) in a 1:40 dilution until bullae resolve
(usually within a few days)
 Compresses with a 1:10.000 solution of potassium permanganate are also effective
 Drain large bullae with a sterile syringe, and leave the roof intact
 Prescribe systemic antibiotics that cover Staphylococcus aureus and group A streptococci
Activity
Bed rest 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.
Deterrence
Advise dyshidrotic eczema patients to avoid known contact irritants or allergens, to reduce stress (may help
some patients), to follow a hand care regimen, and to use regular prophylactic emollients.
Consultations
Consultation with a psychologist may be helpful for stress reduction using biofeedback therapy and other
techniques. [37] Consultation with an allergist may be helpful for oral provocation tests for nickel, cobalt, or
chromium salts. Oral challenges occasionally are positive in patients who demonstrate negative patch tests
to these metals. The test is considered positive if a patient's dyshidrotic eczema flares after metal is ingested.
Ultraviolet A Light
Paradoxically, although sometimes linked as a possible cause, UVA or UVA-1 alone or with oral or topical
psoralen has been used in treatment. Hand and/or foot UVA therapy (UVA or UVA-1 alone or with oral or
topical psoralen) improves the eruption and pruritus when administered 2-3 times per week. The dose
typically starts at 0.5 J per treatment and is increased by 0.5 J at every other or every third treatment. [38,39]
Topical application of 8-methoxypsoralen plus UVA (bath-PUVA) has been demonstrated to be the preferred
method for the treatment of dyshidrotic eczema, compared with oral PUVA. [40] Local, narrow-band UVB has
been shown to be as effective as bath-PUVA in patients with chronic hand eczema of dry and dyshidrotic
types. [41]
Corticosteroids
Topical corticosteroids are the mainstay of treatment. Typically, use class I steroids initially, then class II or
III steroids. Ointments penetrate the skin better than creams do, although patients may prefer creams during
the day. Topical antipruritics with pramoxine are useful.
Systemic corticosteroids can also be used. Either oral prednisone or intramuscular triamcinolone suspension
may be administered for severe episodes. Tapering of prednisone can follow intramuscular treatment.
Schedule follow-up and check blood pressure 1 week after initiating prednisone.
Calcineurin Inhibitors
Topical calcineurin inhibitors may be helpful. Some patients may benefit from topical tacrolimus or
pimecrolimus. Several studies have demonstrated their efficacy and tolerability in the treatment of chronic
hand dermatitis, [42] and long-term occlusive therapy has also been determined to be efficacious, particularly
in persons with severe dyshidrotic eczema. [42]
Advantages of topical calcineurin inhibitors over topical corticosteroids include the lack of development of
tachyphylaxis, telangiectasias, and thinning and atrophy of the skin. [43] Personal experience of the coauthor
has shown effective control with topical calcineurin inhibitor therapy alone in several patients followed in
her practice. Note that topical calcineurin inhibitors can exacerbate irritant hand dermatitis.
OnabotulinumtoxinA
OnabotulinumtoxinA injections may be helpful in some patients. OnabotulinumtoxinA intradermal
injections as an adjuvant to topical corticosteroids has been tested in a study in which 6 patients who
completed an 8-week trial achieved significant reductions in their Dyshidrotic Eczema Area and Severity
Index scores and faster reductions of pruritus and vesiculation. [43] In another study, 7 of 10 vesicular
pompholyx patients achieved good to very good responses after the injection of OnabotulinumtoxinA alone,
with a reduction of pruritus. [44]
Immunosuppressive Agents
For severe refractory pompholyx, azathioprine, methotrexate, [45] mycophenolate mofetil, cyclosporine, [46] or
etanercept may be helpful. In one study, etanercept was administered subcutaneously to a patient with
recalcitrant hand pompholyx at a dose of 25 mg twice a week. The patient achieved complete remission for 4
months, after which the patient had a relapse. The etanercept dose was increased to 50 mg twice a week
without improvement. [47] Consider measuring thiopurine methyltransferase levels, which may help to guide
azathioprine therapy. Accurate dosing avoids toxicity and underdosing.
Nickel Chelators and Khellin
Nickel chelators, such as disulfiram (Antabuse), occasionally are used in nickel-sensitive patients who
demonstrate a positive oral provocation test. [48]
Khellin, a furanochromone similar to methoxypsoralen, may be used in combination with
photochemotherapy (sun exposure) for recalcitrant palmoplantar cases. [34]Khellin, unlike other psoralens,
does not induce skin phototoxicity (erythema) and hyperpigmentation of healthy skin after UVA radiation
therapy.
Alitretinoin
Alitretinoin (9-cis retinoic acid) activates the retinoid X receptor and all retinoic receptors. In one study,
alitretinoin treatment produced significant clinical improvements in patients with chronic hand dermatitis,
but it was not effective specifically against dyshidrotic eczema. The randomized, double-blind, placebo-
controlled, multicenter trial involved 319 patients with chronic hand dermatitis (70 with pompholyx) that
was refractory to standard therapy. Oral alitretinoin was administered at doses of 10 mg, 20 mg, or 40 mg
once daily for 12 weeks. Although alitretinoin induced a significant clinical improvement in a dose-
dependent fashion (53% improvement in disease status and 70% reduction in clinical features) in the patient
group as a whole, no difference was noted in the patients with pompholyx compared with placebo. [43, 49]
However, evidence from another study indicated that alitretinoin is effective against dyshidrotic eczema In
this investigation, another randomized, double-blind, placebo-controlled, multicenter trial, oral alitretinoin
showed a response rate of 33% at a dose of 30 mg/d, compared with 23% at a dose of 10 mg/d and 16% with
placebo, in 377 patients with pompholyx. [50]
Headache and mucocutaneous adverse events, including dry skin, rash, alopecia, exfoliative dermatitis, and
hyperlipidemia, were the most common adverse events in these trials.
Alitretinoin 1% gel has been evaluated for the treatment of classic Kaposi sarcoma,
[51]
photoaging, [52] pyogenic granuloma, [53] and cutaneous T-cell lymphoma. [54]Currently, alitretinoin 1% gel
has not been used for the topical treatment of pompholyx.
Three phase III studies (1 open-label study and 2 double-blind, randomized, controlled trials) evaluated the
safety [55] and efficacy [56] of once-daily oral alitretinoin at 10 mg or 30 mg versus placebo in 1032 patients
with chronic hand eczema, including pompholyx, in whom treatment with potent topical corticosteroids had
failed.
According to physician assessment, "clear" or "almost-clear" status was achieved in up to 48% of patients in
the alitretinoin groups and 17% in the placebo group. Median percentage reduction in disease symptoms was
75%. Alitretinoin at 30 mg had faster responses (median 85 d) than did placebo (median 141 d). Among
complete responders who relapsed, 80% in the alitretinoin groups responded to the same alitretinoin dose
and 8-10% of patients in the placebo group responded to retreatment with placebo.
Common adverse effects included headache, flushing, erythema, and xerosis. Headache was the most
common adverse effect with alitretinoin at 30 mg. Also in the treatment group, dry skin, dry eyes, dry
mouth, dry lips, and cheilitis were reported in 10% of patients, compared with 4% of patients in the placebo
group. Lipid abnormalities were similar to those seen with other retinoids.
A phase III trial--a randomized, double-blind (subject, investigator), placebo-controlled, parallel-assignment,
safety/efficacy study--has been conducted on the treatment of chronic hand dermatitis (including
pompholyx) using oral alitretinoin at 30 mg/d (1 capsule) for up to 24 weeks. [57] Results are not yet
available.
Additional Agents
Potential agents for the treatment of pompholyx, such as topical bexarotene, systemic alitretinoin,
leukotriene receptor antagonists, leukotriene synthesis inhibitors, phosphodiesterase-4 inhibitors, and
monoclonal antibodies, have been shown to be effective for the treatment of chronic hand dermatitis and
other inflammatory conditions, including atopic dermatitis. Controlled studies need to be conducted to
establish their efficacy and safety for the treatment of dyshidrotic eczema (pompholyx).
Diet
For nickel-sensitive patients, consider a low-nickel diet for 3-4 weeks. However, 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. [17]
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. [3] Some patients have reported improvement by avoiding
foods rich in heavy metal salts.
Medication Summary
Dyshidrotic eczema treatment can be quite challenging because of the severe inflammatory process that can
be involved and because of frequent recurrences. Pharmacologic treatment begins with high-strength, topical
corticosteroids. In recalcitrant cases, systemic corticosteroids are the next line of treatment. Two case reports
also note some success with other immunosuppressants (eg, methotrexate, mycophenolate mofetil).
The long-term efficacy of occlusive therapy with pimecrolimus (Elidel), a topical calcineurin inhibitor, was
reported in patients with severe dyshidrosiform hand and foot eczema. [42] However, the authors recommend
caution in the extended use of calcineurin inhibitors.
Other treatment options include onabotulinumtoxinA injections and a topical form known as bexarotene gel,
as well as plant-based pharmaceuticals; new types of anti-inflammatory oral drugs, such as leukotriene
inhibitors and phosphodiesterase-4 (PDE4) inhibitors; and phototherapy with high-dose UVA-1 and UV-free
phototherapy. [43]
Corticosteroids
Class Summary
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They
modify the body's immune response to diverse stimuli. Topical ointments are more potent, but greasier, than
creams.
Topical corticosteroids are the first-line therapy. Steroid potency choice is based on the patient's response to
treatment; however, the higher-strength steroids are usually necessary for disease control.
Clobetasol (Temovate, Clobex, Cormax, Olux)
Clobetasol is for severe episodes. It is a class I superpotent topical steroid; it suppresses mitosis and increases
the synthesis of proteins that decrease inflammation and cause vasoconstriction.
Fluocinonide (Vanos)
Fluocinonide is a class II steroid. It has high potency and, like all topical steroids, possesses anti-inflammatory,
antipruritic, and vasoconstrictive properties.

Prednisone
This immunosuppressant is used in the treatment of autoimmune disorders. It is a potent anti-inflammatory
agent that has salt-retaining properties and varied metabolic effects. Prednisone may decrease
inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN)
activity.
A glucocorticoid, prednisone is readily absorbed from gastrointestinal tract. It is used as second-line
pharmacologic treatment for dyshidrotic eczema.
Betamethasone (Celestone, Diprolene, Luxiq)
Betamethasone is used for severe, acute episodes. It has a rapid onset (within 1 h) and a 72-hour duration. It
can be administered for inflammatory dermatosis that is responsive to steroids. It decreases
inflammation by suppressing the migration of PMN leukocytes and reversing capillary permeability.

Triamcinolone (Aristospan, Kenalog)

Triamcinolone is for inflammatory dermatosis that is responsive to steroids; it decreases inflammation by
suppressing migration of PMN leukocytes and reversing capillary permeability. This agent has a long
duration (4-6 wk).
Immunosuppressives
Class Summary
These agents are for the treatment of severe, acute episodes.
Tacrolimus topical (Protopic)
Tacrolimus topical is used for short-term treatment or for intermittent, long-term treatment in unresponsive or
intolerant cases. It inhibits T-lymphocyte activation. Some patients may benefit from tacrolimus topical
or pimecrolimus. Patients may achieve disease control with topical calcineurin inhibitors alone.
Tacrolimus topical is available in a 0.03% and a 0.1% ointment.
Pimecrolimus cream (Elidel)
Pimecrolimus cream is used for short-term treatment or for intermittent, long-term treatment in unresponsive
or intolerant cases. It is available in a 1% cream.
This was the first nonsteroid cream approved in the United States for mild to moderate atopic dermatitis. It
is derived from ascomycin, a natural substance produced by the fungus Streptomyces hygroscopicus var.
ascomyceticus. Pimecrolimus cream selectively inhibits the production and release of inflammatory
cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The
resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release.
Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.
Pimecrolimus cream is indicated only after other treatment options have failed.
Methotrexate (Rheumatrex, Trexall)
Methotrexate has an unknown mechanism of action in the treatment of inflammatory reactions; it may affect
immune function. Methotrexate ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). It
is an antimetabolite that inhibits deoxyribonucleic acid (DNA) synthesis and cell reproduction in
malignant cells; it may suppress immune system. A satisfactory response is seen within 3-6 weeks
following the administration of methotrexate. Adjust the dose gradually to attain a satisfactory
response.
Azathioprine (Imuran, Azasan)
Azathioprine antagonizes purine metabolism and inhibits the synthesis of DNA, ribonucleic acid (RNA), and
proteins. It may decrease the proliferation of immune cells, thus lowering autoimmune activity.

Cyclosporine (Neoral. Gengraf, Sandimmune)

Cyclosporine is a 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
the dosing on ideal body weight.
Antibiotics
Class Summary
Antibiotics are used for dyshidrosis with secondary impetiginization.
Dicloxacillin
Dicloxacillin binds to 1 or more penicillin-binding proteins, which, in turn, inhibits the synthesis of bacterial
cell walls. This agent is used for infections caused by penicillinase-producing staphylococci. It may be
used to initiate therapy when staphylococcal infection is suspected

Cephalexin (Keflex)
Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall
synthesis. It has bactericidal activity against rapidly growing organisms. The drug's primary activity is
against skin flora; it is used for skin infections and for prophylaxis in minor procedures.

Erythromycin (E.E.S., Erythro RX, Ery-Tab)

Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer RNA (tRNA) from
ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of
staphylococcal and streptococcal infections.
Age, weight, and the severity of infection determine the proper dosage in children. When twice-daily dosing
is desired, one half of the total daily dose may be taken every 12 hours. Double the dose for more severe
infections.
Antihistamines
Class Summary
Antihistamines are used to treat pruritus associated with dyshidrosis. Desloratadine (Clarinex) is a long-
acting, tricyclic histamine antagonist that is selective for the H1 receptor. It is a major metabolite of
loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.
The dose for adults and children over age 12 years is 5 mg by mouth daily. Decrease the dose in hepatic
impairment. Data are 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.
Loratadine (Claritin, Alavert, Loradamed)
This is a nonsedating agent that selectively inhibits peripheral histamine H1 receptors.

Hydroxyzine (Vistaril)
Hydroxyzine antagonizes H1 receptors in the periphery. It has sedating qualities and may suppress histamine
activity in the subcortical region of the central nervous system (CNS).

Pramoxine topical (Pramosone, Zypram, Epifoam)

This is a topical antihistamine and mild anti-inflammatory. It blocks nerve conduction and impulses by
inhibiting the depolarization of neurons. This agent is available alone or as a 1% or 2.5% cream or
ointment. It is available over the counter as Prax.
Nickel Chelators
Class Summary
These minimize the effects of nickel in eczema.
Disulfiram (Antabuse)
Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. It is for patients with severe,
vesicular hand dermatitis who are highly allergic to nickel. The chelating effect of disulfiram helps to
reduce the body's nickel burden in individuals who are allergic to nickel. Do not administer this drug if
the patient has ingested alcohol within last 12 hours. Disulfiram is supplied as a 250-mg tablet.
https://emedicine.medscape.com/article/1122527-overview

Pompholyx (dyshidrotic eczema)

Pompholyx (dyshidrotic eczema) is a type of eczema that causes tiny blisters to develop across the
fingers, palms of the hands and sometimes the soles of the feet.

It can affect people of any age, but it's most often seen in adults under 40.

Pompholyx can sometimes be confused with similar-looking conditions. See your GP if you have any sort of
blistering skin condition.

Signs and symptoms of pompholyx

Pompholyx usually starts as intense itching and burning of the skin on the hands and fingers. The palms and
sides of the fingers (and sometimes the soles of the feet) then erupt into tiny itchy blisters that may weep
fluid.

In severe cases, the blisters may be quite large and may spread to the backs of the hands, feet and limbs.
 The skin can sometimes become infected. Signs of an infection can include the blisters becoming very
painful and oozing pus or becoming covered in a golden crust.

The blisters will usually heal within a few weeks. The skin tends to become dry and crack or peel as it starts
to heal.

What causes pompholyx?

It's not clear exactly what causes pompholyx, but it may be triggered or made worse by:
 a fungal skin infection – this may be on the hands or at a distant site from the blisters (such as in
between the toes) and will need treating
 a reaction to something that has touched your skin – such as certain metals (particularly nickel),
detergents, household chemicals, soap, shampoo, cosmetic products or perfume
 stress
 sweating – pompholyx is more common in spring and summer, in warmer climates, and in people
with hyperhidrosis (excessive sweating)

How long does it last?

In many cases, pompholyx will clear up on its own within a few weeks. The treatments below may help
relieve your symptoms in the meantime.

Sometimes pompholyx may just occur once and never come back, but it often comes and goes over several
months or years. Any of the triggers mentioned above can cause it to flare up again.

Occasionally, pompholyx can be more continuous and difficult to treat.

Treatments for pompholyx

Protecting your skin

You should try to avoid contact with anything that might irritate your skin, including soaps, shampoos and
other household chemicals.

Use an emollient as a soap substitute (see below) and wear cotton-lined gloves when you're at risk of contact
with other potentially irritating substances, such as when washing your hair or doing housework.

Don't burst the blisters – let them heal on their own. If they're particularly big, your GP may be able to drain
them.
 Treating the symptoms

The main treatments your GP may recommend to treat the symptoms of pompholyx are similar to those used
when treating atopic eczema, including:
 emollients (moisturisers) – use these all the time and instead of soap to stop your skin becoming dry
 steroid cream – this reduces the inflammation and irritation and helps the skin to heal

Your GP will probably prescribe a strong steroid cream to use for a short period of time, to minimise risk
of steroid side effects. You may be advised to wear cotton gloves at night to help the cream sink into the
skin.

You can also try:

 soaking your hands in a dilute solution of potassium permanganate(1:10,000) for 10 to 15
minutes once or twice a day for up to 5 days
 antihistamines to relieve the itching and help you sleep if the itchiness is keeping you awake at
night

These treatments are available from pharmacies without a prescription. Your pharmacist can advise whether
they're suitable for you and how you should use them.

Antibiotics may be prescribed if your skin becomes infected.

Specialist treatments

If your pompholyx keeps returning or is severe and doesn't get better with the above treatments, your GP
may refer you to a specialist in treating skin conditions (dermatologist).

A dermatologist may recommend one of the following treatments:

 phototherapy – controlled exposure to ultraviolet (UV) light
 steroid tablets or very strong steroid cream
 immunosuppressant creams or ointments, such as pimecrolimus or tacrolimus
 immunosuppressant tablets or capsules, such as ciclosporin or azathioprine
 alitretinoin capsules – medication that helps improve severe eczema affecting the hands when other
treatments haven't worked

Similar skin conditions

Conditions that can look similar to pompholyx include:

 bullous impetigo – a contagious skin infection that mainly affects children and causes sores and
blisters
 bullous pemphigoid – a blistering skin condition that tends to affect the elderly
 contact dermatitis – a type of eczema caused by skin contact with a substance that causes irritation
or an allergic reaction
 hand, foot and mouth disease – a viral infection that mainly affects young children, which can
cause small blisters to develop on the fingers and palms of the hands
 herpetic whitlow (whitlow finger) – an abscess (collection of pus) at the end of the finger that can
cause it to become suddenly red, swollen, painful and blistered
 pustular psoriasis – an uncommon type of psoriasis that causes pus-filled blisters to appear on your
skin
https://www.nhs.uk/conditions/pompholyx/

1. Lee WJ, Lee DW, Kim CH, et al. Pompholyx with bile-coloured vesicles in a patient with jaundice:
are sweat ducts involved in the development of pompholyx?. J Eur Acad Dermatol Venereol. 2010
Feb. 24(2):235-6. [Medline].
2. 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. 2007 Oct. 33(10):1289-90. [Medline].

3. Stuckert J, Nedorost S. Low-cobalt diet for dyshidrotic eczema patients. Contact Dermatitis. 2008
Dec. 59(6):361-5. [Medline].

4. Thierse HJ, Gamerdinger K, Junkes C, Guerreiro N, Weltzien HU. T cell receptor (TCR) interaction
with haptens: metal ions as non-classical haptens. Toxicology. 2005 Apr 15. 209(2):101-7. [Medline].

5. Shenefelt PD. Update on psychodermatological disorders. Expert Rev Dermatol. 2010 Feb. 5(1):95-
107.

6. Gerstenblith MR, Antony AK, Junkins-Hopkins JM, Abuav R. Pompholyx and eczematous reactions
associated with intravenous immunoglobulin therapy. J Am Acad Dermatol. 2011 May 19. [Medline].

7. Kotan D, Erdem T, Acar BA, Boluk A. Dyshidrotic eczema associated with the use of IVIg. BMJ
Case Rep. 2013 Feb 15. 2013:[Medline]. [Full Text].

8. Lee KC, Ladizinski B. Dyshidrotic eczema following intravenous immunoglobulin treatment. CMAJ.
2013 Aug 6. 185(11):E530. [Medline]. [Full Text].

9. Brazzelli V, Grassi S, Savasta S, Ruffinazzi G, Carugno A, Barbaccia V, et al. Pompholyx of the

hands after intravenous immunoglobulin therapy for clinically isolated syndrome: a paediatric
case. Int J Immunopathol Pharmacol. 2014 Jan-Mar. 27(1):127-30. [Medline].

10. 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. 2006 Feb. 126(2):300-4. [Medline].

11. Molin S, Vollmer S, Weiss EH, Ruzicka T, Prinz JC. Filaggrin mutations may confer susceptibility to
chronic hand eczema characterized by combined allergic and irritant contact dermatitis. Br J
Dermatol. 2009 Oct. 161(4):801-7. [Medline].

12. Soler DC, Bai X, Ortega L, Pethukova T, Nedorost ST, Popkin DL, et al. The key role of aquaporin 3
and aquaporin 10 in the pathogenesis of pompholyx. Med Hypotheses. 2015 May. 84 (5):498-
503. [Medline].
13. Guillet MH, Wierzbicka E, Guillet S, Dagregorio G, Guillet G. A 3-year causative study of
pompholyx in 120 patients. Arch Dermatol. 2007 Dec. 143(12):1504-8. [Medline].

14. Man I, Ibbotson SH, Ferguson J. Photoinduced pompholyx: a report of 5 cases. J Am Acad Dermatol.
2004 Jan. 50(1):55-60. [Medline].

15. Tamer E, Ilhan MN, Polat M, Lenk N, Alli N. Prevalence of skin diseases among pediatric patients in
Turkey. J Dermatol. 2008 Jul. 35(7):413-8. [Medline].

16. Nalluri R, Rhodes LE. Photoaggravated pompholyx. Photodermatol Photoimmunol Photomed. 2016
Feb 12. [Medline].

17. Lofgren SM, Warshaw EM. Dyshidrosis: epidemiology, clinical characteristics, and
therapy. Dermatitis. 2006 Dec. 17(4):165-81. [Medline].

18. Magina S, Barros MA, Ferreira JA, Mesquita-Guimaraes J. Atopy, nickel sensitivity, occupation, and
clinical patterns in different types of hand dermatitis. Am J Contact Dermat. 2003 Jun. 14(2):63-
8. [Medline].

19. Iannaccone S, Sferrazza B, Quattrini A, Smirne S, Ferini-Strambi L. Pompholyx (vesicular eczema)

after i.v. immunoglobulin therapy for neurologic disease. Neurology. 1999 Sep 22. 53(5):1154-
5. [Medline].

20. Llombart M, Garcia-Abujeta JL, Sanchez-Perez RM, Hernando de Larramendi C. Pompholyx

induced by intravenous immunoglobulin therapy. J Investig Allergol Clin Immunol. 2007. 17(4):277-
8. [Medline].

21. Colebunders R, Zolfo M, Lynen L. Severe dyshidrosis in two patients with HIV infection shortly
after starting highly active antiretroviral treatment. Dermatol Online J. 2005 Aug 1.
11(2):31. [Medline].

22. 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].

23. Molin S, Diepgen TL, Ruzicka T, Prinz JC. Diagnosing chronic hand eczema by an algorithm: a tool
for classification in clinical practice. Clin Exp Dermatol. 2011 Aug. 36(6):595-601. [Medline].

24. 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].

25. Hsu CY, Wang YC, Kao CH. Dyshidrosis is a risk factor for herpes zoster. J Eur Acad Dermatol
Venereol. 2015 Apr 27. in press. [Medline].

26. Yasuda M, Miyachi Y, Utani A. Two cases of dyshidrosiform pemphigoid with different
presentations. Clin Exp Dermatol. 2009 Jul. 34(5):e151-3. [Medline].

27. Veien NK. Bullous pemphigoid masquerading as recurrent vesicular hand eczema. Acta Derm
Venereol. 2010. 90(1):4-5. [Medline].

28. Chang YY, van der Velden J, van der Wier G, et al. Keratolysis exfoliativa (dyshidrosis lamellosa
sicca): a distinct peeling entity. Br J Dermatol. 2012 Nov. 167(5):1076-84. [Medline].

29. Bittencourt AL, Mota K, Oliveira RF, Farré L. A dyshidrosis-like variant of adult T-cell
leukemia/lymphoma with clinicopathological aspects of mycosis fungoides. A case report. Am J
Dermatopathol. 2009 Dec. 31(8):834-7. [Medline].
30. Bittencourt AL, Mota K, Oliveira RF, Farré L. A dyshidrosis-like variant of adult T-cell
leukemia/lymphoma with clinicopathological aspects of mycosis fungoides. A case report. Am J
Dermatopathol. 2009 Dec. 31(8):834-7. [Medline].

31. National Institute for Clinical Excellence. Frequency of application of topical corticosteroids for
atopic eczema. London, England: National Institute for Clinical Excellence (NICE); 2004. 34.

32. Wollina U, Abdel Naser MB. Pharmacotherapy of pompholyx. Expert Opin Pharmacother. 2004 Jul.
5(7):1517-22. [Medline].

33. Boyle RJ, Bath-Hextall FJ, Leonardi-Bee J, Murrell DF, Tang ML. Probiotics for treating
eczema. Cochrane Database Syst Rev. 2008 Oct 8. CD006135. [Medline].

34. Capella GL. Topical khellin and natural sunlight in the outpatient treatment of recalcitrant
palmoplantar pompholyx: report of an open pilot study. Dermatology. 2005. 211(4):381-
3. [Medline].

35. 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. 1996 Nov. 76(6):472-4. [Medline].

36. Markantoni V, Kouris A, Armyra K, Vavouli C, Kontochristopoulos G. Remarkable improvement of

relapsing dyshidrotic eczema after treatment of coexistant hyperhidrosis with oxybutynin. Dermatol
Ther. 2014 Nov-Dec. 27(6):365-8. [Medline].

37. Koldys KW, Meyer RP. Biofeedback training in the therapy of dyshidrosis. Cutis. 1979 Aug.
24(2):219-21. [Medline].

38. 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. 2004 Jan. 50(1):68-72. [Medline].

39. Polderman MC, Govaert JC, le Cessie S, Pavel S. A double-blind placebo-controlled trial of UVA-1
in the treatment of dyshidrotic eczema. Clin Exp Dermatol. 2003 Nov. 28(6):584-7. [Medline].

40. Tzaneva S, Kittler H, Thallinger C, Honigsmann H, Tanew A. Oral vs. bath PUVA using 8-
methoxypsoralen for chronic palmoplantar eczema. Photodermatol Photoimmunol Photomed. 2009
Apr. 25(2):101-5. [Medline].

41. Sezer E, Etikan I. Local narrowband UVB phototherapy vs. local PUVA in the treatment of chronic
hand eczema. Photodermatol Photoimmunol Photomed. 2007 Feb. 23(1):10-4. [Medline].

42. 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].

43. Wollina U. Pompholyx: what's new?. Expert Opin Investig Drugs. 2008 Jun. 17(6):897-
904. [Medline].

44. 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. 2002 Jan.
16(1):40-2. [Medline].

45. Egan CA, Rallis TM, Meadows KP, Krueger GG. Low-dose oral methotrexate treatment for
recalcitrant palmoplantar pompholyx. J Am Acad Dermatol. 1999 Apr. 40(4):612-4. [Medline].
46. Petersen CS, Menne T. Cyclosporin A responsive chronic severe vesicular hand eczema. Acta Derm
Venereol. 1992 Nov. 72(6):436-7. [Medline].

47. Ogden S, Clayton TH, Goodfield MJ. Recalcitrant hand pompholyx: variable response to
etanercept. Clin Exp Dermatol. 2006 Jan. 31(1):145-6. [Medline].

48. Menne T, Kaaber K. Treatment of pompholyx due to nickel allergy with chelating agents. Contact
Dermatitis. 1978 Oct. 4(5):289-90. [Medline].

49. Cheer SM, Foster RH. Alitretinoin. Am J Clin Dermatol. 2000 Sep-Oct. 1(5):307-14; discussion 315-
6. [Medline].

50. Ruzicka T, Larsen FG, Galewicz D, et al. Oral alitretinoin (9-cis-retinoic acid) therapy for chronic
hand dermatitis in patients refractory to standard therapy: results of a randomized, double-blind,
placebo-controlled, multicenter trial. Arch Dermatol. 2004 Dec. 140(12):1453-9. [Medline].

51. Rongioletti F, Zaccaria E, Viglizzo G. Failure of topical 0.1% alitretinoin gel for classic Kaposi
sarcoma: first European experience. Br J Dermatol. 2006 Oct. 155(4):856-7. [Medline].

52. Baumann L, Vujevich J, Halem M, et al. Open-label pilot study of alitretinoin gel 0.1% in the
treatment of photoaging. Cutis. 2005 Jul. 76(1):69-73. [Medline].

53. Maloney DM, Schmidt JD, Duvic M. Alitretinoin gel to treat pyogenic granuloma. J Am Acad
Dermatol. 2002 Dec. 47(6):969-70. [Medline].

54. Bassiri-Tehrani S, BA BA, Cohen DE. Treatment of cutaneous T-cell lymphoma with alitretinoin
gel. Int J Dermatol. 2002 Feb. 41(2):104-6. [Medline].

55. Bissonnette R, Maares J, Shear N. Alitretinoin is Well Tolerated in the Treatment of Severe Chronic
Hand Eczema. Poster P1409 presented a the 68th Annual Meeting of American Academy of
Dermatology. March 5-9, 2010, Miami, Fla. J Am Acad Dermatol. Mar 2010. 62(3 Supp):AB51.

56. Lynde C, Haarsch M, Poulin Y. Alitretinoin is Effective in Clearing Severe Crhonic Hand Ezcema.
Poster P1405 presented a the 68th Annual Meeting of American Academy of Dermatology. March 5-
9, 2010, Miami, Fla. J Am Acad Dermatol. Mar 2010. 62(3 Supp):AB50.

57. Maares J. Efficacy and Safety of Alitretinoin in the Treatment of Severe Chronic Hand Eczema
Refractory to Topical Therapy. ClinicalTrials.gov identifier: NCT00817063. ClinicalTrials.gov.
Available at http://clinicaltrials.gov/ct2/show/study/NCT00817063. Accessed: May 13, 2009.