Nummular dermatitis (discoid eczema)
Salient
features
·
Also
known as nummular dermatitis and discoid eczema.
·
A
chronic inflammatory skin disorder of unknown etiology.
·
Papules
and papulovesicles coalesce to form nummular plaques with oozing, crust, and
scale.
·
Most
common sites of involvement are upper extremities in men and women,
particularly the dorsal hands in women, and the lower extremities in men.
·
Pathology
may show acute, subacute, or chronic eczema.
Introduction
Nummular (meaning
round or "coin shaped") dermatitis or eczema is an inflammatory skin
condition characterized by the presence of well-demarcated round-to-oval
erythematous plaques. The term nummular dermatitis has been used both as an
independent disease and as a description of lesion morphology that can be found
in many different diseases, including atopic dermatitis, contact dermatitis,
asteatotic eczema and stasis dermatitis.
Epidemiology
Frequency
The prevalence of nummular
eczema is two cases per 1000 people.
Sex
Nummular eczema is more common
in males than in females.
Age
Nummular eczema,
also known as discoid eczema is predominantly a disease of adulthood. It has
two peaks of age distribution. The most common is in the sixth to seventh
decade of life and is most often seen in males. A smaller peak occurs in the
second to third decade of life, which is most often seen in association with
atopic dermatitis. This is more often seen in females. It
is uncommon in children.
Etiology and Pathogenesis
The etiology of nummular eczema is unknown and likely
multifactorial. Most patients with nummular eczema have associated
contact sensitization as well as very dry (xerotic) skin and
venous hypertension. Local trauma, such as arthropod bites, contact with chemicals,
or abrasions, may precede an outbreak.
Like
most other forms of dermatitis, the cause is likely to be a combination of
epidermal lipid barrier dysfunction and an immunologic response. Dryness of the
skin results in leaking of the epidermal lipid barrierdysfunction; this allows
environmental agents to penetrate the skin and induce an allergic or irritant contact dermatitis. About one‐third
of patients have a clinically relevant underlying allergic contact dermatitis
with a positive patch test reaction, most often to potassium
dichromate, nickel sulfate and cobalt chlorideand reported
improvement in their nummular dermatitis as a result of avoidance of these
allergens.
Nummular eczema has been
associated with medications. Any medication that induces dryness of the skin
can theoretically initiate nummular eczema, particularly diuretics and statins.
Onset of severe, generalized nummular lesions has been reported in association
with interferon and ribavirin therapy for hepatitis C. Other
medications that influence immune response have also been reported to induce
lesions of nummular eczema, including inhibitors of tumor necrosis factor.
Venous insufficiency (and
varicosities), stasis dermatitis, and edema may be related to the development
of nummular eczema on the affected lower extremities.
Clinical features
There are two forms of discoid eczema:
·
Exudative acute discoid eczema:
oozy vesicles, papulesand plaques
·
Dry discoid eczema:
subacute or chronic erythematous, dry plaques
Both forms of discoid eczema are usually more
prevalent on the limbs than the trunk, but the rash may
be widespread. Although often bilateral,
the distribution is often asymmetrical.
Well- demarcated coin shaped erythematous
plaques form from coalescing papules and papulovesicles. Plaques may be several centimeters. In the acute phase the lesions are highly pruritic, very oozing with crusting; crusts may cover the entire surface of
the plaques. The surrounding skin is generally normal but may be xerotic particularly in
patients with AD. Within
a few days, they
progress towards a less vesicular and scalier stage, often with central
clearing, and peripheral extension, causing ring‐shaped
or annular lesions. Chronic plaques are
dry, scaly, lichenified and hyper pigmented that may form particularly in patients with
AD. As they fade, the lesions flatten to macules, usually with
brown post-inflammatory hyperpigmentation that gradually lightens. It is very characteristic of this disease that patches which
have apparently become dormant may become active again, i.e. recurrence at prior sites of involvement is a feature of the
disease. The classic distribution of lesions is the extensor aspects of the
extremities, often the lower legs in men and the forearms and dorsal aspects of
the hands in women and less commonly on the trunk. A single lesion often
precedes the eruption and may be present for some time before other lesions
appear. Stasis
dermatitis may occur simultaneously on
the lower extremities, and venous stasis may lead to the concomitant
development of both conditions.
Disease course and prognosis
Nummular eczema tends to be a chronic condition that remits and
relapses. Patients need to be informed that once nummular eczema develops, it
is often recurrent. Relapse may occur at variable intervals and
most are worse during the colder months of the year when xerosis is
maximal. Avoidance
of exacerbating factors and close attention to moisturizing the skin may help
reduce the frequency.
Pruritus, often worst at night,
may cause irritability, insomnia, or both.
Nummular eczema lesions may
become secondarily infected due to excoriation with heavy purulent exudate. The
most common organism revealed by culture is Staphylococcus aureus.
Investigations
Exogenous contact
dermatitis should be suspected if the condition is unusually severe and
persistent or if patches are few, asymmetrical or of unusual configuration.
Irritants and, occasionally, sensitizers, may provoke this discoid type of
response. When the history suggests this, patch tests should be performed.
Differential Diagnosis
Nummular dermatitis must be
distinguished from nummular lesions of atopic dermatitis and dissemination
secondary to contact dermatitis or stasis dermatitis.
Treatment
General considerations such as the
avoidance of irritants and ambient conditions of low humidity should be
corrected.
Treatment is aimed at
rehydration of the skin, repair of the epidermal lipid barrier, reduction of
inflammation and treatment of any infection.
Hydration
of the skin is the most important factor in treating nummular eczema. Use of hypoallergenic,
fragrance-free creams, lotions, or ointments is the first step in therapy. Lukewarm
or cool baths or showers reduce itching and help rehydrate the skin; a gentle
soap or liquid cleanser may be used. Skin should be patted dry and then moisturizers
are applied to still-damp skin. The "soak-and-smear" therapeutic
regimen includes a 20-minute plain water soak each night followed by
application of steroid ointment or petrolatum to wet skin and includes
alteration of cleansing habits so that soap is applied only to the axilla and
groin.
Wet wrap treatments are often
helpful. This involves dampening the skin with lukewarm water until it is well
hydrated (usually 10 min). Then, petrolatum or steroid ointment is applied
liberally, followed by occlusion for 1 hour with damp pajamas or a non breathable
sauna suit. For small areas of involvement, plastic wrap may be used to occlude
the area. This process may be repeated 5-6 times a day with petrolatum. Caution
must be used when prescription steroid medications are used because overuse of
these medications can cause striae, thinning of the skin, and, rarely, enough
systemic absorption of steroid to affect the hypothalamic-pituitary-adrenal
axis.
Steroids are the most commonly used therapy to reduce inflammation
and combination with a topical
antibiotic can be considered. Less erythematous, less pruritic lesions
may be treated with low-potency (class III-VI) steroids. Severely inflamed
lesions with intense erythema, vesicles, and pruritus require high-potency
(class I-II) preparations. Penetration of the medication is enhanced by
occlusion and/or presoaking in a tub of plain water followed immediately
(without drying) by application of the steroid-containing ointment.
Ointments are usually more
effective than creams because they are more occlusive, form a barrier between
the skin and the environment, and more effectively hold water into the skin.
However, patients may be more likely to use a cream formulation; education and
discussion is key to patient compliance.
Oral or intramuscular steroid
may be required in cases of severe, generalized eruptions.
Tar preparations are helpful to
decrease inflammation, particularly in older, thickened, scaly plaques.
Topical immune modulators
(tacrolimus and pimecrolimus) also reduce inflammation. These
are often initiated a few days after the topical steroid to decrease the risk
of a burning sensation that may occur when applied to extremely irritated skin.
When eruptions are generalized
and prolonged, more aggressive therapy is warranted. Phototherapy (generally
with ultraviolet [UV] B) may be helpful. Broadband or
narrowband UVB is most commonly used, although psoralen plus UVA (PUVA) may be
used in severe cases.
Oral sedative antihistamines
may help reduce itching and improve sleep.
Oral antibiotics, such as
cephalexin, or clarithromyin, should be used in cases of secondary infection. Swab
cultures of the skin guide selection of antibiotics.
Once the eruption has resolved,
ongoing aggressive hydration may decrease the frequency between flares,
particularly in dry climates. Heavy moisturizers (preferably a sensitive-skin
formulation) or petroleum jelly applied to damp skin after showering may be
helpful.
In severe disease refractory to
the above treatments, immunomodulator such as methotrexate have been described
to be safe and effective in these severely affected patients.
Therapeutic ladder
First line
·
Emollient, topical corticosteroid ±
topical or oral antibiotic
Second line
·
Topical calcineurin inhibitor
Third line
·
Phototherapy (narrow‐band UVB/PUVA), oral
immunosuppressants including methotrexate or oral steroids
