Definition of Eczema

Often used interchangeably with the term atopic dermatitis (AD).

• Is a broad-spectrum condition that is subdivided into different clinical presentations, i.e., infantile, childhood and adult.
• Eczema is a clinical diagnosis that must meet a set of diagnostic criteria: [Williams HC, et al. Br J Dermatol 131(3):383-416 (1994 Sep.).]
  • Pruritus, plus 3 or more of the following
  • Early age of onset
  • Typical distribution (i.e., extensors in infants and children, flexures in adults)
  • Personal or familial history of atopy (e.g., asthma, hay fever, eczema)
  • Xerosis (dry skin)
  • Chronicity and relapses
• Increased levels of IgE are not necessary to make the diagnosis.
• There are no diagnostic lab tests.

Incidence

• The prevalence of eczema is increasing, especially over the past 30 years.
• Current studies find a prevalence of 20% in children in North America, Northern Europe, and Japan, [Laughter D, et al. J Acad Dermatol 43:649-55 (2000 Oct.)]. With lower figures elsewhere in the world, [Williams HC, et al. J Allergy Clin Immunol 103:125-38 (1999 Jan.)] though reasons for this remain unclear.
• There is a strong genetic component.

Presentation of Eczema

• Can either be acute or chronic in nature.
• Acute eczema shows marked inflammation of skin, erythema and juicy papules.
• Chronic eczema shows lichenification (thickening of the skin) from repeated rubbing or scratching, postinflammatory hyper- or hypopigmentation.
• Both types can show excoriations.
• There is commonly a secondary infection, usually with Staphylococcus aureus (S. aureus).

Management

• Chronicity of disease must be emphasized – there is no cure for eczema.
• Preventative measures, including avoidance of trigger factors and skin hydration, are mainstays of treatment.
• Therapeutic measures include the use of topical and oral medications, and the treatment of secondary infections, if present.
• General strategy involves induction of remission, stabilization and maintenance, and the rescue of flares.

Preventative Measures

• Avoid irritants and allergens such as harsh detergents , wool or other itch-inducing fabrics, and common allergens such as pet dander, dust, smoke, and pollens.
• The trigger need not be allergic in nature to induce eczema.
• Moisturizers
  • Need to be used on at least a daily basis because of the inherent xerosis of the skin.
  • Moisturizers that are occlusive prevent water loss.
  • Oils tend to stay on the surface of the skin and are not absorbed.
• Maintain hydration of the skin
  • Use mild or soapless cleanser that does not disrupt the barrier of the skin.
• Bathing
  • Warm, not hot, baths or showers are encouraged.
  • It is crucial to moisturize immediately after bathing.
• Cool temperatures
  • Sweat is aggravating to eczematous skin, and can promote pruritus.

Therapeutic Measures

Topical Corticosteroids

• Most effective for an acute onset of eczema (flare) because of rapid onset of action.
• Potency of the agent depends on the location of the eczema (mild for face and groin, moderate for body).
  • Use the lowest potency possible to control the flare.
  • Greater potency exists when the drug is delivered as an ointment as compared to a cream or a lotion.
• Rarely, skin atrophy, tachyphylaxis (loss of effectiveness), or adrenal suppression is seen with prolonged, daily use. Use of more potent topical steroids is associated with increased risk of development of adverse effects. Risk is higher for younger children because of their surface area-to-weight ratio and because their skin is more permeable.
• To be applied only on the area of active disease.
• Can be used in combination with topical calcineurin inhibitors for local control of eczema.
• Allergic contact dermatitis to corticosteroids is rare.

Topical Calcineurin Inhibitors

• New class of anti-inflammatory agents, available as pimecrolimus 1% cream (Elidel^®), and tacrolimus 0.03% (children 2–12 years) and 0.1% (adults) ointment (Protopic^®).
• Calcineurin inhibitors block cytokine transcription mediated by NF-AT in T cells.
• Pimecrolimus is approved for short-term and intermittent long-term therapy of mild-to-moderate eczema, whereas tacrolimus is approved for therapy of moderate-to-severe AD.
• Both are excellent for long-term management of AD [Meurer M, et al. Dermatol 205(3):271-7 (2002); Hanifin JM, et al. J Am Acad Dermatol 53(2 Suppl 2):S186-94 (2005 Aug).]
  • Reduces the intensity of the flare
  • Helps maintain remission
• Pimecrolimus has been shown to increase the time between flares.[Meurer M, et al. Dermatol 205:271-7 (2002).]
• To be applied only on areas of disease.
• Most common side-effects are local burning and stinging of the skin, which are transient.
• In response to black box warnings for calcineurin inhibitors initiated by Health Canada and the US FDA, the Canadian Dermatology Association has stated that the topical use of calcineurin inhibitors does not lead to an increased risk of malignancy, specifically lymphoma, and so can be used with the same precautions as with topical corticosteroids.[Maddin S. Skin Therapy Lett10(4):1-3 (2005 May).] Their position still holds as of May 2006.

Oral Anti-itch Medications:

• Sedating antihistamines, such as hydroxyzine or diphenhydramine, can be useful adjuncts when taken at bedtime, especially with flares.
• Mast cell stabilizers, such as ketotifen, can be useful when there are other atopic manifestations, such as asthma, rhinitis.

Antibiotic Therapy:

• There may be a secondary infection with S. aureus, even without obvious impetigo, that can lead to a flare.
• Usually topical therapy, such as mupirocin (Bactroban^®) or fusidic acid ointment (Fucidin^®), is sufficient to help clear the eczema.
• In rare widespread cases, oral cloxacillin or a cephalosporin is required, after swabbing for cultures and sensitivities.

Second-line Therapies:

• For very resistant cases systemic treatments such as PUVA, UVB, cyclosporine, azathioprine, or methotrexate can be used. Systemic steroids are sometimes used short-term.

Department of Dermatology, McGill University, Montréal, Québec, Canada

Rosacea is a common condition that is prevalent worldwide. Its incidence is higher in fairer skin types, however it is also seen in Asians, and African-Americans. Rosacea occurs in males and females, often after the age of 30 years.

There are currently no laboratory tests to diagnose rosacea; it remains a clinical diagnosis. The actual pathophysiology and etiology of rosacea also remain unclear; however, quite recently the spectrum of rosacea has been classified and standardized.[Wilkin JK, et al. J Am Acad Dermatol 46:584-7 (2002).] The defining clinical finding is persistent erythema of the central face for at least 3 months. Other primary findings include flushing (transient erythema), papules and pustules, and telangectasias (dilated blood vessels). Secondary findings include stinging, burning, dryness, edema, plaques, ocular manifestations, and phymatous changes.

There are four recognized subtypes of rosacea, and it’s important to distinguish among them, as they require different modes of therapy.

Subtypes of Rosacea

• Erythematotelangectatic rosacea: Flushing and persistent central facial erythema is seen, as well as telangectasias. Often, central facial edema, stinging and burning of the skin, and dryness occurs.
• Papulopustular rosacea: Papules and pustules are seen, often along with persistent facial erythema.
• Phymatous rosacea: Thickening of the skin, often presenting as rhinophyma. Irregular surface nodules, enlarged follicles, sebaceous appearance seen. The chin, forehead, cheeks, and ears may be involved.
• Ocular rosacea: Sensation of burning, grittiness, dryness, burning, “foreign body sensation”, and telangectasia of the sclera. Often, blepharitis, conjunctivitis, chalazions, and styes present. Rarely corneal manifestations (keratitis, infiltrates, and ulcers) may occur.

These subtypes are then graded into mild, moderate, and severe. They may overlap; however, it is currently believed that patients do not progress from one subtype to the next.

Postulated Pathophysiology

• Vasomotor lability
• Exposure to UV radiation, heat
• Degeneration of dermal matrix
• Perifollicular inflammatory process

The role of Demodex and Helicobacter pylori are not at present considered to be pathogenic in the development of rosacea.

Aggravating Factors

• UV exposure
• Extremes of temperature
• Consumption of hot beverages, spicy foods, alcohol
• Topical irritating products containing glycolic acid, alcohol, acetone, exfoliants, astringents, perfumes
• Medications that can cause flushing such as vasodilatation agents, nicotinic acid, amyl nitrate, calcium channel blockers, and opiates

Differential Diagnosis

These diseases must be excluded before making the diagnosis of rosacea:

• Systemic lupus erythematosus, dermatomyositis, mixed connective tissue disease, and other connective tissue diseases
• Polycythemia vera
• Carcinoid
• Mastocytosis

Other situations to be considered include photosensitivity and allergic contact dermatitis. Perioral dermatitis is no longer considered to be a variant of rosacea; it presents with erythematous papules around the mouth or periorbitally. Seborrheic dermatitis can co-exist with rosacea; it presents with orange-red scaling in the T-zone of the face, scalp, and chest.

Treatment Options for Rosacea

• Erythematotelangiectatic rosacea: Topical metronidazole, sodium sulfacetamide with sulfur, and azeleic acid help decrease erythema. Telangiectasias are best treated with laser and light therapies.
• Papulopustular rosacea: Topical metronidazole, sodium sulfacetamide with sulfur, azeleic acid, benzoyl peroxide, erythromycin, clindamycin, and tretinoin decrease inflammatory papules and pustules. For a more rapid response, oral antibiotics are used. Low dose oral isotretinoin (to avoid excessive dryness) can also be used.
• Phymatous rosacea: In early stages, topical therapies can decrease the papules and pustules often present centrally. Isotretinoin can also be used to control the nodules and cysts, as well as temporarily decreasing excessive sebum production. However, rhinophyma itself is treated surgically, including dermabrasion, electrosurgery, cryosurgery and laser surgery.
• Ocular rosacea: General lid care, tear supplements are essential. Often, oral tetracycline is used to treat the inflammatory lesions. If corneal involvement is suspected, consultation with ophthalmology is advised.

Basic Nonprescription Guidelines to Give Patients Include

• Daily use of broad spectrum sunscreens that include titanium dioxide and zinc oxide as UV blockers.
• Use of non-fragranced moisturizers that contain silicone (as dimethicone or cyclomethicone) to protect the skin barrier.
• Soap-free cleansing of the skin.
• Green-tinted foundations in powder, liquid, or cream form to help camouflage erythema.
• Avoidance of aggravating factors (listed above).

Patient Communication

It is important to inform patients that rosacea is a chronic disease, that there is no cure for rosacea, but there exist effective therapies to maintain control. Remission of the disease can be obtained using maintenance treatment to which the patient may have to adhere for life and avoiding aggravating factors. Patients should be counseled that progression of disease can occur when therapy and avoidance behaviors are not maintained.

Dosage and Course of Prescription Treatment for Rosacea