AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Atopic dermatitis (AD) is a chronically relapsing skin disorder with an immunologic basis. The clinical presentation varies from mild to very severe. In the worst cases, AD may interfere with normal growth and development. Treatment consists of adequate skin hydration, avoidance of allergenic precipitants, topical anti-inflammatory medications, systemic antihistamines, and antibiotic coverage of secondary infections.

Although often used interchangeably, the terms eczema and AD are not equivalent. Eczema is a reaction pattern with various causes, the most common pediatric cause being AD. Other causes of eczematous dermatitis include allergic contact dermatitis, irritant contact dermatitis, seborrheic dermatitis, nummular eczema, dyshidrotic eczema, asteatotic eczema, and lichen simplex chronicus. Eczematous reactions can be classified as acute, subacute, or chronic, depending on historical and physical characteristics.

Pathophysiology

The etiology of AD remains unclear. Histologically, AD has been shown to be a complex inflammatory process involving mast cells, lymphocytes, and infiltrating leukocytes. One causative theory is that AD results from a hyperactive T helper cell 2 (Th2) and down-regulation of T helper cell 1 (Th1) activity. Th2 cells normally secrete interleukin (IL)–4, IL-5, and IL-13, of which IL-4 and IL-13 serve to promote the synthesis of immunoglobulin E (IgE) from B lymphocytes and to activate the vascular endothelium. IL-5 enhances eosinophil-mediated responses. This theory is supported by the frequent occurrences of elevated serum IgE levels and peripheral blood eosinophilia in AD patients. Furthermore, evidence is accumulating that administration of IL-2 or gamma-interferon, the cytokines of the Th1 immune response system, to atopic patients results in improvement in disease severity.

Another theory is that AD may be a result of problems with fatty acid metabolism. Specifically, deficient levels of omega-6 fatty acids have been observed in the blood and adipose tissues of individuals affected by AD as well as in the breast milk of mothers of some affected infants. Infants fed formula, which has a relatively low yield of omega-6 fatty acids in comparison with breast milk, have a higher incidence of AD than infants fed human milk. Furthermore, prostaglandin E1 (PGE1) and prostaglandin E2 (PGE2), major metabolites of omega-6 fatty acid biosynthesis, have been shown to suppress synthesis of IgE and are necessary for the optimal stimulation of Th1 cell activities by thymic hormones.

Frequency

United States

AD occurs in approximately 10-15% of children. Areas in the Western Hemisphere have prevalence estimated at 10%, while areas in Asia have much lower disease prevalence. Interestingly, populations that migrate from areas of low prevalence to areas of higher prevalence have shown an increased incidence of AD, bolstering the idea of strong environmental influences in the development of AD. Children with concurrent asthma or hayfever have a 30-50% incidence of developing AD.

Race

No clear racial predilections have been identified.

Sex

Males and females are affected with equal incidence and severity.

Age

AD may occur in people of any age, but it often starts in infants aged 2-6 months. Seventy-five percent of individuals experience marked improvement in the severity of AD by age 10-14 years, but the remaining 25% continue to have relapses during their adult life.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

• Diagnostic criteria for AD have been proposed by Hanifin and Rajka (1980) and largely adopted by the American Academy of Allergy, Asthma, and Immunology. Appropriate cases must have at least 3 major characteristics and at least 3 minor characteristics.
• Major characteristics include the following:
• • Pruritus
  • Typical morphology and distribution (ie, flexural lichenification and linearity in adults, facial and extensor involvement in infants and young children)
  • Chronic or chronically relapsing dermatitis
  • Personal or family history of atopy (eg, asthma, allergic rhinoconjunctivitis, AD)
• Minor characteristics are as follows:
• • Xerosis (dry skin)
  • Ichthyosis/palmar hyperlinearity/keratosis pilaris
  • Hand and/or foot dermatitis
  • Cheilitis
  • Nipple eczema
  • Susceptibility to cutaneous infection (eg, with Staphylococcus aureus, herpes simplex virus [HSV], other viruses, warts, molluscum, dermatophytes)
  • Erythroderma
  • Perifollicular accentuation
  • Pityriasis alba
  • Early age of onset
  • Impaired cell-mediated immunity
  • Recurrent conjunctivitis
  • Orbital darkening
  • Infraorbital fold (eg, Dennie pleat, Morgan fold)
  • Anterior neck folds
  • Keratoconus
  • Anterior subcapsular cataracts
  • Sensitivity to emotional factors
  • Food intolerance
  • Pruritus with sweating
  • Intolerance of wool
  • White dermographism
  • Immediate type I skin test response
  • Elevated total serum IgE
  • Peripheral blood eosinophilia
• Most atopic children relate a history notable for intense pruritus and dry skin. The quality of the pruritus is referred to as a spreading itch. Affected children often have a lowered itch threshold, resulting in increased levels of cutaneous reactivity in response to stimuli. Patients may succumb to a vicious itch-scratch-itch cycle, in which pruritus stimulates a bout of scratching. This, in turn, increases skin inflammation and triggers a greater sensation of itching, thus exacerbating flares.
• Altered cell-mediated immunity has been noted in patients with AD. This is observed clinically as a history of repeated unusual cutaneous infections (eg, eczema herpeticum, warts, molluscum, dermatophytes).

Physical

• Three classes of skin lesions exist.
• • Acute - Intensely pruritic erythematous papules and vesicles overlying erythematous skin; frequently associated with extensive excoriations and erosions accompanied by serous exudates
  • Subacute - Erythema, excoriation, and scaling
  • Chronic - Thickened plaques of skin, accentuated skin markings (lichenification), fibrotic papules (prurigo nodularis); possible coexistence of all 3 types of lesions in chronic AD
• Typical locations of lesions by age
• • Nonmobile infant - Face and scalp
  • Crawling infant - Extensor surfaces of extremities, trunk, face, and neck
  • Older child and adolescent - Wrists, ankles, antecubital fossae, popliteal fossae, and neck
  • Adult - May be limited to hand and foot eczema
• Associated findings in AD include keratosis pilaris; accentuated palmar creases; lichenification; atopic pleats; allergic shiners; transverse nasal crease; pallor around the nose, mouth, and ears; white dermographism; cataracts; and keratoconus.
• Keratosis pilaris, or plucked chicken skin, consists of large cornified plugs in the upper part of hair follicles and produces a stippled appearance of the skin on the outer aspects of the arms and legs and on the buttocks and trunk.
• Hyperlinear palms are usually present at birth and persist throughout life. These consist of an increased number of fine lines and accentuated markings on the palms.
• Lichenification of the wrists, ankles, popliteal fossae, or antecubital fossae is characteristic of chronic AD. It is observed as thickened, leathery, hyperpigmented patches of skin with a deepening of normal skin creases.
• Atopic pleats, also referred to as Morgan-Dennie folds, Morgan folds, Dennie pleats, or mongolian lines, are skin folds observed just below the lower lid of both eyes and are retained throughout life.
• Allergic shiners are violet-gray infraorbital discolorations caused by underlying vascular stasis. Increased pressure on nasal and paranasal venous plexuses causes edema in these areas, leading to development of atopic pleats and allergic shiners.
• A prominent transverse nasal crease is a common sign of concurrent allergic rhinitis and, along with allergic shiners and atopic pleats, may be a clue to the diagnosis of an atopic diathesis.
• Dermographism is a normal reaction in 5% of the population. After a firm pointed instrument is stroked against the skin, the path of the instrument is observed as a red line followed by an erythematous flare that ultimately develops into a wheal. This response occurs within 3 minutes of the insult. White dermographism is a paradoxical reaction wherein the initial red line is replaced within 10 seconds by a white line and an absence of a wheal. This reaction can be observed in AD and allergic contact dermatitis.
• Atopic cataracts affect 4-12% of patients with AD and occur much earlier in life than senile cataracts. They typically are bilateral, central, and shield-shaped, and they mature rapidly. Because patients generally are asymptomatic, diagnosis is usually made by slit lamp examination. Incidence of cataracts in atopic patients appears to be unrelated to the use of topical steroids.
• Keratoconus is an elongation of the corneal surface that is thought to be caused by long-term eye rubbing and may be a degenerative change in the cornea. Keratoconus affects approximately 1% of children with AD and generally can be alleviated with the use of contact lenses.

Causes

The etiology of AD appears to be linked both to genetic causes and to environmental agents.

• The prevalence of AD in children with 1 affected parent is 60% and rises to nearly 80% for children of 2 affected parents. Additionally, nearly 40% of patients with newly diagnosed cases report a positive family history for AD in at least 1 first-degree relative. Much higher concordance of AD exists in monozygotic twins than in dizygotic twins.
• Environmental allergens repeatedly have been shown to trigger exacerbations of AD in susceptible individuals. Contact irritants, climate, sweating, aeroallergens, microbial organisms, and stress/psyche are common culprits.
• • Contact irritants (eg, soaps, solvents, wool clothing, mechanical irritants, detergents, preservatives, perfumes) compromise the integument, creating inflammation, irritation, and a portal of entry for further environmental insult. These surface irritants, along with the macerative effects of sweating and the drying effects of low humidity, lower the pruritic threshold. A vicious cycle of itching and scratching ensues, in which added cutaneous damage caused by scratching further lowers the pruritic threshold and subsequently causes increased itching.
  • Aeroallergens (eg, house dust mite, molds, pollen, dander) induce peripheral eosinophilia and elevate serum IgE levels. These early effects lead to increased histamine release from IgE-activated mast cells and elevated activity of the T-helper cell–mediated immune system. The increased release of vascular mediators (eg, bradykinin, histamine, slow-reacting substance of anaphylaxis [SRS-A]) induces vasodilation, edema, and urticaria, which in turn stimulate pruritus and inflammatory cutaneous changes.
  • Microbial agents (eg, S aureus, Pityrosporum yeasts, Candida organisms, Trichophyton dermatophytes) act in 2 different ways to promote the flares of AD. The microorganisms directly invade the skin, creating local injury and inflammation, and they induce a systemic allergic response to specific antigens, causing a rise in serum IgE and enhanced activity of the immune system.
  • Food allergy is implicated in one third to one half of children with AD. The most common food allergens are egg, soy, milk, wheat, fish, shellfish, and peanut, which together account for 90% of food-induced cases of AD in double-blind placebo-controlled food challenges. Fortunately, many food allergies fade in intensity after age 1 year, eliminating the need for long-term restrictive diets.
  • Stress may trigger AD at the sites of activated cutaneous nerve endings, possibly by the actions of substance P, vasoactive intestinal peptide (VIP), or via the adenyl cyclase–cyclic adenosine monophosphate (cAMP) system.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Seborrheic dermatitis
Psoriasis

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• No definitive laboratory tests to diagnose AD exist.
• Elevated serum IgE levels and peripheral blood eosinophilia occur in most individuals with AD, and these findings may be useful in confirming the atopic status of suspected cases.
• The presence of serum IgE directed against the cell wall of S aureus is observed in hyper-IgE syndrome and AD.
• Common infections that mimic or complicate AD can be tested for as follows: conduct a Tzanck smear for HSV, a potassium hydroxide (KOH) preparation for dermatophytes, and a Gram stain for bacterial infections.

Other Tests

• Prick skin testing to common allergens can help identify specific triggers of AD. For accuracy, antihistamines must be discontinued for 1 week and topical steroids for 2 weeks prior to testing. Although used most often in young children with moderate-to-severe disease, false-negative and false-positive test results are not uncommon in children younger than 8 years. If positive, these tests do not necessarily indicate clinically significant triggers. Prick skin tests only indicate that the patient has been sensitized to the particular antigens. For example, most children shown to have multiple food allergies by skin tests only demonstrate clinically detectable allergic reactions to 3 or fewer foods when tested by double-blind randomized provocative testing.
• Radioallergosorbent test (RAST) and enzyme-linked immunosorbent assay (ELISA) in vitro tests identify serum IgE directed toward specific allergens. As with prick skin tests, these diagnostic methods show a poor predictive value for clinically significant food allergies and may produce false-positive results when the patient's serum contains elevated IgE levels.

Histologic Findings

Acute eczematous lesions show histologic markings of hyperkeratosis, parakeratosis, and acanthosis with a decreased or absent granular cell layer. Important features in histologic diagnosis include spongiosis (accumulation of fluid in the intercellular and intracellular areas) and exocytosis (infiltration of leukocytes through the epidermis). Chronic eczematous lesions display hyperkeratosis with areas of parakeratosis and papillomatosis (upward proliferation of dermal papillae).

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

• The most fundamental and important step in combating atopic dermatitis (AD) is rehydration of the stratum corneum. Adequate rehydration preserves the stratum corneum barrier, minimizing the direct effects of irritants and allergens on the skin and maximizing the effect of topically applied therapies, thus decreasing the need for topical steroids.
• • Lukewarm soaking baths lasting 20-30 minutes are ideal. Very hot water should be avoided to prevent both vasodilation, which can trigger pruritus, and the damage to the skin barrier caused by scalding.
  • Small amounts of bath oils or emulsification agents may be used for added hydration benefits in older children and adolescents. Bath oils or emulsification agents result in slippery conditions; warn patients and parents of the resultant risks of trauma and drowning after a fall. Readily available over-the-counter bath agents include Aveeno Colloid Oatmeal, RoBathol, Maypo, cottonseed oil with Brij 93, or mineral oil.
  • Recommended soaps are mild and unscented with a neutral pH. Examples include Dove, Oil of Olay, Caress, Camay, Aveeno, and Purpose. Even these mild soaps are often too drying for atopic skin. If the children are prepubertal, bathing in water alone may be preferable. Postpubertal patients need to use soap in the axillae and groin but do not need it elsewhere.
  • If soaps are too irritating to the skin, hydrophobic lotions and creams, such as Cetaphil, Diprobase, and Unguentum Merck, may be used. These agents have excellent cleansing properties and low potential for irritation. They should be applied without water and rubbed gently over the skin surface until a light foaming occurs. A soft cotton cloth or tissue can then be applied to wipe away the agent, leaving behind a protective film of stearyl alcohol and propylene glycol.
  • Baby shampoo may be used to manage scalp dermatitis.
• Baths should be followed by the immediate application of an occlusive emollient over the entire skin surface to retain moisture in the epidermis. If an emollient is not applied within 3 minutes of leaving the bath, evaporation causes excess drying of the skin. Skin should not be completely dried with a towel prior to application of the emollient; rather, lightly patting the skin with a towel to remove excess moisture is sufficient.
• • Frequently recommended emollients are hydrophobic and ointment-based; these include Vaseline petrolatum jelly, Crisco, vegetable oil, Aquaphor, and Elta. Occasionally, parents may find these agents too greasy for everyday use, and cream-based alternatives may be offered. Common creams are DML Forte, Moisturel, Aveeno, Curel, Purpose, Dermasil, Neutrogena, and Eucerin. This latter group of moisturizers is less effective because of the weaker occlusive effects of creams as compared to ointments; thus, they should be used only if the ointment-based emollients are not well tolerated.
  • The newest type of moisturizing product is a ceramide-dominant, lipid-based emollient (TriCeram) aimed at repairing the stratum corneum barrier function lost in atopic dermatitis. One study showed a significant decrease in clinical severity scores and a decrease in transepidermal water loss in children whose traditional moisturizers were replaced by TriCeram for 3 weeks.
  • Urea-containing products have been shown to soften and moisturize dry skin. Commonly available preparations include Aquacare cream or lotion and Ureacin Crème. Alpha-hydroxy and lactic acid preparations also are helpful as moisturizers. Name brands include Aqua Lacten Lotion, AmLactin Lotion, LactiCare Lotion, Lac-Hydrin Lotion, and Nutraderm 30. In addition, 12% ammonium lactate lotion has been shown to improve skin barrier function and even to mitigate dermal or epidermal atrophy induced by corticosteroids. Because of the stinging sensation experienced by children with acute or fissured dermatoses, the 10% urea concentration is preferred over the higher concentrations, and care should also be used in the application of the alpha-hydroxy and lactic acid preparations. LactiCare-HC Lotion also contains hydrocortisone to further benefit acute flares of AD.
  • For children with repeated cutaneous infections, adding 2 teaspoons of household bleach (eg, Clorox) per gallon of bath water can help reduce incidence of such infections. A typical bathtub holds approximately 25-40 gal of water. During acute AD exacerbations, pouring 1 cup of table salt into the bath may ameliorate the stinging effect these children frequently experience while bathing.
  • Wet dressings are very useful for diverse types of atopic dermatitic flares. They can be used on dry lichenified lesions to improve hydration and increase the penetration of topical corticosteroids; they also work well to dry weeping or oozing lesions via evaporation.
  • Burow solution 1:40 is a commonly used wet dressing because it is germicidal and directly suppresses weeping lesions by precipitation of protein. The solution is prepared easily by dissolving one Domeboro packet or effervescent tablet in a pint of tepid or lukewarm tap water. Hot water induces vasodilatation with increased weeping and pruritus; cold water causes vasoconstriction and secondary vasodilation. Submerge a soft cloth (eg, handkerchief, thin diaper, strips of bed sheets) into the solution until moderately wet but not dripping. Place the dressing over the affected skin site, periodically rewetting the compress. In severe cases, a topical corticosteroid may be applied after the compress for enhanced penetration and action of the medication. A final benefit of wet dressings is to provide a physical barrier against scratching.
  • Seek psychologic counseling, biofeedback, relaxation techniques, massage therapy, and behavioral modifications if emotional stressors are a contributing factor to AD.
• Ultraviolet light may benefit some patients. Ultraviolet light in the UVB range may provide control and eliminate or markedly reduce the need for steroids. The new narrow band units are especially effective. Ultraviolet light in the UVA range has been used alone, in combination with oral psoralen administration (PUVA), or with high-dose UVA 1 (ie, 340-400 nm spectrum units).

  A significant decline in the usage of UVA light therapy and psoralen has taken place in recent years as this regimen clearly accelerates photoaging and increases the risk of skin cancer. UVA 1 spectrum light works by reducing cellular immunoglobulin E (IgE) binding sites and inducing apoptosis in inflammatory cells and has demonstrated significant efficacy in treating atopic dermatitis. However, UVA 1 light sources continue to be prohibitively expensive and are not yet standardized equipment in nonacademic treatment centers nor readily available enough to recommend. A small number of patients develop erythema or disease flares with lighttreatment.

Consultations

Consider consultation with an allergist, immunologist, or dermatologist for the following conditions:

• AD that is severe (eg, 20% skin involvement, 10% skin involvement with eyelids/hands/intertriginous areas affected) or is refractory to first-line treatments
• Erythroderma or extensive exfoliation
• Infectious complications
• Ocular complications
• Psychosocial complications
• Coexisting asthma, allergic rhinitis
• Impaired quality of life
• Identification of triggers and allergens
• AD requiring hospitalization or more than 1 course of systemic steroids
• Uncertain diagnosis

Diet

• Studies regarding the protective effect of breastfeeding on AD have yielded conflicting results. A recent meta-analysis concluded that exclusive breastfeeding has a protective effect for the first 3 months of life on the later development of AD in childhood. However, this effect was only significant in children with a family history of atopy and not in the general population or in children without atopic first-degree relatives. More studies need to be performed to delineate the exact mechanism and nature of this protection.
• Many physicians are currently advocating elimination of specific commonly allergenic foods during the first 1-2 years of life in children with acute AD. The short list includes cow's milk, eggs, tomatoes, citrus fruits, chocolate, wheat products, spiced foods, fish, nuts, and peanut butter. These foods may be reintroduced after controlling the initial acute flare of AD, or parents may elect to wait until after the child is aged 2 years because food reactivity diminishes markedly with age.
• For children older than 5 years, nutritionally adequate elimination diets are the goal if double-blind placebo-controlled trials indicate a clinically significant food allergy. However, most skin tests, RAST, and ELISA tests that reveal positive results against food allergens are not borne out to cause disease flares in clinical trials; thus, elimination diets are only rarely indicated.
• Chinese herbal teas have been shown to be efficacious in inducing remission in some children and patients with recalcitrant disease. Because these teas can contain up to 10 different herbs, which have various anti-inflammatory, antihistaminic, or immunosuppressant activities, these effects have not yet been specifically linked to any one ingredient. Reports exist of liver, kidney, and cardiac damage as well as hypersensitivity; thus, risks and benefits need to be further evaluated.
• Probiotics have become much more popular within the last few years as treatments for a wide variety of ailments, including skin disorders. A recent study demonstrated improvement in eczematous dermatitis symptoms in allergic patients (ie, elevated IgE level or at least one positive skin-prick test) when given certain probiotic Lactobacillus strains. However, these results were not seen in patients who did not have the aforementioned allergic markers. More prospective, blinded studies are needed to confirm these findings.

Activity

• In the subgroup of children with AD who also experience respiratory allergies to animal allergens, parents should consider removing animals from the home or confining them to areas of the house where susceptible children do not come into contact with their dander or saliva.
• Prohibit smoking in the home and other areas that are frequented by children with allergies.
• Implement dust mite and mold control measures for allergic children. Counsel parents to use dust mite–proof plastic cases around pillows, mattresses, and box springs. Wash bedding in hot water weekly to remove offending agents. For children who have tested positive for sensitivity to house dust mite by skin test, natamycin spray and benzyl benzoate (Acarosan) may be helpful in controlling mites in carpets and drapes.
• Avoid irritants that trigger the itch-scratch-itch cycle (eg, soaps, detergents, chemicals, abrasive clothing, extremes of temperature and humidity).
• • Use pH-neutral minimally defatting soaps (eg, Dove). Avoid excessive drying of the skin with alcohol-containing astringents. Launder new clothes before wearing to remove manufacturing chemicals. Use liquid detergent rather than powder detergent and add a second rinse cycle to remove all residual detergent.
  • Wear loose fitting open-weave cotton or cotton-blend clothing; avoid wool.
  • Use a humidifier in the winter to prevent excessive skin dryness and an air conditioner in the summer to prevent sweating and associated macerative effects on the skin. Decreased humidity indoors helps prevent the growth of mold.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Topical corticosteroids are the mainstay of treatment of AD. These medications reduce inflammation and pruritus primarily by inhibiting the transcriptional activity of various proinflammatory genes. Topical steroids should be applied only to areas of acute exacerbations, whereas emollients should be used over the remainder of the skin. The absorption of topical steroids is much better through hydrated skin; thus, the ideal time for application is in the first 3 minutes after a bath or shower. The various topical steroid formulations, in ascending order of occlusiveness, include lotions, creams, gels, and ointments.

Lotions contain water and may be drying because of the evaporative effect; thus, they are used mostly in scalp and beard areas where drying effects are not as problematic. Lotions containing alcohol may cause a burning sensation upon application, especially on skin with fissured or ulcerated areas. Lotions may contain preservatives, solubilizers, and fragrances that can irritate the skin.

Creams are generally well tolerated but are less moisturizing than ointments. Creams are popular for their nongreasy appearance on treated skin and are more convenient during hot weather because they cause less occlusion of eccrine sweat glands than ointments and gels. As with lotions, creams may contain preservatives, solubilizers, and fragrances that can irritate the skin.

Gels are highly occlusive, but the propylene glycol base is irritating to the skin and promotes dryness. Therefore, gels, similar to lotions, are used mostly in scalp and beard areas where the drying effects are not as problematic. They are very effective in the management of acute weeping or vesicular lesions of AD.

Ointments are the most moisturizing of the topical steroid vehicles, but their occlusiveness may not be well tolerated because of their interference with sweat gland function and resultant development of sweat retention dermatitis, especially in warm humid climates. Ointments work the best on thickened lichenified plaques of AD.

Systemic corticosteroids have been used in severe chronic AD, but usage has been limited in the pediatric population because of the risk of severe adverse effects associated with chronic usage, including growth retardation and immune suppression.

Oral antihistamines are effective as systemic antipruritics, sedatives, and mild anxiolytics. These are beneficial especially at nighttime because pruritus is usually worse at night. Commonly used oral antihistamines include diphenhydramine, hydroxyzine, and doxepin. Pramoxine is a topical antipruritic agent and can be found as Prax, Pramosone, or PrameGel.

Coal tar topical preparations have antipruritic and anti-inflammatory effects. They work as disinfectants and astringents and help to correct abnormal keratinization by decreasing both epidermal proliferation and dermal infiltration. They are effective as second-line agents for subacute, chronic, and lichenified AD. Cosmetically acceptable preparations recently have been made available and include AquaTar, Estar, Fototar, PsoriGel, and Neutrogena T/Derm Tar Emollient. Tar shampoos, such as Neutrogena T-Gel, are effective for scalp involvement. Adverse effects may include folliculitis and photosensitivity.

Topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus) are the newest class of topical medications for atopic dermatitis. These nonsteroidal immunomodulators act by down-regulating the mediator release or cytokine expression of various cells, including T1 helper cells, T2 helper cells, mast cells, eosinophils, keratinocytes, and Langerhans cells. Calcineurin inhibitors may be especially useful for treating face, groin, or axillary areas, where steroid-sparing treatments are preferred.

Systemic cyclosporine A can dramatically reverse severe flares of AD. Because of the risk of severe adverse effects, this treatment should be limited in duration. Once control is obtained, alternative maintenance therapy should be instituted.

Experimental treatments for AD have included trials of gamma-interferon and IL-2; both are inhibitors of Th2 cell functions and have been promising. Oral mycophenolate mofetil, an inhibitor of purine synthesis, has also recently been shown in 2 small series to be an effective alternative form of treatment for severe disease.

Drug Category: Topical corticosteroids

In older children and adolescents, treat mild cases of AD with a low-potency (class VI or VII) topical steroid twice a day to decrease inflammation. Examples include hydrocortisone cream or ointment, 1% and 2.5%. For moderate cases of AD, intermediate-potency steroids (class III, IV, V) may be used for brief periods (<2 wk) to control an eczematous flare. Subsequently, low-potency steroids can be used to maintain remission. For severe cases of AD, pulse therapy with high-potency topical steroids (class II) or PO steroids may be beneficial in adolescents. Remember to use only lower potency steroids on the face, axillae, groin, and intertriginous areas because of increased absorption.

For mild AD in infants, class VI or VII topical steroids should be effective. If the infant has more severe AD, a moderate-potency steroid can be prescribed for up to 1 week and then tapered down to a lower-potency medication for maintenance therapy. In general, do not treat infants with topical steroids in the high-potency classes (class II or above) without a referral to a dermatologist.

Cordran tape is a corticosteroid-impregnated polyethylene film that enhances topical steroid penetration up to 100-fold. Occlusion of a topical steroid under plastic wrap seems to work equally as well. These methods are especially useful for chronic lichenified plaques of AD.

In order to achieve a quick, complete remission of AD symptoms, adequate amounts of topical steroid must be used. Many patients initially use suboptimal amounts of topical steroid products, leading to poor control of their AD symptoms and ultimate discontinuation of their therapy. Approximately 30 grams of medication is needed to cover the entire surface area of an adult body. For children, the fingertip unit (FTU) has been shown to accurately measure an appropriate amount of medication. The FTU is defined as the amount of topical medication that will cover the child's index finger from the tip to the metacarpophalangeal joint. For topical steroids, 1 FTU will cover the hand or groin, 2 FTUs for the face or foot, 3 FTUs for an arm, 6 FTUs for a leg, and 14 FTUs for the trunk.

Drug Category: Systemic corticosteroids

Symptoms typically improve dramatically in the first few days of treatment with systemic steroids, only to be followed by an equally dramatic rebound flare after cessation of treatment. Tapering oral steroids over 10-14 days may mitigate this effect. In addition, an intensified focus on hydration with bathing and appropriate use of topical steroids should be emphasized to prevent rebound phenomena after discontinuation of systemic steroids.

Drug Category: Antimicrobials

Antistaphylococcal antibiotics (eg, topical mupirocin or bacitracin, first-generation cephalosporins, macrolides, penicillinase-resistant extended-spectrum penicillins such as oxacillin or dicloxacillin if resistant strains of S aureus are encountered, amoxicillin-clavulanate) are helpful in secondary bacterial infections. Herpes simplex superinfections (eczema herpeticum) should be suspected if vesicles are present or if no improvement is observed with PO antibiotics. Tzanck smear of the base of vesicles is positive in 70% of cases. Treat with PO or IV acyclovir for 10 days. Varicella infections may become severe in the setting of AD, and early treatment with acyclovir is recommended. Counsel all children with AD as to the benefits of vaccination against varicella. Treat dermatophyte infections with topical or PO antifungals, such as topical ketoconazole cream or shampoo.

Drug Category: Antipruritics

Topical local anesthetics or antihistamines (topical or systemic) may be used to decrease pruritus.

Drug Category: Immunomodulators

Topical tacrolimus ointment and pimecrolimus cream have both been shown to diminish pruritus and inflammation markedly within 3 days of initiating therapy and to have persistent effects for up to 12 months. Several studies have documented the rapid and prolonged improvement in clinical severity scores in children and adults with a range of severity of AD. The most common adverse effect is a local burning sensation upon application, but this symptom tends to diminish after the first few days of use.

Oral cyclosporine has proven beneficial in patients with severe AD refractory to treatment with topical steroids. Discontinuation of cyclosporine frequently results in rapid relapse of skin disease. Significant adverse effects (eg, nausea, abdominal discomfort, hypertrichosis, paresthesias, hypertension, hyperbilirubinemia, renal impairment) have diminished enthusiasm for this drug, especially with the advent of the topical immunomodulators mentioned above.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Outpatient Care

• Frequent follow-up is needed early in the disease course to ensure compliance and assess patient responsiveness to therapy. Analyze treatment failures for the presence of resistant organisms, contact dermatitis to a medication (eg, preservatives in steroid preparations, bacitracin), or parental noncompliance.

Deterrence/Prevention

• Prevention of acute flares and the subsequent development of chronic lesions of AD are indicators of successful treatment for this disease. Maintenance of adequate hydration of the stratum corneum, avoidance of known or probable allergens and irritants, rapid self-treatment with the proper class of topical steroids, and judicious use of complementary therapies (eg, antipruritics, stress relievers, antibiotics) are the cornerstones of ensuring a high quality of life unimpeded by the more severe aspects of this disease.

Complications

• The most common complication of AD is secondary infection.
• • Staphylococcus species and group A beta-hemolytic streptococci are the most frequent organisms cultured from skin lesions. Superinfected eczematoid lesions appear as erythema associated with serous or purulent exudates and crusting. Greasy moist scales on the surface of the lesions and small pustules at the advancing edges may be present. Always consider infection in acute flares of chronic AD or in cases that are unresponsive to appropriate therapy.
  • Osteomyelitis has been described in patients with superinfected AD. Topical antibiotic therapy is useful for localized infections; however, systemic treatment is preferred for recurrent or widespread infections. The agent of choice is penicillin G if group A streptococci is the known infectious organism. Use erythromycin or a semisynthetic penicillin (eg, nafcillin, oxacillin, dicloxacillin) if S aureus is a possible cause. Hospitalization and use of intravenous antibiotics are indicated in cases of invasive infection (eg, osteomyelitis). Perform urinalysis and closely observe patients for symptoms for at least 7 weeks after treatment in endemic areas because systemic antibiotic treatment does not prevent postinfectious glomerulonephritis after a cutaneous infection with nephritogenic M strains of streptococci.
  • Less commonly, patients with AD may develop an explosive vesicular eruption known as Kaposi varicelliform eruption or eczema herpeticum. Vesicles and pustules typically are umbilicated and initially confined to eczematous skin but may later spread to normal skin. Later in the course of the disease, erosions may be commonplace and confluent, resulting in denuded areas. Tzanck smear of vesicles or a viral culture confirms the diagnosis. Treatment is with acyclovir (if mild, administer 25-30 mg/kg/d, up to 200 mg 5 times per d orally; if severe, administer 5 mg/kg 8h or 1.5 g/m²/d IV).

Prognosis

• Twenty to 40% of atopic children remain atopic as adults. Many children outgrow severe AD and only experience itchy or inflamed skin if exposed to exogenous irritants as adults.

Patient Education

• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Eczema.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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Article Last Updated: May 24, 2006