atopic dermatitis

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ATOPIC DERMATITIS

Elizabeth Harrigan, MD, and Linda G. Rabinowitz, MD

Atopic dermatitis (AD) is a chronic condition that affects nearly 10% of all children and is often the first clinical manifestation of atopy. It is a complex multifactorial disorder that typically has its onset during the first year of life. The diagnosis is established by noting the presence of pruritus, a chronic relapsing course, and a personal or family history of atopy, in addition to particular morphologic features, a characteristic distribution, and associated physical findings (Table 1). Although the exact cause is not known, AD occurs in genetically predisposed individuals, with 80% of affected children having a personal or family history of atopy. The precise pathogenesis is unclear, but eosinophil, mast cell, and lymphocyte activation triggered by elevated production of interleukin- 4 ( IL4) by specific T-helper lymphocytes seems to be involved.

CLINICAL FEATURES

AD can develop at any age but most' often has its onset during the first 6 months of life. Approximately 50% of affected individuals will have symptoms during the first year, and the majority of patients with AD will develop allergic rhinitis or asthma later in childhood. In infants, atopic dermatitis typically involves the face, scalp, trunk, and extensor surfaces of the limbs (Fig. 1). Older children and adolescents have involvement primarily of the flexural areas, including the antecubital and popliteal fossae, wrists, and ankles (Fig. 2). Pruri- tus is the hallmark of atopic dermatitis. The primary skin lesions are papules or vesicles and are typically associated with erythema and white scale. In the acute phase, scratching leads to excoriation and subsequent oozing and crusting. Chronic skin changes include thickening, lichenification, and hypo- or hyperpig- mentation. Follicular prominence, which gives the skin a goosebump-like tex- ture, is often seen in patients with AD.

From the Department of Pediatrics (EH, LGR) (Dermatology [LGR]) and Division of Allergy and Immunology (EH), Medical College of Wisconsin, Milwaukee, Wisconsin

IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA

VOLUME 19 NUh4BER 2 - MAY 1999 383

384 HARRIGAN & RABINOWlTZ

Table 1. DIAGNOSTIC CRITERIA FOR ATOPIC DERMATITIS IN CHILDREN

Major criteria Pruritus Facial and extensor involvement Chronic relapsing course Personal or family history of atopy Minor criteria Xerosis Ichthyosis, palmar hyperlinearity or keratosis pilaris Skin prick test reactivity Elevated total serum IgE Early age of onset Propensity for cutaneous infections Nipple eczema Cheilitis Dennie-Morgan fold Kera toconus Anterior subcapsular cataracts Facial pallor or erythema Pityriasis alba Intolerance to wool Food intolerance Worsening of symptoms with emotional or enviromental changes Worsening of itch with perspiration

Data from Hanifin JM, Rajka G: Diagnostic features of atopic dermatitis. Acta Dermatol 9244-47, 1980.

Figure 1. Erythema and scaling of the face, particularly the cheeks, is a common presentation of atopic dermatitis in children.

ATOPIC DERMATITIS 385

figure 2. Flexural areas, such as the antecubital fossae, are typically involved during childhood.

Diagnosis and Identification of Triggers

The clinical criteria for the diagnosis of atopic dermatitis according to Hanifin and RajkaX7 are outlined in TabIe 1. No single laboratory marker exists for the diagnosis of AD. Atopic individuals typically have an elevated IgE level and eosinophilia. These findings are nonspecific and are not necessary to estab- iisfi the diagnosis of AD. One third to one half of all children with AD have a food allergy that is thought to trigger a late-phase IgE response. Sampson evaluated over 300 children with moderate to severe AD and found 63% to have food hypersensitivity confirmed by double-blind placebo-controlled food challenges.39 A recent study demonstrated that seven foods-milk, egg, peanut, soy, wheat, cod, and cashew-account for 90% of confirmed food allergy, with skin prick testing correlating in 99% of these patients? Early identification and elimination of the allergenic food can produce significant improvement in AD ~ymptoms.3~ Thus, skin-prick testing for foods is warranted in infants and young children with AD whose disease persists for several months or is unresponsive to conventional therapy.

In older children and adults, aeroallergens and contactants, rather than foods, are more common triggers of AD. Contact with irritants such as wool, feathers, fragrances and perfumes, and pet dander can trigger flares of AD and should be avoided as much as possible. The dust mite ~ e ~ u t o ~ ~ g u ~ d e s pferonyssinus is a major trigger for atopic dermatitis. Reducing the mite burden in the home environments of patients with AD has been shown to result in significant improvement in disease symptoms.B5 Because patients with AD typically demonstrate elevated IgE against mite antigen, they frequently exhibit reactivity on skin-prick testing to dust mite; the significance of this is controver-

386 HARRIGAN & RABINOWITZ

sial. Studies to establish a standardized patch test technique for delayed hypersensitivity reaction to dust mite may be a more reliable indicator of immunologic sensitivity in AD patients.ll

For those patients who have extensive skin involvement or are dependent on oral antihistamines for symptom relief, radioallergosorbent test (RAST) may be used to identify IgE directed against specific allergens, Patients with elevated total serum IgE levels, however, can have false-positive RAST results because of nonspecific allergen bindk1g.2~

IMMUNOLOGY OF ATOPIC DERMATITIS

The immune dysregulation associated with AD occurs via several mechanisms. A relative imbalance between Th-2 and Th-1 lymphocyte activity exists in patients with this disorder. Patients with AD have predominant activation of Th-2 lymphocytes, resulting in relatively high levels of IL-4, IL-5, and total IgE, with underproduction of interferon gamma (IFN-y)F6 IL-4 inhibits IFN-y production and downregulates Th-1 lymphocytes.48 In addition, IL-4 serves as an IgE isotype-specific switch factor and stimulates the expression of vascular adhesion molecule1 (VCAM-l), which promotes monocyte and eosinophil mi- gration to sites of inflammation.26

IL-5 stimulates the differentiation and endothelial adhesion of eosinophils and the release of histamine from’ba~ophils.~~ The local expression of these cytokines appears to directly affect the way in which inflammation manifests in AD. A recent in situ hybridization study demonstrated IL-4 expression primarily in acute inflammatory AD lesions, whereas chronic lesions manifested IL-5 expression and infiltration of eosinophils.16

The ceIlular phenotype in AD is thought to contribute to the pathogenesis of the disease by the expression of specific cell surface markers that appear to play a role in T-cell activation. Lymphoaytic infiltrates found in acute and chronic skin lesions of AD consist primarily of CD3, CD4, and CD45RO memory T cells, which express CD25 and HLA-DR.z7,36 These cells also express cutaneous lymphocyte antigen (CLA), a skin T-cell homing receptor that can be induced by staphylococcal superantigen to enhance cutaneous inflammation and promote colonization with Staphylococcus aureus in AD.28

Increased numbers of Langerhans’ cells are found in the chronic skin lesions of patients with AD. These cells express CDlb, CD36 (not found in the Langer- hans’ cells of normal patients), and HLA-DRZ7 Keratinocytes in AD lesions have increased levels of ICAM-1, CD36, and CDla but specifically lack expression of HLA-DR (found on the keratinocytes of patients with allergic contact derma- ti ti^.)^ Eosinophils are found in increased numbers in chronic AD skin lesions. Major basic protein derived from eosinophils is found in increased amounts in AD lesions% and may contribute to tissue injury.

Patients with AD have fewer and less functional CD8+ cytotoxic T cells than healthy controls.z6 B cells from AD patients have increased expression of the low-affinity IgE receptor, CD23, which i s modulated by IL-4 production. Increased expression of CD23 has been associated with increased disease severity in patients with AD.50 Monocytes from atopic individuals also produce increased amounts of IL-10, cyclic AMP-phosphodiesterase and prostaglandin (PG) ED which inhibit IFN-y production.12, 4o IL-10 also inhibits cell-mediated immunity to bacterial pathogens, which may explain why AD patients are prone to develop secondary bacterial infections.

IgE appears to have a multifactorial role in the Th-2-mediated inflammation


in AD, which differs from the typical delayed-type hypersensitivity (DTH) reactions produced by Th-1 lymphocytes. IgE produces a mononuclear cell infiltrate in response to sigruficant allergen exposure in a biphasic manner. Immediate reactions, manifested in AD patients as intense pruritus and erythema, Occur when mediators are released by mast cells bearing allergen-specific IgE in response to allergen exposure. This is followed by an IgE-dependent late- phase reaction (LPR) characterized by a T-lymphocyte infiltrate that exhibits mRNA for IL-3, IL-4, and IL-5 but not for IFN-y." These cells resemble the Th- 2-like lymphocytes found in AD skin lesions. IgE is also expressed on the surfaces of Langerhans' cells of AD patients where it facilitates allergen capture for processing and presentation to Th-2 lymphocytes in an apparent effort to sustain local T-cell

The inflammation in AD reflects a chronic component that is thought to have several causes. Patients with AD typically undergo repeated or ongoing exposure to allergic triggers, perpetuating both immediate and late-phase reactions as well as Th-2 cell proliferation. Th-2-like cells, in turn, produce cytokines that inhibit IFN-y, thus promoting persistent elevation of IgE and eosinophil proliferation. In addition, enhanced survival of inflammatory cells may contribute to chronic inflammation. Monocytes from patients with AD have been shown to be less likely to undergo spontaneous or IL-&induced apoptosis than normal controls.6 The itch-scratch cycle also appears to play a role. Keratinocytes, injured by trauma from scratching, have been shown to release cytokines and mediators that attract cells to sites of Finally, patients with AD may have an impaired response to steroids because recent studies have shown that monocytes from AD patients demonstrate reduced glucocorticoid receptor binding affinity.13

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of atopic dermatitis includes all eczematous disorders, including contact dermatitis and seborrheic dermatitis. It may also be difficult to distinguish scabies from atopic dermatitis because severe pruritus and excoriation can occur in both conditions. Hyper-IgE syndrome must be differentiated from other disorders in which IgE levels may be elevated, such as atopic dermatitis and Wiskott-Aldrich syndrome. These latter entities are not associated with cutaneous abscesses that are so prevalent in hyper-IgE syndrome. Patients with Wiskott-Aldrich syndrome have thrombocytopenia and hemorrhagic skin lesions and do not usually have the atopic diatheses, such as allergic rhinitis and reactive airway disease, often seen in patients with atopic dermatitis.

TREATMENT

Atopic dermatitis is typically managed by implementing a skin care regimen consisting of daily skin hydration, use of moisturizers, avoidance of irritants, use of oral antihistamines, and application of topical corticosteroids which, in combination, decrease pruritus and improve skin integrity. Management should be individualized because choice of treatment depends on the severity of the condition. The following guidelines may be used for managing most patients, but these may need to be modified in some situations.

388 HARRIGAN 81 RABINOWITZ

Bathing

Patients with AD have suboptimal skin barrier function that is associated with significant evaporative losses and inability to retain moisture. Daily bathing is recommended to hydrate the skin, but baths should be limited to 10 or 15 minutes, and hot water should be avoided. Excessive soaking in the tub or frequent baths during the day can lead to increased dryness of the skin. Bath oils may be used as long as they are not substituted for moisturizers. All products used in the bath should be fragrance-free and designed for sensitive Skin.

Cleansers

Atopic patients should use gentle soaps or soap substitutes (that do not contain soap) such as Basis or Cetaphil products to avoid overdrying the skin and disrupting the epidermal barrier even further. Unscented products are recommended because perfumes can trigger flares of atopic dermatitis. Scrub- bing should be avoided. '

Shampoos

Mild shampoos, such as baby shampoo, are recommended. Shampoos that contain zinc, tar, or selenium sulfide may be too harsh and irritating for patients whose eczema affects their scalp. Specially formulated shampoos and condition- ers are available for patients with extremely sensitive scalps.

Moisturizers

Moisturizers are probably the most important ingredient in the skin care regimen of patients with AD. They should be applied after bathing and at least one other time during the day. The most effective moisturizers are those that do not contain water, such as plain petroleum jelly. Lotions contain predominantly water and, thus, are less effective in preventing evaporative losses from the skin. Thick creams such as Eucerin or Nivea are more effective than lotions because they contain more lipid products, but they have more additives and preserva- tives than bland petrolatum. Emollients have been shown to be topical corticosteroid-sparing agents in the treatment of mild to moderate AD in children.32

Antihistamines

Systemic antihistamines can be used to help control the itch-scratch cycle of atopic dermatitis. Hydroxyzine and diphenhydramine can be used if sedation is a desired effect. Less sedating antihistamines, such as cetirizine, have been studied in the management of AW4 with moderate success. They offer some relief without affecting school performance and other daytime activities. Topical antihistamines are not recommended because of their potential for skin sensitization. Doxepin 5% cream, a potent combination HJH2 antagonist, has been used successfully in adults with AD. In a short-term double-blind study, topical doxepin was shown to be superior to placebo in controlliig pruritus and improv-

ATOPIC D E ~ ~ S 389

ing overall skin condition. No apparent sensitization occurred.l4 Mild sedation was a frequent side effect when doxepin was applied over a large body surface ma. The safety and efficacy of topical doxepin in children have not yet been established.

Topical Corticosteroids

Topical corticosteroids continue to be the mainstay of treatment of AD. These medications reduce the inflammation and decrease the pruritus of the disorder. Seven classes of topical corticosteroids exist, ranked according to potency. Table 2 summarizes the relative potency of some of the more commonly used preparations. The strength of a corticosteroid product is determined by the steroid molecule itself, in addition to its vehicle. Several products are available in multiple forms, as a lotion, gel, solution, cream, or ointment. Ointments are more potent than the comparable cream, owing to the more occlusive nature of an ointment vehicle. Class I and 11 are potent corticosteroids that should not be used for mild or moderate atopic dermatitis. If necessary, they can be used to control severe AD but should not be used on the face, groin, or intertriginous areas. Mid-~trength topical steroids can control most cases of mild to moderate AD and low potency steroids are used for mild eczema and for facial and intertriginous eczema.

Side effects from topical corticosteroids may occur with prolonged use. Local side effects include thinning and atrophy of the skin, telangiectases, striae, and possible steroid-induced rosacea. Systemic side effects, although less frequent, include potential suppression of the hypothalamic-pituitary-adrenal axis and are related to the potency of the steroid, the surface area over which it i s used, and the duration of treatment." Although one study group found no suppression in adrenal glucocorticoid function in patients with mild to moderate AD treated chronically with topical corticosteroids,35 it remains a serious concern. The risk of adrenal suppression from topical steroids is greatest in infants and young children because increased percuta.neous absorption can occur because of their greater body surface area to weight ratio.

Table 2. POTENCY OF TOPICAL CORTICOSTEROIDS

~ t r a ~ t e n ~ Temovate (clobetasol propionate) cream and ointment 0.05% Ultravate (halobetasol propionate) cream and ointment 0.05% Diprolene (betamethasone dipropionate) cream and ointment 0.05%

Halog (halcinonide) cream 0.1% Topicort (desoximetasone) ointment and cream 0.25% Diprosone (betamethasone dipropionate) ointment 0.05% Synalar (fluocinolone acetonide) ointment 0.025% Kenalog (triamcinolone acetonide) ointment 0.1% Elocon (mometasone furoate) cream 0.1% Ik-matop (prednicarbate) cream 0.1% Westcort (hydrocortisone valerate) cream 0.2% DesOwen (desonide) cream and ointment 0.05% Aclovate (aclometasone dipropionate) cream and ointment 0.05% Hydrocortisone cream and ointment 1%, 2.5%

Strong Lidex (fluocinonide) ointment 0.5%

Moderate

Mild

Verv Mild

390 HAREUGAN & RABINOWITZ

Antibiotics

Patients with AD are colonized with S. aureus that frequently causes secondary infection of primary eczematous lesions. Studies have demonstrated s. aureus at a density of 1 X lo6 colony-forming units (CFU)/cm2 to be aggravating to AD lesions but not indicative of secondary infection. Those with a density of S. aureus greater than 1 X lo7 CFU/cmz likely are secondarily infected.' Thus, patients whose lesions are devoid of purulence, weeping, or cellulitis but are significantly excoriated warrant treatment with antibiotics. Cephalexin, dicloxa- cillin or erythromycin are generally effective for most patients. Long-term therapy should be avoided in order to help prevent microbial resistance to the antibiotic. Mupirocin is a broad-spectrum antibiotic used topically for the treatment of cutaneous infections. It is effective in reducing s. aureus colony counts and is associated with a reduction in the severity of lesions in patients with AD?' Although 10% povidone-iodine solution has been shown to reduce S. aureus colony counts on the skin lesions of patients with AD, it is irritating and has been associated with transient congenital h~othyroidism when used in pregnant and lactating patients.' Thus, its routine use in this condition is not recommended.

Systemic Cortieosteroids

Patients with severe, chronic AD may experience marked improvement with a short course of oral corticosteroids. The dose should be tapered, however, and used in conjunction with aggressive hydration, moisturizing, and topical corticosteroid application to minimize rebound flares of eczema when the oral corticosteroid is withdrawn.

P hototherapy

Ultraviolet (W) light therapy has been shown to be moderately effective in the treatment of AD, although its mechanism of action is not well understood. Short-wave W B light therapy is readily available in many dermatologists' offices. In one pediatric study, UVB light reduced the pruritus of AD and reduced the need for topical corticosteroid but did not clear lesions completely? Photochemotherapy with methoxypsoralen and W A light was used successfully in a study of adolescent patients with severe AD3; however, this modality has a fairly high incidence of side effects, including nausea, itching, hyperpigmenta- tion, premature aging and development of skin cancer.

Cyclosporine

As the immune system's role in the development of atopic dermatitis becomes better understood, immune modulators are being evaluated for their potential efficacy in the treatment of this disease. Cyclosporine inhibits T-cell immune responses and was first used as an immune suppressant in organ transplantation. The efficacy of cyclosporine in the treatment of several immune- modulated skin disorders, including psoriasis and AD, has been demonstrated. One study showed that cyclosporine decreased the number of activated T cells and IL-2 receptors and suppressed IL-5 expression by mononuclear cells in a


pediatric patient with ADT1 In another study, administration of cyclosporine to two children with AD produced an increase in IFN-y production and a reduction in IL-4 production compared with nonatopic patients.l0

Results of multiple controlled trials in adult patients with AD have demonstrated that 5 mg/kg per day of oral cyclosporine given for 2 to 8 weeks was safe and effective but was associated with a high relapse rate. Disease severity, however, declined after discontinuation of cyclosporine. Several recent pediatric studies showed that a 6-week course of 5 mg/kg per day of cyclosporine produced significant improvement in the majority of patients?, 51 Most side effects were minor (including headache and abdominal pain) but occurred with fairly high frequency. In addition, most patients had a relapse of their rash within several weeks of discontinuing treatment. An international committee on the use of cyclosporine in AD recently developed a set of guidelines for its use. Cyclosporine should not be used in patients with immunodeficiency, renal insufficiency, or compliance problems. It should not be used in conjunction with erythromycin or antifungal agents. Patients should be watched closely for the development of S. aureus or herpes simplex virus infections? Further studies are needed to establish ideal dosing and duration of therapy for the long-term use of cyclosporine in children.

Tacrolimus

Tacrolimus, or FK-506, is an immune suppressant used, like cyclosporine, to inhibit organ rejection after ~ansplantation. Recent studies have shown that 0.3% tacrolimus ointment is effective in controlling pruritus and improving skin condition in adult and pediatric AD patients, with low systemic absorption and only transient side effects.2 Tacrolimus is as effective as a class I topical corticosteroid in reducing cutaneous inflammation. It has not been shown to cause the atrophic skin changes seen with prolonged topical corticosteroid use. Recent studies have demonstrated systemic absorption of topically applied tacrolimus; however, topical tacrolimus is significantly less bioavailable than intravenous or oral tacrolimus. Furthermore, the amoFt of tacrolimus absorbed decreases with its continued use? The most common side effect is burning at the site of application.38

Thy mopentin

Thymopentin (TP-5) is a synthetic peptide derived from the thymic hormone thymopoietin. It has been shown to increase production of IL-2 and IFN-y and suppress IL-4 producti~n.~~ Several double-blind, controlled studies indicate that TP-5 administered subcu~neously three times per week for 12 weeks can be effective in reducing severity of symptoms in AD.30 TP-5 was effective in an open trial of 16 pediatric patients with AD using a similar dosing regimen; however, relapse occurred frequently after discontinuationTO The only signhcant side effect noted was pain at the injection site. TP-5 is thought to be a safe adjunctive therapy for severe AD but is less effective than cycl0sporine.3~

Chinese Herbal Therapy

A mixture of ten Chinese herbs has been found to provide symptomatic relief for patients with AD as evidenced by several short-term double-blind,

392 HARRIGAN & RABXNOWITZ

placebwontrolled studies in adults and children." The herbs are assembled in a sachet and boiled in water for 90 minutes. Patients ingest approximately 100 mL of this tea daily until symptoms improve. The dosing interval is then gradually increased. The herbs are known to have NSAID-like properties as well as antihistamine and immunomodulatory effects. It has been postulated that Chinese herbal therapy exerts its effect by reducing expression of the low- affinity IgE receptor, CD23, on Langerhans' cells in the skin.= In one pediatric study, CHT was moderately effective in patients followed for 1 year.4I Elevated liver enzyme levels were noted in 2 of the 37 children enrolled, but these values normalized within 8 weeks of discontinuation of treatment. This herbal formula has an unpleasant odor and taste and is unacceptable to some children.

lmmunotherapy

The major role aeroallergens play in AD exacerbations suggests that desensi- tization to allergens such as D. ptemnyssinus may offer a therapeutic benefit to patients. Such attempts have been moderately successful in studies of adult patients7; however, a double-blind, placebo-controlled study of children with AD found hyposensitization with injections of mite extract to be no better than placebo in improving symptoms.15 In this report, a significant placebo effect was observed, which may have obscured actual results. Further studies are necessary to establish whether or not immunotherapy is effective in the treatment of AD in children.

Cromolyn

Cromolyn has been used with variable success in the treatment of AD. Several investigators have found topical cromolyn .ointment (disodium cromoglycate) to be ineffective in the management of AD; however, daily topical application of 1% cromolyn nebulizer solution to AD lesions in young children has been shown to safely improve eczema, decrease pruritus, and improve sleep over a 3-week study period.= Continued application of the solution is required to prevent recurrence, and older children respond more slowly to this treatment than younger children.

Evening Primrose Oil

Evidence suggests that children with AD have abnormally low serum levels of long chain polyunsaturated fatty acids (LCPs) derived from linoleic acid. In view of this, evening primrose oil (gammaliinolenic acid or Epogam) has been touted as an effective treatment for AD. Results of a recent double-blind study, however, indicate that Epogam is not superior to placebo in improving AD symptoms in pediatric patients.18 There was significant improvement in symptoms in both test patients as well as controls, possibly because of improved patient compliance with prestudy medication regimens that were continued throughout the study. It is also possible that global improvement in AD symptoms was attributable to an increased understanding of the disease and close follow-up and monitoring.


Hypnotherapy

Hypnosis has been used successfully in the treatment of behavior disorders such as phobias, smoking, obesity, and anxiety. Children were previously thought to be incapable of being hypnotizable, largely because adult hypnosis techniques had been used, unsuccessfully, on them. Using age-appropriate techniques, such as storytelling, hypnosis has been shown to be successful in some children. In one recent study, children with severe AD, refractory to conventional therapy, experienced significant long-term improvement in their pruritus, sleep patterns, and general mood after listening to a soothing audio tape nightly for 4 to 8 weeks.@ While larger, controlled studies are necessary to determine whether hypnotherapy is truly effective in the management of AD, it appears to offer an economical treatment alternative with no side effects. In addition, it can help counteract negative psychologic effects that can be associated with this chronic and often frustrating skin disorder.

Patient Education

Education of parents and patients is the key to successful management of AD. Without a firm understanding of the rationale of therapy, parents and patients are less likely to comply with the physician’s instructions. Additionally, they may become less frustrated if they know this is a chronic condition, associated with recurrent flares and remissions. Affected individuals tend to have dry, sensitive skin throughout life, but this disorder usually improves with age.

ASSOCIATED CONDITIONS

Keratosis Pilaris

A skin condition frequently associated with atopic dermatitis is keratosis pilaris. On examination, there are numerous follicular keratotic papules that are typically distributed on the lateral cheeks and extensor aspects of the upper arms and thighs. When present on the cheeks, these papules are often misdiagnosed as acne or molluscum contagiosum. The lesions may or may not be associated with inflammation around each hair follicle. Facial lesions often disappear with age. Lesions on the upper arms frequently persist into adulthood. This condition represents a skin type, rather than a disease that needs to be cured. Treatments consist of topical medications that contain either lactic acid, retinoic acid, or urea and use of moisturizers. If inflammation is present, topical corticosteroids may be beneficial also. Patients and parents should understand that the follicular papules will usually recur when topical treatment is discontinued. The lesions are usually asymptomatic and are often treated for cosmetic reasons. If the patient does not find the problem bothersome, no treatment is necessary.

lchthyosis Vulgaris

Ichthyosis vulgaris is the most common form of ichthyosis and has an autosomal dominant inheritance pattern. Approximately one half of affected patients have concomitant AD. The cause and pathogenesis of this disorder,

394 HAlUUGAN & RABINOWITZ

characterized by fine white scales that have a “pasted on” appearance, are unknown. Sites of predilection include the extensor surfaces of the limbs and the trunk, whereas flexural areas such as the antecubital and popliteal fossae are spared. The back may be involved, as may the forehead and cheeks, but scaling in these areas diminishes with age.

Ichthyosis vulgaris is managed with emollients, such as petroleum jelly or less greasy creams. Salicylic acid, urea, lactic acid, and other alpha-hydroxy acids can also be used to improve the appearance of the skin. These medications can loosen scale and improve binding of water to the epidermis. Skin irritation, stinging, or burning are possible side effects of these preparations and may limit their use. In addition, if patients have coexisting inflammatory AD, they will probably not be able to tolerate these topical agents. As with keratosis pilaris, ichthyosis vulgaris may not need to be treated.

SUMMARY

AD is a chronic and complex immunologic disorder. Although a significant percentage of the population is affected, most patients with AD improve over time. For children with moderate to severe AD, consultation with a dermatolo- gist or allergist is advisable to help identify specific triggers and assure judicious use of medications. Guidelines established by the Joint Task Force on Practice Parameters/Work Group on Atopic Dermatitis (September 1997 issue of Annals of Asthma, Allergy and Immunology) help to standardize the approach to the management of patients with AD. As the immunological aspects of AD are better understood, treatments directed toward immune regulation, including the modulation of Th-2 cells and their associated cytokines, may expand available therapeutic options. Keratosis pilaris and ichthyosis vulgaris are often associated with AD. Recognition of these conditions is necessary to better educate patients and their parents and provide treatment when indicated.

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Address reprint requests to Linda G. Rabinowitz, MD

Department of Pediatrics (Dermatology) Medical College of Wisconsin 9000 West Wisconsin Avenue

Milwaukee, WI 53201

atopic dermatitis

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