eMedicine Specialties > Dermatology > Allergy & Immunology

Atopic Dermatitis: Treatment & Medication

Author: Bernice R Krafchik, MBChB, FRCPC, Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto
Contributor Information and Disclosures

Updated: Oct 16, 2008

Treatment

Medical Care

Patients with atopic dermatitis (AD) do not usually require emergency therapy, but they may visit the emergency department for treatment of acute flares caused by eczema herpeticum and bacterial infections. For further information on treatment, see the NICE Guidelines Issued for Treating Atopic Eczema in Children.13

  • Moisturization
    • Depending on the climate, patients usually benefit from 5-minute, lukewarm baths followed by the application of a moisturizer such as white petrolatum. Frequent baths with the addition of emulsifying oils (1 capful added to lukewarm bath water) for 5-10 minutes hydrate the skin. The oil keeps the water on the skin and prevents evaporation to the outside environment. In infants, 3 times a day is not a great burden; in adults, once or twice a day is usually all that can be achieved. Leave the body wet after bathing.
    • Advise patients to apply an emollient such as petrolatum or Aquaphor all over the body while wet, to seal in moisture and allow water to be absorbed through the stratum corneum. The ointment spreads well on wet skin. The active ingredient should be applied before the emollient. Newer emollients such as Atopiclair and Mimyx have been advocated as having superior results, but they are expensive and need further evaluation. 
  • Topical steroids
    • Topical steroids are currently the mainstay of treatment. In association with moisturization, responses have been excellent.
    • Ointment bases are preferred, particularly in dry environments.
    • Initial therapy consists of hydrocortisone 1% powder in an ointment base applied 3 times daily to lesions on the face and in the folds.
    • A midstrength steroid ointment (triamcinolone or betamethasone valerate) is applied 2-3 times daily to lesions on the trunk until the eczematous lesions clear.
    • Steroids are discontinued when lesions disappear and are resumed when new patches arise.
    • Flares may be associated with seasonal changes, stress, activity, staphylococcal infection, or contact allergy.
    • Contact allergy is rare but accounts for increasing numbers of flares. These are seen mostly with hydrocortisone.
  • Immunomodulators
    • Tacrolimus (topical FK506) is an immunomodulator that acts as a calcineurin inhibitor. Studies have shown excellent results compared with placebo and hydrocortisone 1%. Little absorption occurs. A stinging sensation may occur following application, but this can be minimized by applying the medication only when the skin is dry. The burning usually disappears within 2-3 days. Tacrolimus is available in 2 strengths, 0.1% for adults and 0.03% for children, although some authorities routinely use the 0.1% preparation in children. Tacrolimus is an ointment and is indicated for moderate-to-severe AD. It is indicated for children older than 2 years.
    • Pimecrolimus 1% is also an immunomodulator and calcineurin inhibitor. It is more effective than placebo. Pimecrolimus is produced in a cream base for use twice a day; it is indicated for mild AD in persons older than 2 years and is particularly useful on the face.
    • A 2006 black box warning has been issued in the United States based on research that has shown an increase in malignancy in association with the calcineurin inhibitors. While these claims are being investigated further, the medication should likely only be used as indicated (ie, for AD in persons older than 2 y and only when first-line therapy has failed).
    • These agents are much more expensive than corticosteroids and should only be used as second-line therapy.
  • Other treatments, effective and ineffective
    • Probiotics have been explored as a therapeutic option for the treatment of AD. The rationale for their use is that bacterial products may induce an immune response of the TH 1 series instead of TH 2 and could therefore inhibit the development of allergic IgE antibody production. This research has yet to be proven.
    • UV-A, UV-B, a combination of both, psoralen plus UV-A (PUVA), or UV-B1 (narrow-band UV-B) therapy may be used. Long-term adverse effects of skin malignancies in fair-skinned individuals should be weighed against the benefits.
    • In patients with eczema herpeticum, acyclovir is effective.
    • In patients with severe disease, and particularly in adults, phototherapy, methotrexate (MTX), azathioprine, cyclosporine, and mycophenolate mofetil14  have been used with success.
    • Both hydroxyzine and diphenhydramine hydrochloride provide a certain degree of relief from itching but are not effective without other treatments.
    • Ketotifen (a calcium channel blocker) may be effective.
    • Oil of evening primrose was believed to be effective, but in a randomized controlled study, it showed no benefit in children and little improvement in adults.
    • Results with many other medications, such as thymopentin, gamma interferon, and Chinese herbs, have been disappointing. Many medications are not practical to use, and they can be expensive. Some Chinese herbal preparations contain prescription medications, including prednisone, and have been associated with cardiac and liver problems.
    • Antibiotics are used for the treatment of clinical infection caused by S aureus or flares of disease. They have no effect on stable disease in the absence of infection. Laboratory evidence of S aureus colonization is not evidence of clinical infection because staphylococcal organisms commonly colonize the skin of patients with AD.
  • Nonmedical efforts
    • Clothing should be soft next to the skin. Cotton is comfortable and can be layered in the winter.
    • Cool temperatures, particularly at night, are helpful because sweating causes irritation and itch.
    • A humidifier (cool mist) prevents excess drying and should be used in both winter, when the heating dries the atmosphere, and in the summer, when air conditioning absorbs the moisture from the air.
    • Clothes should be washed in a mild detergent with no bleach or fabric softener.
    • Food avoidance is discussed in Diet, below, and in Causes.

Consultations

Consulting an allergist may be necessary, particularly if the patient develops asthma and/or hay fever or an acute reaction to a food.

Diet

Avoid foods that provoke acute allergic reactions (hives, anaphylaxis). Most frequently, allergic reactions occur to peanuts (peanut butter), eggs, seafood, milk, soya, and chocolate. Additionally, advise patients to apply a barrier of petroleum jelly around the mouth prior to eating to prevent irritation from tomatoes, oranges, and other irritating foods.

Activity

Advise patients to avoid activities that cause excessive sweating. Also, swimming in an outdoor pool (or wading pool for babies) in summer provides therapeutic benefit by exposing the person to the sun but avoiding the heat.

Medication

The basis of treatment for atopic dermatitis (AD) is to provide moisturization for dryness, allay pruritus, and manage inflammation of the eczematous lesions.

Anti-inflammatory agents

Provide relief of inflammation of eczematous lesions. Ointment base provides moisturization. White petrolatum is useful to avoid potential sensitization to preservatives in water-based moisturizers.


Hydrocortisone ointment 1% (Cortaid)

Mild topical corticosteroid mixed in petrolatum. Has mineralocorticoid and glucocorticoid effects and anti-inflammatory activity.
Use 1% ointment 2-3 times daily.

Adult

Apply sparingly to affected areas bid/tid; discontinue when cleared

Pediatric

Apply as in adults

Documented hypersensitivity; clinical viral, fungal, and bacterial skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution around eyes, prolonged use, and application over large surface areas; occlusive dressings may increase systemic absorption of corticosteroids


Betamethasone valerate (Beta-Val)

Medium-strength topical corticosteroid for body areas. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.
Use 0.05-0.1% ointment in adults and 0.05% ointment in pediatrics.

Adult

Apply topically bid/tid until response; discontinue when cleared

Pediatric

Administer as in adults

Documented hypersensitivity; skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause atrophy of groin, face, and axillae; may cause striae distensae in teenagers or rosacealike eruption; may increase skin fragility; rarely, may suppress HPA axis; if infection is present, discontinue use until infection is under control

Antihistamines

Provide symptomatic relief of pruritus.


Hydroxyzine hydrochloride (Atarax)

Antihistamine with antipruritic, anxiolytic, and mild sedative effects. Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.
Syr available as 10 mg/5 mL.

Adult

25-50 mg PO tid/qid prn

Pediatric

<6 years: 30-50 mg/d PO (2 mg/kg/d) in divided doses
>6 years: 50-100 mg/d PO in divided doses

CNS depression may increase with alcohol or other CNS depressants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness; caution operating automobiles and other dangerous machinery; anticholinergic effects (ie, dry mouth) may occur


Diphenhydramine (Benadryl)

Antihistamine used for pruritus and allergic reactions.

Adult

Cap: 25-50 mg tid/qid prn
Elix: 10-20 mL (12.5 mg/5 mL) q4-6h; not to exceed 4 doses/d

Pediatric

Cap
<10 years: Not recommended
>10 years: 25 mg PO tid/qid prn
Elix (12.5 mg/5 mL)
6-12 years: 12.5-25 mg every 4-6 hours
>12 years: Administer as in adults
Children's liquid (6.25 mg/5 mL)
<2 years: 2.5 mL q6h prn
2-6 years: 5 mL q6h prn
6-12 years: 10-20 mL q6h prn; not to exceed 4 doses/d or 5 mg/kg/d

Potentiates effect of CNS depressants; as a result of alcohol content, do not administer elix to patient taking medications that can cause disulfiramlike reactions

Documented hypersensitivity; children with chronic lung disease; glaucoma

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; xerostomia may occur; caution operating automobiles and other dangerous machinery because of possible sedation; as a result of atropinelike action, caution in history of bronchial asthma, increased intraocular pressure, hyperthyroidism, cardiovascular disease, or hypertension

Immunomodulators

For treatment of patients with severe disease in whom conventional therapy is ineffective. In more severe cases and particularly in adults, consider using both MTX and cyclosporine. The latter is more efficacious, but lesions recur when it is stopped.


Cyclosporine (Neoral, Sandimmune)

Demonstrated to be helpful in a variety of skin disorders, especially psoriasis. Acts by inhibiting T-cell production of cytokines and ILs. Like tacrolimus and pimecrolimus (ascomycin), cyclosporine binds to macrophilin and then inhibits calcineurin, a calcium-dependent enzyme, which, in turn, inhibits phosphorylation of nuclear factor of activated T cells and inhibits transcription of cytokines, particularly IL-4. Discontinue treatment if no response within 6 wk.

Adult

2 mg/kg/d PO divided bid; if no improvement within 1 mo, may be increased gradually; not to exceed 5 mg/kg/d
As skin lesions improve, reduce dose by 0.5-1 mg/kg/d/mo; lowest effective dose for maintenance

Pediatric

5 mg/kg/d PO for 6 wk (see note in Contraindications)

Erythromycin, clarithromycin, azithromycin, norfloxacin ciprofloxacin, cephalosporins, doxycycline, ketoconazole, itraconazole, fluconazole, ritonavir, indinavir, saquinavir, nelfinavir, diltiazem, verapamil, nicardipine, cimetidine, methylprednisolone, dexamethasone, thiazides, furosemide, allopurinol, bromocriptine, danazol, amphotericin B, metoclopramide, oral contraceptive pills, warfarin, and grapefruit juice increase levels
Rifampin, rifabutin, nafcillin, carbamazepine, phenobarbital, phenytoin, valproate, octreotide, and ticlopidine decrease levels
Tobramycin, gentamicin, ketoconazole, azapropazone, TMP-SMZ, vancomycin, sulindac, amphotericin B, indomethacin, naproxen, cimetidine, ranitidine, diclofenac, tacrolimus, and melphalan potentiate renal toxicity

Absolute: Significantly decreased renal function, uncontrolled hypertension, hypersensitivity to cyclosporine, clinically cured or persistent malignancy (except nonmelanoma skin cancer)
Relative: Age <18 y or >64 y (however, cyclosporine A at 5 mg/kg/d for 6 wk has been shown to be effective and well tolerated in children aged 2-16 y with severe AD), controlled hypertension, planning to receive a live-attenuated vaccine, active infection or evidence of immunodeficiency, concurrent phototherapy, coal tar, MTX (or other immunosuppressive agents), pregnancy or lactation, unreliable patient, severe hepatic dysfunction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver function often by measuring BUN, serum creatinine, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for patients who cannot take PO; development of malignancies (particularly skin) has been reported; perform biopsy on skin suggestive of malignancy or premalignancy and, if malignant, discontinue use


Methotrexate (Folex PFS, Rheumatrex)

Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction. Satisfactory response seen 3-6 wk following administration.
Adjust dose gradually to attain satisfactory response.

Adult

10-25 mg/wk PO/IM or 2.5-7.5 mg PO q12h for 3 doses/wk

Pediatric

Not established

Salicylates, NSAIDS, dipyridamole, probenecid, retinoids, ethanol, triamterene, pyrimethamine, sulfonamides, tetracycline, chloramphenicol, penicillin or other broad-spectrum antibiotics, trimethoprim, dapsone, theophylline, phenytoin, phenothiazines, barbiturates and nitrofurantoin (impair folic acid absorption), ascorbic acid, phenylbutazone, cyclosporin, and aminoglycosides

Absolute: Pregnancy or desire to become pregnant, active peptic ulcer, alcoholism, primary/secondary immunodeficiency, blood dyscrasias, active hepatitis, cirrhosis, chronic renal failure, active infections
Relative: History of excessive alcohol intake or substance abuse, increased LFT results, recent hepatitis, diabetes, obesity, family history of heritable liver disease, unreliable patient, CrCl <50 mL/min, male contemplating conception (must not take for 3 mo)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC count, renal panel, urinalysis, and LFTs at 1 wk initially and after dose increases, and monitor liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood cell counts occurs; fatal reactions reported when administered concurrently with NSAIDs


Tacrolimus (Protopic) ointment 0.03% or 0.1%

Immunomodulator that suppresses humoral immunity (T-lymphocyte) activity. Used for refractory disease.

Adult

Apply a thin layer to affected areas bid; continue for 1 wk after symptoms clear

Pediatric

<2 years: Not established
2-15 years: Only the 0.03% ointment is indicated

Topical tacrolimus is minimally absorbed; however, levels may increase with diltiazem, nicardipine, clotrimazole, verapamil, erythromycin, ketoconazole, itraconazole, fluconazole, bromocriptine, grapefruit juice, metoclopramide, methylprednisolone, danazol, cyclosporine, cimetidine, or clarithromycin; levels may reduce with rifabutin, rifampin, phenobarbital, phenytoin, and carbamazepine

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use with occlusive dressings; may be associated with an increased risk of folliculitis in adults; may cause local burning sensation, stinging, soreness, or pruritus (typically improve as lesions heal); for external use only; minimize exposure to natural or artificial sunlight (eg, tanning beds or UVA/B treatment); be sure skin is completely dry before application; product insert for tacrolimus revised in January 2006 and contains a black box warning stating the long-term safety of calcineurin inhibitors has not been established; although a causal relationship has not been established, rare cases of malignancy (eg, skin, lymphoma) reported; only 0.03% ointment is indicated for use in children aged 2-15 y

Antiviral agents

For management of herpetic infections and to treat AD in patients who develop chickenpox.


Acyclovir (Zovirax)

Inhibits activity of both HSV-1 and HSV-2. Has affinity for viral thymidine kinase and, once phosphorylated, causes DNA-chain termination when acted on by DNA polymerase. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h of rash onset. May prevent recurrent outbreaks. Early initiation of therapy is imperative. Zoster dose is 4 times higher than that for herpes simplex. Duration of therapy varies.

Adult

200-800 mg PO qid for 5-10 d started within 24 h of appearance of rash

Pediatric

5-20 mg/kg PO qid for 5-10 d (susp 200 mg/5 mL) started within 24 h of appearance of rash

Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or when using nephrotoxic drugs; has caused mutagenesis in some studies at high concentrations

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For the treatment of clinical infection by S aureus, cloxacillin or cephalexin is used. In streptococcal infections, cephalexin is preferred. If not effective, penicillin and clindamycin in combination are effective. Consider staphylococcal infection in every flare of AD.


Cephalexin (Keflex)

First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections or prophylaxis in minor procedures.
Available susp include mauve granules (125 mg/5 mL) and peach granules (250 mg/5 mL).

Adult

1-4 g/d PO in divided doses

Pediatric

25-50 mg/kg/d PO divided q6h

Coadministration with aminoglycosides increase nephrotoxic potential

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy


Cloxacillin (Cloxapen, Tegopen)

For treatment of infections caused by penicillinase-producing staphylococci. May be used to initiate therapy when a staphylococcal infection is suspected.

Adult

250-500 mg PO q6h

Pediatric

<20 kg: 50-100 mg/kg/d PO divided q6h
>20 kg: 250 mg PO q6h

May decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor PT in patients taking anticoagulant medications; toxicity may increase in renal impairment


Penicillin VK (Beepen-VK, Betapen-VK, Veetids)

Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached, and most effective during stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Adult

500 mg PO q6h for 10d

Pediatric

<12 years: 25-50 mg/kg/d divided tid/qid up to 3 g/d
>12 years: Administer as in adults

Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment


Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Adult

150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d

Pediatric

8-20 mg/kg/d PO as hydrochloride or 8-25 mg/kg/d as palmitate divided tid/qid

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile

More on Atopic Dermatitis

Overview: Atopic Dermatitis
Differential Diagnoses & Workup: Atopic Dermatitis
Treatment & Medication: Atopic Dermatitis
Follow-up: Atopic Dermatitis
Multimedia: Atopic Dermatitis
References
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References

  1. Jansén CT, Haapalahti J, Hopsu-Havu VK. Immunoglobulin E in the human atopic skin. Arch Dermatol Forsch. May 28 1973;246(4):209-302. [Medline].

  2. Callard RE, Harper JI. The skin barrier, atopic dermatitis and allergy: a role for Langerhans cells?. Trends Immunol. Jul 2007;28(7):294-8. [Medline].

  3. Irvine AD. Fleshing out filaggrin phenotypes. J Invest Dermatol. Mar 2007;127(3):504-7. [Medline].

  4. Sandilands A, Smith FJ, Irvine AD, McLean WH. Filaggrin's fuller figure: a glimpse into the genetic architecture of atopic dermatitis. J Invest Dermatol. Jun 2007;127(6):1282-4. [Medline].

  5. Horii KA, Simon SD, Liu DY, Sharma V. Atopic dermatitis in children in the United States, 1997-2004: visit trends, patient and provider characteristics, and prescribing patterns. Pediatrics. Sep 2007;120(3):e527-34. [Medline].

  6. Williams HC, Pembroke AC, Forsdyke H, Boodoo G, Hay RJ, Burney PG. London-born black Caribbean children are at increased risk of atopic dermatitis. J Am Acad Dermatol. Feb 1995;32(2 Pt 1):212-7. [Medline].

  7. Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol (Stockh). 1980;92 (suppl):44-7.

  8. Morar N, Willis-Owen SA, Moffatt MF, Cookson WO. The genetics of atopic dermatitis. J Allergy Clin Immunol. Jul 2006;118(1):24-34; quiz 35-6. [Medline].

  9. Novak N, Bieber T, Leung DY. Immune mechanisms leading to atopic dermatitis. J Allergy Clin Immunol. Dec 2003;112(6 Suppl):S128-39. [Medline].

  10. Williams H, Flohr C. How epidemiology has challenged 3 prevailing concepts about atopic dermatitis. J Allergy Clin Immunol. Jul 2006;118(1):209-13. [Medline].

  11. Zutavern A, Hirsch T, Leupold W, Weiland S, Keil U, von Mutius E. Atopic dermatitis, extrinsic atopic dermatitis and the hygiene hypothesis: results from a cross-sectional study. Clin Exp Allergy. Oct 2005;35(10):1301-8. [Medline].

  12. [Best Evidence] Weston S, Halbert A, Richmond P, Prescott SL. Effects of probiotics on atopic dermatitis: a randomised controlled trial. Arch Dis Child. Sep 2005;90(9):892-7. [Medline].

  13. Baumer JH. Guideline review: atopic eczema in children, NICE. Arch Dis Child. Apr 1 2008;[Medline].

  14. Heller M, Shin HT, Orlow SJ, Schaffer JV. Mycophenolate mofetil for severe childhood atopic dermatitis: experience in 14 patients. Br J Dermatol. Jul 2007;157(1):127-32. [Medline].

  15. Leung DY, Bieber T. Atopic dermatitis. Lancet. Jan 11 2003;361(9352):151-60. [Medline].

  16. Abramovits W. Atopic dermatitis. J Am Acad Dermatol. Jul 2005;53(1 Suppl 1):S86-93. [Medline].

  17. Bieber T. Atopic dermatitis. N Engl J Med. Apr 3 2008;358(14):1483-94. [Medline].

  18. Boguniewicz M, Eichenfield LF, Hultsch T. Current management of atopic dermatitis and interruption of the atopic march. J Allergy Clin Immunol. Dec 2003;112(6 Suppl):S140-50. [Medline].

  19. Krafchik BR. Eczematous dermatitis. In: Schachner LA, Hansen RD, eds. Pediatric Dermatology. Vol 1. 2nd ed. New York, NY: Churchill Livingstone; 1998:685-721.

  20. Lebwohl M, Friedlander S. New strategies for optimizing the treatment of inflammatory dermatoses with topical corticosteroids in an era of corticosteroid-sparing regimens. J Am Acad Dermatol. Jul 2005;53 (1 Pt 2):S1-S2.

  21. Leung DY, Boguniewicz M, Howell MD, Nomura I, Hamid QA. New insights into atopic dermatitis. J Clin Invest. Mar 2004;113(5):651-7. [Medline].

  22. Simpson EL, Hanifin JM. Atopic dermatitis. J Am Acad Dermatol. Jul 2005;53(1):115-28. [Medline].

  23. Williams HC. Clinical practice. Atopic dermatitis. N Engl J Med. Jun 2 2005;352(22):2314-24. [Medline].

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Further Reading

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Keywords

atopic dermatitis, eczema, infantile eczema, Besnier's prurigo, intrinsic eczema, extrinsic eczema, atopiform eczema, asthma, food allergy, peanut allergy, allergic reaction

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Contributor Information and Disclosures

Author

Bernice R Krafchik, MBChB, FRCPC, Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto
Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Peter Fritsch, MD, Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria
Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Van Perry, MD, Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas Health Science Center
Van Perry, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Laser Medicine and Surgery
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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