Atopic Dermatitis Medication

  • Author: Brian S Kim, MD; Chief Editor: William D James, MD   more...
 
Updated: Apr 4, 2012
 

Medication Summary

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

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Anti-inflammatory agents

Class Summary

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.

Betamethasone topical (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.

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Antihistamines

Class Summary

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.

Diphenhydramine (Benadryl)

 

Antihistamine used for pruritus and allergic reactions.

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Immunomodulators

Class Summary

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.

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.

Tacrolimus (Protopic) ointment 0.03% or 0.1%

 

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

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Antiviral agents

Class Summary

For management of herpetic infections and to treat atopic dermatitis 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.

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Antibiotics

Class Summary

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 atopic dermatitis.

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).

Cloxacillin (Cloxapen, Tegopen)

 

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

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.

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.

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Contributor Information and Disclosures
Author

Brian S Kim, MD  Clinical Instructor, Department of Dermatology, Hospital of the University of Pennsylvania, Perelman School of Medicine, University of Pennsylvania

Brian S Kim, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster 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.

Van Perry, MD  Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

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.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Additional Contributors

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.

References
  1. Jansen 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. Spergel JM. From atopic dermatitis to asthma: the atopic march. Ann Allergy Asthma Immunol. Aug 2010;105(2):99-106; quiz 107-9, 117. [Medline].

  3. Koga C, Kabashima K, Shiraishi N, Kobayashi M, Tokura Y. Possible pathogenic role of Th17 cells for atopic dermatitis. J Invest Dermatol. Nov 2008;128(11):2625-30. [Medline].

  4. Molfino NA, Gossage D, Kolbeck R, Parker JM, Geba GP. Molecular and clinical rationale for therapeutic targeting of interleukin-5 and its receptor. Clin Exp Allergy. Sep 23 2011;[Medline].

  5. Siracusa MC, Saenz SA, Hill DA, et al. TSLP promotes interleukin-3-independent basophil haematopoiesis and type 2 inflammation. Nature. Aug 14 2011;477(7363):229-33. [Medline]. [Full Text].

  6. Ito Y, Satoh T, Takayama K, Miyagishi C, Walls AF, Yokozeki H. Basophil recruitment and activation in inflammatory skin diseases. Allergy. Aug 2011;66(8):1107-13. [Medline].

  7. Hershko AY, Suzuki R, Charles N, et al. Mast cell interleukin-2 production contributes to suppression of chronic allergic dermatitis. Immunity. Oct 28 2011;35(4):562-71. [Medline].

  8. Osawa R, Akiyama M, Shimizu H. Filaggrin gene defects and the risk of developing allergic disorders. Allergol Int. Mar 2011;60(1):1-9. [Medline].

  9. Smith FJ, Irvine AD, Terron-Kwiatkowski A, et al. Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris. Nat Genet. Mar 2006;38(3):337-42. [Medline].

  10. Palmer CN, Irvine AD, Terron-Kwiatkowski A, et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet. Apr 2006;38(4):441-6. [Medline].

  11. Saenz SA, Taylor BC, Artis D. Welcome to the neighborhood: epithelial cell-derived cytokines license innate and adaptive immune responses at mucosal sites. Immunol Rev. Dec 2008;226:172-90. [Medline]. [Full Text].

  12. Brandt EB, Sivaprasad U. Th2 Cytokines and Atopic Dermatitis. J Clin Cell Immunol. Aug 10 2011;2(3):[Medline]. [Full Text].

  13. Kubo A, Nagao K, Amagai M. Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases. J Clin Invest. Feb 1 2012;122(2):440-7. [Medline]. [Full Text].

  14. 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].

  15. 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].

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

  17. Sun LD, Xiao FL, Li Y, et al. Genome-wide association study identifies two new susceptibility loci for atopic dermatitis in the Chinese Han population. Nat Genet. Jun 12 2011;43(7):690-4. [Medline].

  18. Paternoster L, Standl M, Chen CM, et al. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis. Nat Genet. Dec 25 2011;44(2):187-92. [Medline]. [Full Text].

  19. 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].

  20. 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].

  21. [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].

  22. Lee CH, Chuang HY, Hong CH, et al. Lifetime exposure to cigarette smoking and the development of adult-onset atopic dermatitis. Br J Dermatol. Mar 2011;164(3):483-9. [Medline]. [Full Text].

  23. Schmitt J, Chen CM, Apfelbacher C, et al. Infant eczema, infant sleeping problems, and mental health at 10 years of age: the prospective birth cohort study LISAplus. Allergy. Mar 2011;66(3):404-11. [Medline].

  24. Nikkels AF, Piérard GE. Occult varicella. Pediatr Infect Dis J. Dec 2009;28(12):1073-5. [Medline].

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

  26. Haeck IM, Rouwen TJ, Timmer-de Mik L, et al. Topical corticosteroids in atopic dermatitis and the risk of glaucoma and cataracts. J Am Acad Dermatol. Feb 2011;64(2):275-81. [Medline].

  27. Heil PM, Maurer D, Klein B, Hultsch T, Stingl G. Omalizumab therapy in atopic dermatitis: depletion of IgE does not improve the clinical course - a randomized, placebo-controlled and double blind pilot study. J Dtsch Dermatol Ges. Dec 2010;8(12):990-8. [Medline].

  28. Michail S. The role of Probiotics in allergic diseases. Allergy Asthma Clin Immunol. Oct 22 2009;5(1):5. [Medline].

  29. 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].

  30. Van Velsen SG, Haeck IM, Bruijnzeel-Koomen CA. Severe atopic dermatitis treated with everolimus. J Dermatolog Treat. 2009;20(6):365-7. [Medline].

  31. Feldman SR. Adherence must always be considered: is everolimus really ineffective as a treatment for atopic dermatitis?. J Dermatolog Treat. 2009;20(6):317-8. [Medline].

  32. Huang JT, Abrams M, Tlougan B, Rademaker A, Paller AS. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Pediatrics. May 2009;123(5):e808-14. [Medline].

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

  34. Armstrong AW, Kim RH, Idriss NZ, Larsen LN, Lio PA. Online video improves clinical outcomes in adults with atopic dermatitis: a randomized controlled trial. J Am Acad Dermatol. Mar 2011;64(3):502-7. [Medline].

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

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Typical atopic dermatitis on the face of an infant.
Flexural involvement in childhood atopic dermatitis.
Dirty neck sign in chronic atopic dermatitis.
Irritation around mouth of an infant with atopic dermatitis.
 
 
 
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