This report reflects the best data available atthe time the report was prepared, but caution should be exercisedin interpreting the data; the results of future studies mayrequire alteration of the conclusions or recommendations setforth in this report. Reprint requests: American Academy ofDermatology, P.O. Box 4014,
Schaumburg, IL 60168-4014.
J AM ACAD DERMATOL 1992;26:485-8
Copyright 1992 by the American Academy of Dermatology, Inc. Guidelines of care for atopic dermatitis Committee onGuidelines of Care: Lynn A. Drake, MD, chairman, Roger I. Ceilley, MD, Raymond L.Cornelison, MD, William A. Dobes, MD,William Dorner, MD, Robert W. Goltz, MD, Charles W. Lewis, MD,Stuart J. Salasche, MD, and Maria L. Chanco Turner, MD Task Force onAtopic Dermatitis: William Dorner, MD, chairman, Kenneth W. Baylock, MD, Jon M.Hanifin, MD, William R. Holder, MD, and G.Thomas Jensen, MD I. Introduction The American Academy of Dermatology’s Committee on Guidelines of Care is developing guidelines of care for our profession. The development of guidelines will promote the continued delivery of quality care and assist those outside our profession in understanding the complexities and scope of care provided by dermatologists. II. Definition Atopic dermatitis is an acute, subacute, or chronic pruritic dermatosis with other cutaneous findings, such as xerosis, excoriations, and lichenification, often occurring in persons with asthma, allergic rhinoconjunctivitis, contact urticaria, or with a family history of the same. There is no biologic marker for the disease. III. Rationale A. Scope Atopic dermatitis is a disease that may cause physical suffering, pronounced and total disability, and anguish for the patient and family. The reported incidence of atopic dermatitis indicates that a significant percentage of the general population is affected at some time in their lives. B. Issue The diagnosis of atopic dermatitis may be made with reasonable certainty, in most cases, from family history, patient history, and examination of the skin. IV. Diagnosticcriteria A. Clinical 1. Major characteristics may include the following: a) Pruritus with or without excoriation b) Typical morphology and distribution (1) Eczematous dermatitis (2) Flexural lichenification or linearity in adults (3) Facial and extensor involvement in infants and children (4) Any of these patterns or combination of patterns can appear in both adults and children. c) Chronic or chronically relapsing dermatitis d) Personal or family history of atopy (asthma, allergic rhinoconjunctivitis, atopic dermatitis, contact urticaria) 2. Other characteristics may include the following: a) Xerosis b) Ichthyosis/palmar hyperlinearity/keratosis pilaris c) Early age of onset d) Cutaneous colonization and/or overt infections (1) Staphylococcus aureus (2) Herpes simplex and other viral infections (3) Warts (4) Molluscum (5) Other e) Nonspecific hand and/or foot dermatitis, increased susceptibility to irritant contact dermatitis f) Nipple eczema g) Cheilitis h) Recurrent conjunctivitis i) Infraorbital fold j) Keratoconus k) Anterior subcapsular cataracts l) Orbital darkening m) Facial pallor/facial erythema n) Erythroderma o) Pityriasis alba p) Anterior neck folds q) Perifollicular accentuation r) White dermographism/delayed blanch s) I mpaired cell-mediated immunity t) Other 3. Characteristic flare factors may include the following: a) Sweating with enhanced pruritus b) Intolerance to wool, any coarse fabric or non-absorptive occlusive garment, lipid solvents, and wet working conditions c) Environmental or emotional factors d) Food intolerance e) Physical trauma f) Other B. Diagnostic tests Uncomplicated atopic dermatitis with clear clinical markers does not usually require diagnostic tests. Definitive diagnosis or complicating factors, including flare factors, however, may require laboratory confirmation. Tests may include the following: 1. Complete blood cell count and differential, total count for eosinophilia 2. Serum IgE or antistaphylococcal IgE level 3. Smears for infectious agents (e.g., Tzanck test, KOH preparation) and immunofluorescence 4. Bacterial culture with antibiotic sensitivity, viral and fungal cultures 5. Skin biopsy 6. Patch tests 7. Scratch/prick/intradermal tests 8. Radioallergosorbent tests may be appropriate in special cases. 9. Immunologic testing 10. Food elimination 11. Psychological evaluation: Atopic dermatitis does appear to have a distinct tendency to flare in response to psychic stress such as anxiety, depression, anger, embarrassment, shame, and resentment. Patients subjected to experimental stress interviews manifest erythema and then pruritus in skin areas subject to dermatitis. If factors cannot be adequately evaluated and treated by the dermatologist, psychological evaluation and care, including testing, may be of value and should be considered. C. Inappropriate diagnostic tests Not applicable D. Exceptions Not applicable E. Evolving diagnostic tests 1. Phenotyping and quantification of cellular aspects of immune response cells 2. Other V. Recommendations A. Treatment There are no specific therapeutic modalities for complete control of atopic dermatitis. Management must be individualized to improve morbidity (itching and scratching) with the goal to allow most patients to function in a normal productive manner. 1. Nonsurgical a) Systemic treatment may include the following: (1) Antihistamines: single or multiple agents (a) Hydroxyzine hydrochloride (b) Doxepin hydrochloride (c) Other (2) Antiinfective agents (3) Systemic corticosteroids in selected cases (4) Others, which may include the following: (a) Nonsteroidal anti-inflammatory drugs (b) Antidepressants (c) Phenothiazine b) Intralesional corticosteroids in selected cases c) Topical treatment may include the following: (1) Corticosteroids, with the use of mid- to high-potency compounds for brief periods and low-potency compounds for maintenance therapy. When extensive areas of dermatitis are being treated ultra-high-potency corticosteroid compounds may be used for brief periods. Certain vehicles may cause irritation; thus alternative products or compounded preparations may be indicated. (2) Tar preparations (3) UV light (a) UVA, with or without psoralen (b) UVB (c) Goeckerman and/or Ingram (4) Emollients (5) Pramoxine hydrochloride (6) Therapeutic baths, compresses, and cleansers (a) Tars (b) Emollients (c) Colloidals (d) Skin cleansers (7) Wet dressings (8) Other d) Hospitalization may be indicated or required for patients with severe flares or complications. 2. Surgical Not applicable 3. Other and/or evolving a) Immunotherapy (1) Cyclosporine (2) Methotrexate (3) Azathioprine (Imuran) (4) Interferon gamma (5) Other b) Oral ketotifen (a mast cell stabilizer) c) Caffeine administered topically, 10% to 30% in petrolatum or water-in-oil base d) Dietary (1) Elimination diet (2) Supplements (a) Evening primrose oil (b) Linoleic acid (c) g -Linoleic acids (d) Fish oil (e) Other e) Hyposensitization f) Others may include but are not limited to the following: (1) Occupational and/or psychological counseling (2) Bed rest (3) Grenz ray, in carefully selected patients with localized disease (4) Biofeedback (5) Psychotherapy B. Miscellaneous treatment considerations Flare factors may include but are not limited to the following: 1. Infection a) Bacterial b) Viral c) Fungal and yeast 2. Dry skin a) Improper bathing b) Use of strong soap, bubble bath, and detergent 3. Psychological stress a) Psychotropic drugs may be used in selected cases. b) Psychological counseling may be indicated. 4. Antigenic exposure 5. Contactants a) Immunologic b) Nonimmunologic c) Irritants (1) Wool or rough fabrics or materials (2) Lipid solvents (3) Wet working conditions 6. Sweating a) Overheating b) Saunas and steam c) Excessive physical exertion 7. Physical trauma 8. Environmental factors 9. Food intolerance VI. Supportingevidence See Bibliography (Appendix) VI. Disclaimer Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the propriety of any specific procedure must be made by the physician in light of all the circumstances presented by the individual patient. Appendix.Bibliography
Adinoff AD, Clark FAF. The allergic nature of atopic dermatitis. Immunol AllergyPract 1989;11:191-202.
Andersen L, Thestrup-Pedersen K. Sweat pore density on thefingertips of atopic patients. Br J Dermatol 1987;117:225-30.
Atherton D, Carabott F, Glover M, et al. The role of psoralenphotochemotherapy (PUVA) in the treatment of severe atopic eczemain adolescents. Br J Dermatol 1988;118:791-5.
Bjorneboe A, Soyland E, Bjorneboe G, et al. Effect of dietarysupplementation with eicosapentaenoic acid in the treatment ofatopic dermatitis. Br J Dermatol 1987;117:463-9.
Finlay A, Nicholls S, King C, et al. The "dry"non-eczematous skin associated with atopic eczema. Br J Dermatol1980;103:249-56.
Friedman S, Schroeter A, Homburger H. IgE antibodies to Staphylococcusaureus. Arch Deramtol 1985;121:869-72.
Morris E. Pharmacotherapy of allergic disease. Prim Care1987;14:605-21.
Nilsson G, Rak S, Ahlstedt S. The influence of substance P on theproliferation of peripheral blood lymphocytes from normalindividuals and birch pollen-allergic patients. Allergy1987;42:516-23..
Norris P, Schofield O, Camp R. A study of the role of house dustmite on atopic dermatitis. Br J Dermatol 1988;118:435-40.
Paller A. Allergy in atopic dermatitis. Prim Care1987;14:491-501.
Roberts N, Page C, Chung K, et al. Effect of a PAF antagonist,BN52063, on antigen-induced, acute, and late-onset cutaneousresponses in atopic subjects. J Allergy Clin Immunol1988;82:236-41.
Rocklin R, Pincus S. Atopic dermatitis. In: Samter M, Talmage D,Frank M, et al. Eds. Immunological disease; vol 2. 4thed. Boston: Little, Brown, 1988:1228-36.
Rystedt I. Work-related hand eczema in atopics. ContactDermatitis 1985;12:164-71.
Sampson H. Immunologically mediated reactions to foods: IgE ineczema. Ann Allergy 1987;59:71-6.
Savin J, Dow R, Harlow B, et al. The effect of a new non-sedativeH1 receptor antagonist (LN2974) on the itching andscratching of patients with atopic eczema. Clin Exp Dermatol1986;11:600-2.
Schalin-Karrila M, Mattila L, Jansen C, et al. Evening primroseoil in the treatment of atopic eczema: effect on clinical status,plasma phospholipid fatty acids and circulating blood prostaglandins. Br J Dermatol 1987;117:11-9.
Uehara M. Clinical and histological features of dry skin inatopic dermatitis. Acta Derm Venereol (Stockh) (Suppl)1985;114:82-6. | 
