Guidelines for Treatment of Atopic Eczema (Atopic Dermatitis) Part II
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DOI: 10.1111/j.1468-3083.2012.04636.x JEADV GUIDELINES Guidelines for treatment of atopic eczema (atopic dermatitis) Part II J. Ring,†,* A. Alomar,‡ T. Bieber,§ M. Deleuran,– A. Fink-Wagner,†† C. Gelmetti,‡‡ U. Gieler,§§ J. Lipozencic,–– T. Luger,††† A.P. Oranje,‡‡‡ T. Scha¨ fer,§§§ T. Schwennesen,––– S. Seidenari,†††† D. Simon,‡‡‡‡ S. Sta¨ nder,††† G. Stingl,§§§§ S. Szalai,–––– J.C. Szepietowski,††††† A. Taı¨eb,‡‡‡‡‡ T. Werfel,§§§§§ A. Wollenberg,––––– U. Darsow,† For the European Dermatology Forum (EDF), and the European Academy of Dermatology and Venereology (EADV), the European Task Force on Atopic Dermatitis (ETFAD), European Federation of Allergy (EFA), the European Society of Pediatric Dermatology (ESPD), and the Global Allergy and Asthma European Network (GA2LEN) †Department of Dermatology and Allergy Biederstein, Christine Ku¨ hne-Center for Allergy Research and Education (CK-CARE), Technische Universita¨ tMu¨ nchen, Munich, Germany and Division of Environmental Dermatology and Allergy, Helmholtz Zentrum Mu¨ nchen ⁄ TUM, ZAUM-Center for Allergy and Environment, Munich, Germany ‡Department of Dermatology, Hospital de Sant Pau, Universitat Autonoma Barcelona, Barcelona, Spain §Department of Dermatology and Allergy, University Bonn, Bonn, Germany –Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark ††EFA Project and Fundraising Officer, Konstanz, Germany ‡‡Istituto di Scienze Dermatologiche, Universita` di Milano, Milano, Italy §§Department for Psychosomatics and Psychotherapy, University of Gießen and Marburg GmbH, Gießen, Germany ––Department of Dermatology and Venereology, University Hospital Center Zagreb, Zagreb, Croatia †††Competence Center Chronic Pruritus, Department of Dermatology, University Hospital of Mu¨ nster, Mu¨ nster, Germany ‡‡‡Department of Pediatric Dermatology, Erasmus MC – Sophia Children ‘s Hospital, Rotterdam, The Netherlands §§§Institute for Social Medicine, University Lu¨ beck, Lu¨ beck, Germany –––Deutscher NEURODERMITIS Bund (DNB), Hamburg, Germany ††††Department of Dermatology, University of Modena and Reggio Emilia, Modena, Italy ‡‡‡‡Department of Dermatology, Universita¨ tsklinik fu¨ r Dermatologie, Bern, Switzerland §§§§Department of Dermatology, University of Vienna, Vienna, Austria ––––Department of Dermatology, Heim Pa´ l Children’s Hospital, Budapest, Hungary †††††Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, Wroclaw, Poland ‡‡‡‡‡Department of Dermatology & Pediatric Dermatology, Hoˆ pital St Andre´ , Bordeaux, France §§§§§Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany –––––Department of Dermatology and Allergy, Ludwig-Maximilian University, Munich, Germany *Correspondence: J. Ring: E-mail: [email protected] Abstract The existing evidence for treatment of atopic eczema (atopic dermatitis, AE) is evaluated using the national standard Appraisal of Guidelines Research and Evaluation. The consensus process consisted of a nominal group process and a DELPHI procedure. Management of AE must consider the individual symptomatic variability of the disease. Basic therapy is focused on hydrating topical treatment, and avoidance of specific and unspecific provocation factors. Anti-inflammatory treatment based on topical glucocorticosteroids and topical calcineurin inhibitors (TCI) is used for exacerbation management and more recently for proactive therapy in selected cases. Topical corticosteroids remain the mainstay of therapy, but the TCI tacrolimus and pimecrolimus are preferred in certain locations. Systemic immune-suppressive treatment is an option for severe refractory cases. Microbial colonization and superinfection may induce disease exacerbation and can justify additional antimicrobial treatment. Adjuvant therapy includes UV irradiation preferably with UVA1 wavelength or UVB 311 nm. Dietary recommendations should be specific and given only in diagnosed individual food allergy. Allergen-specific immunotherapy to aeroallergens may be useful in selected cases. Stress-induced exacerbations may make psychosomatic counselling recommendable. ‘Eczema school’ educational programs have been proven to be helpful. Pruritus is targeted with the majority of the recommended therapies, but some patients need additional antipruritic therapies. ª 2012 The Authors JEADV 2012 Journal of the European Academy of Dermatology and Venereology ª 2012 European Academy of Dermatology and Venereology 2 Ring et al. Conflict of interest A. Alomar has been speaker for Almirall, Astellas, Leti. T. Bieber has been advisor, speaker or investigator for ALK Abello´ , Astellas, Bencard, Galderma, Glaxo SmithKline, Leo, Novartis, Stallergenes. U. Darsow has been speaker, investigator and ⁄ or been a member of advisory boards for Allergopharma, ALK Abello´ , Bencard, GSK, Hermal, Novartis Pharma, Stallergenes, Stiefel. M. Deleuran has been a speaker, participated in clinical trials and ⁄ or been a member of advisory boards for Merck, Novartis, Astellas, Leo Pharma, NatImmune, Pergamum, Pierre Fabre and Janssen-Cilag. A.-H. Fink-Wagner received honorarium from Pharmaxis and Chiesi during the last 3 years and was employed before that by Nycomed. J. Ring has been advisor, speaker or investigator for ALK Abello´ , Allergopharma, Almirall-Hermal, Astellas, Bencard, Biogen-Idec, Galderma, Glaxo SmithKline, Leo, MSD, Novartis, Phadia, PLS Design, Stallergenes. S. Sta¨ nder was or is advisor, speaker and ⁄ or investigator for Aesca Pharma, Almirall ⁄ Hermal, Astellas Pharma, Beiersdorf AG, Birken, Essex Pharma, GSK, Pierre Fabre, Maruho, 3M Medica, Mundipharma, Novartis Pharma, Serentis, and Serono. Z. Szalai is investigator of clinical trials for Astellas, Novartis, Pfizer, Abbott, Pierre Fabre. A. Taı¨eb has received consulting and clinical trial honoraria from Pierre Fabre, Astellas, Almirall ⁄ Hermal, Leo and Novartis. T. Werfel has been advisor, speaker or investigator for ALK Abello´ , Astellas and Novartis. A. Wollenberg has received research funding and lecture honoraria from, conducted clinical trials for, or is a paid consultant to Astellas, Basilea, GSK, Loreal, Merck, Novartis, MSD. Other authors declared no conflict of interest. Phototherapy • UVA + UVB (approx. 280–400 nm). As most patients affected by AE improve during the sunny sum- • Broadband ultraviolet B (BB-UVB = approx. mer season, artificial UV radiation is frequently employed in the 280–320 nm). treatment of AE. • Narrow-band UVB (nbUVB = peak: 311–313 nm). A recent study has confirmed that 74.4% of the patients affected • UVA1 (340–400 nm). by mild-moderate AE had complete resolution during summer Treatment with longer wavelengths has not been sufficiently holidays, 16.3% had improvement and only 9.3% had no modifi- studied for AE and should therefore not be applied. When pre- cation of AE severity, confirming the seasonability of the disease, scribed, phototherapy is usually a part of a total treatment plan, with improvement during summertime and worsening in the i.e. a second-level treatment used especially in adults and much other seasons: More, seaside holidays produced a significantly less in children. Phototherapy in children younger than 12 years greater improvement than mountains holidays, with complete res- should not be applied. olution of the disease in 91.2% vs. 11.1% of patients (P < 0.01).1 As a rule, phototherapy is not indicated in the acute stage of While this difference cannot be explained on the sole basis of UV AE (except UVA1, which is also effective in managing AE flares), exposure, these data support the hypothesis on the positive effect but is more apt to treat chronic, pruritic, lichenified forms and ofUVradiationonAE. should not be prescribed in those patients who experience a VariouspathwaysandmeansthroughwhichtheenergyofUV worsening of their dermatosis during sun exposure. In practise, radiation from natural or artificial sources is ultimately trans- thechoiceofacertainUVtreatmentislimitedbytheavailability formed into biological effects within the skin have been suggested, of the phototherapy equipments: e.g. UVA1 devices are expen- including cutaneous sensory nerves, neuropeptides, neurotrophins sive to buy and to maintain. The biggest drawbacks of UV ther- and certain nerve-related receptors.2 The known mechanism of apy are that the patient must travel between three and five times action targets immunomodulation through apoptosis of inflam- per week and for 6–12 weeks to a site that offers this therapy. In matory cells, inhibition of Langerhans cells and alteration of addition, UV light does not effectively treat hairy areas as scalp cytokine production.3 In addition, UV has an antimicrobial and skin folds. effect reducing the colonization of S. aureus,4 due to its anti- In short, taking into account the individual tolerability, narrow- inflammatory effect and improves skin barrier.5 A different band UVB has been indicated for chronic moderate forms of AE7 explanation could be supported by the role of Vitamin D: a recent and is currently preferred to broadband UV because it is less study demonstrated that a 2-week course of heliotherapy signifi- erythemogenic, whereas high dose UVA1 has been prescribed for cantly improved vitamin D balance by increasing serum calcidiol more severe phases.8 Medium-dose UVA1 appears to be similar in concentration, and caused a marked healing of AE.6 terms of efficacy as narrow-band UVB.9 Furthermore, as high- Present UV sources include equipments able to emit selective lighted in a recent study, there is a small but significant