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ePaper created 2014-09-15, 12:31:02 | version 1.32.01
In the meantime, the first patients with severe eczema were treated with ciclosporin, leading to an increased referral of patients from outside Utrecht and improved experience in treating severe eczema patients with oral immunosuppressants.[7,8] Patient education and information, preferably by trained nurses, became an important quality indicator in the national eczema guideline. In order to make eczema care more efficient, a digital project was started, showing that the provision of care via a protected, dedicated portal was cost-effective and much appreciated by the patients.[9] Translational research using the gene array technique showed a stable down regulation and up regulation of genes involved in T cell proliferation and apoptosis, independent from the effect of therapy.[10] New bio- markers were explored from which thymocyte and activation-regulated chemokine (TARC) turned out to be significantly correlated to disease activity, providing an objective parameter. Gene array techniques were developed and applied to lesional and non-lesional skin and allergen-induced eczema skin, suggesting interesting new possible leads for therapy. Translational research is facilitated by the recent establishment of the central eczema biobank, as well as the eczema database, which contains data of more than 500 well-characterized eczema patients and their sera. The focus for the future will be on further characterizing eczema patients by defining the different phenotypes. References 1. Maat-Bleeker F de. Inhalant allergy and hyposensitization in atopic dermatitis. Thesis Utrecht University 1971. 2. Bruijnzeel-Koomen C, van Wichen DF, Toonstra J , et al. The presence of IgE molecules on epidermal Langerhans cells from patients with atopic dermatitis. Arch Derm Res 1986; 278: 199-205. 3. Reijsen FC van, Bruijnzeel-Koomen CA, de Weger RA, et al. Retention of long-lived, allergen-specific T cells in atopic dermatitis skin. J Invest Dermatol. 1997; 108: 530. 4. Grewe M, Bruijnzeel-Koomen CA, Schöpf E, et al. A role for Th1 and Th2 cells in the immunopathogenesis of atopic dermatitis. Immunol Today. 1998 19: 359-61. 5. Oosting AJ, de Bruin-Weller MS, Terreehorst I, at el. Effect of mattress encasings on atopic dermatitis outcome measures in a double-blind, placebo-controlled study: the Dutch mite avoidance study. J Allergy Clin Immunol. 2002 ; 110: 500-6. 6. Hijnen DJ, de Bruin-Weller M, Oosting B, et al. Serum thymus and activation-regulated chemokine (TARC) and cutaneous T cell-attracting chemokine (CTACK) levels in allergic diseases: TARC and CTACK are disease-specific markers for atopic dermatitis. J Allergy Clin Immunol 2004 ; 113; 334-40. 7. Hijnen DJ, Haeck I, van Kraats AA, et al. Cyclosporin A reduces CD4(+)CD25(+) regulatory T-cell numbers in patients with atopic dermatitis. J Allergy Clin Immunol. 2009 ; 124; 856-8. 8. Knol EF, Haeck IM, van Kraats AA, et al. Modulation of lymphocyte function in vivo via inhibition of calcineurin or purine synthesis in patients with atopic dermatitis. J Invest Dermatol. 2012 ; 132: 2476-9. 9. Os-Medendorp H van, Koffijberg H, Eland-de Kok PC, et al. E-health in caring for patients with atopic dermatitis: a randomized controlled cost-effectiveness study of internet-guided monitoring and online self-management training. Br J Dermatol. 2012 ; 166: 1060-8. 10. Hijnen D, Knol EF, Gent YY, et al. CD8(+) T cells in the lesional skin of atopic dermatitis and psoriasis patients are an important source of IFN-?, IL-13, IL-17, and IL-22. J Invest Dermatol. 2013 ; 133: 973-9. 73 BWEADVSMGFINCORR:Opmaak 1 21-07-2014 17:40 Pagina 73