Please activate JavaScript!
Please install Adobe Flash Player, click here for download
ePaper created 2014-09-15, 12:31:02 | version 1.32.01
The millennium diagnostic criteria for atopic dermatitis (AD) were developed for both children and adults.[4] In cooperation with the department of pediatrics (psychosocial care), the course of life and the disease-related consequences in young adult patients with childhood AD was evaluated. Patients with severe AD in childhood were found to be significantly delayed in their social development later in life.[5] It was shown that AD lesions contain increased levels of IL-31-producing T cells, suggesting that a substantial part of previously reported increased IL-31 mRNA levels in AD skin is T cell-derived and that these cells may be involved in the pathogenesis of AD.[6] The Dutch task force on genodermatoses, with Henk Sillevis Smitt as its secretary and later chairman, described restrictive dermopathy in more detail, based on 12 cases in the Netherlands.[7] Blood and/or tissue DNA of some of these cases was used to unravel the cause of the disease.[8] In a cross-center team, terminology was developed to describe patients showing vascular malformations not only in the face, and combined with growth disturbances. This terminology was used to differentiate the nature, localization and timing of growth disturbances; the nature of co-localization of the vascular malformations and growth disturbances; and the presence or absence of other features. Six subgroups were defined within the group of entities with vascular malformation-deregulated growth. Subsequently a mixed group of both experienced and non-experienced observers evaluated 146 patients (106 from the Netherlands; 40 from the UK) with vascular malformations and disturbed growth. Scoring the patients using the proposed classification yielded a high inter-observer reproducibility.[9] References 1. Sillevis Smitt JH, Weening RS, Krieg SR, et al. Discoid lupus erythematosus-like lesions in carriers of X-linked chronic granulomatous disease. Br J Dermatol 1990; 122: 643-50. 2. Sillevis Smitt JH, Bos JD, Weening RS, et al. Discoid lupus erythematosus-like skin changes in patients with autosomal recessive chronic granulomatous disease. Arch Dermatol 1990; 126: 1656-8. 3. Sillevis Smitt JH, Kuijpers TW. Cutaneous manifestations of primary immunodeficiency. Curr Opin Pediatr 2013; 25: 492-7. 4. Bos JD, Leent EJ van, Sillevis Smitt JH. The millennium criteria for the diagnosis of atopic dermatitis. Exp Dermatol 1998; 7: 132-8. 5. Brenninkmeijer EE, Legierse CM, Sillevis Smitt JH, et al. The course of life of patients with childhood atopic dermatitis. Pediatr Dermatol 2009; 26: 14-22. 6. Szegedi K, Kremer AE, Kezic S, et al. Increased frequencies of IL-31-producing T cells are found in chronic atopic dermatitis skin. Exp Dermatol 2012; 21: 431-6. 7. Smitt JH, Asperen CJ van, Niessen et al. Restrictive dermopathy. Report of 12 cases. Dutch Task Force on Genodermatology. Arch Dermatol 1998; 134: 577-9. 8. Moulson CL, Go G, Gardner JM, et al. Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy. J Invest Dermatol 2005; 125: 913-9. 9. Oduber CE, Horst CM van der, Sillevis Smitt JH, et al. A proposal for classification of entities combining vascular malformations and deregulated growth. Eur J Med Genet 2011; 54: 262-7. 43 BWEADVSMGFINCORR:Opmaak 1 21-07-2014 17:39 Pagina 43