Naslov
Keynote from Japan 5th Georg Rajka International Symposium on Atopic Dermatitis, Kyoto, May 11-13, 2008

Autori
Lipozenčić, Jasna

Izvornik
Acta dermatovenerologica Croatica (1330-027X) 16 (2008), 3; 168-169

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, vijest, stručni

Ključne riječi
hypothesis of atopic dermatitis; WHO Classification of eczematous dermatoses classification

Sažetak
In Keynote lecture Thomas Bieber showed the hypothesis of atopic dermatitis (AD): one or more severe diseases based on WHO Classification of eczematous dermatoses classification before of 6 month and end of 3 years of life with early AD sensitization. In European population but not in Japanese AD patients there are 4 subforms of AD: infancy, childhood, adolescent and adults ; with early onset and late onset ; with genetics variant analysis each of overlapping gene loci of AD and asthma ; with polymorphism in the Filaggrin – gene in ichthyosis vulgaris and AD (loss of function variants R 510x and 288 delta 4 in FFG gene in the epidermal biophysical barrier impairment ; percutane sensitization in AD ; role of staphylococcal aureus in IgE sensitization ; AD as an autoimmune disease ; role of gene-gene and gene environment interaction in the natural history of AD ; environment allergens and autoallergic in AD (sensitization to self proteins) in nonatopic AD. There are no uniform diagnostics criteria for AD: Hanifin & Rajka, UK diagnostic criteria are the most extensively validated but Millenium Criteria from 1994, Japanese criteria, ISAAC Criteria, and Lillenhamer criteria Schultz – Larsen, QUADAS Whiting et al, 2003 are used in many studies. Up-to-date diagnostic criteria are needed to improve AD diagnosis to find visible phenotype of AD. Controversies in AD are based on: genetics (HUGO ; ATOD 1-6 ; 1q21, etc.) ; on pathogenesis: (barrier dysfunction and penetration of allergens and IgE sensitization, on immunocentric hypothesis on immune imbalance – IgE production – organ sensitization ; on epidemiology: different definition in epidemiology ; point prevalence versus period prevalence, not all age groups studied in all countries, explanation of increased AD, hygiene hypothesis: type 2 T-cell persistence after birth ; therapy: tar preparation useful but carcinogeneity not studied, topical corticosteroids once or twice daily, pulse versus continuous corticosteroids, systemic corticosteroids frequent or never ; on diagnosis: WHO definition ; atopy ; atopiform dermatitis ; uniformity of SCORAD, POEMS, EASI as confronts methods. ISSAC International study of asthma and allergies in childhood with 721.601 patients out of 156 centers and 56 countries based on 6-14 year of age and UK diagnostic criteria showed 5-9, 9% prevalence ORs SPT positivity in flexural eczema is associated with AD patients. In Japan is prevalence in 3 year old AD children according the study of 4 month infancy, and 6-7 y of children. There have persisting AD, newly developed AD, regressed AD (70%) and non AD patients (5.5%). Disease activity in AD patients, rather than the use of topical corticosteroids are responsible for the low basal cortisol values in patients with severe AD and low bone mineral density in AD (about 30%) which is not related to the amount of topical corticosteroids used in the past. Plasma levels of platelat-derived microparticles (PDMP) and soluble P-selectin, β -thromboglobulin (β -TG) and platelat factor 4 (PF4) as platelat activation markers in patients with AD, but plasma PDMP and sP-selection may be markers of disease severity in AD. Filaggrin mutations are found in 50% of individuals with eczema the risk factor for AD. Raman spectroscopy is a rapid, non-invasive method to obtain the detailed molecular information of tissue and predisposing factors for AD. Psychological stress (PS) increases the production of endogenous gluccocorticoids and both, systemic and topicals can cause adverse effects or epidermal structure and function similar to those observed with PS. Defects of the skin barrier are influenced by genetic defects in Lekti in AD by cluster of genes with general effects on dermal inflammation (1q21, 17q25, 20p, 3q21, 4q, 6p). Skin barrier function and expression of antimicrobial peptides in AD with pimecrolimus and bethamethasone cream regulates the penetration of Type I and Type IV allergens into the skin. Hot top key notes from Symposium were: Persisting AD since childhood is up 3% to 9% with prevalence in female ; Filaggrin mutations in AD is risk factor for asthma and AD with penetrance 38-40% ; International consensus about the genetics, pathogenesis, epidemiology, diagnosis and therapy of AD is far from sufficient. Thymic-derived CD4+CD25+Fox p3+ natural T-regulatory cells play an important role in maintaining self-tolerance and preventing autoimmunity. The correlation of the plasma levels of platelat-derived microparticles (PDMP) and soluble P-selectin (sP-selectin) levels with the SCORAD index suggests that PDMP and sP-selectin may be markers of disease severity in AD. The confocal Raman sprectroscopy (noninvasive in vivo method) to indicate a filaggrin defect) is rapid tool to screen infants for predisposing factors for AD and detect reduced levels of NMF in stratum corneum. Patients with atopic eczema have a genetic predisposition to enhanced protease activity. Topical corticosteroids induce increased protease expression in the skin which is demonstrated, using in situ zymography and RT-PCR. Chemokines, small secreted molecules (more than 50) that regulate leukocytic trafficking via their corresponding seven-transmembrane-spanning, G-protein coupled receptors (18), participate in the pathophysiology of AD. AD patients are characterized by increased numbers of cutaneous lymphocyte-associated antigens (CLA) +CD4 T-cells that directly affects the expression of skin homing genes in the total CD4+ population. However, these CLA+CD4+ T-cells are qualitatively different from healthy controls by the decreased expression of apopthosis – related genes. Prostanoids are one of the lipid mediators to play pathophysiologic roles in the body (PGE2, PGD2, PG12, PGF2 and thromboxane (TX)A2, but they play some roles on antigen exposure to the skin and have biphasic roles. Cyclosporin treatment in vivo significantly decreased the percentage of CD4 CD25 regulatory T cells and reduces FOXP3 and GADD45A expression in CD4 + T cells from patients with AD. Interleukin-13 and interferon gamma producing skin resident CD8 Tcells: a vicious circle of barrier disruption of the skin in AD. Augmented interleukin-18 secretin may enhance the immune dysfunction observed in AD, leading to constant skin inflammation. The house dust mite (Dermatophagoides pteronisimus-Dp) can trigger allergic response through the increased expression of pro-inflammatory cytokines and the cytokine measurement after DpE treatment may be used as a helpful screening system for the treatment of AD other allergic diseases. Allergen tests in AD are important to treat and care the AD patients (atopy patch test, skin prick test, patch test, repeated open application test and use test). The wet wrap techniques is a kind of occlusive treatment and is suitable for long-term treatment with a potent diluted corticosteroid cream in children, but also in adults and is more effective than treatment with topical immunomodulators. Foods play an important role in irregular aggravation of skin lesions in children with AD. Infection of children with AD from their own emollients should be considered as a possible cause of recurrent infective exacerbations. More severly affected individuals may require systemic anti-inflammatory agents, particularly azathioprine or cyclosporine, mycophenolatemofetil and methotrexate may be associated with fewer side effects, and efalizumab is showing promise among the biologicals. It was very successful Meeting organized by Japanese colleagues.

Izvorni jezik
Engleski

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Kliničke medicinske znanosti

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