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      FCεRI Gene Promoter Polymorphisms and Total IgE Levels in Susceptibility to Atopic Dermatitis in Korea

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          Abstract

          IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor ( FcεRI) is involved in the pathogenesis of allergen-induced immune responsiveness in atopic diseases like atopic dermatitis (AD). We sought to determine FcεRI gene polymorphisms are associated with AD in Korean patients, and analyzed the relevance of FcεRI gene polymorphisms and serum IgE levels. We conducted a case-control association analysis (175 patients and 56 controls) of Korean subjects. Genotyping was performed using the TaqMan fluorogenic 5' nuclease assay, and serum levels of IgE were measured using a fluorescence enzyme immunoassay. We found that there were no significant relationships between FcεRI and AD, although there were trends towards an association between the 66T>C (rs2251746) polymorphism and total serum IgE levels in the Korean AD patients. In conclusion, while the 66T>C (rs2251746) of the FcεRIα polymorphism may be linked to AD and higher serum IgE levels, polymorphisms in the FcεRIβ gene did not confer susceptibility to AD in our patient sample.

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          Most cited references31

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          Atopic dermatitis and the atopic march.

          J. Spergel (2003)
          Atopic dermatitis (AD), one of the most common skin disorders seen in infants and children, usually has its onset during the first 6 months of life. The prevalence of AD is similar in the United States, Europe, and Japan and is increasing, similar to that of other atopic disorders, particularly asthma. AD has been classified into 3 sequential phases: infantile, childhood, and adult, each with characteristic physical findings. AD has a tremendously negative effect on the quality of life of patients as well as family, most commonly disturbing sleep. The condition also creates a great financial burden for both the family and society. The cutaneous manifestations of atopy often represent the beginning of the atopic march. On the basis of several longitudinal studies, approximately half of AD patients will develop asthma, particularly with severe AD, and two thirds will develop allergic rhinitis. Epicutaneous sensitization has been thought to be responsible, with subsequent migration of sensitized T cells into the nose and airways, causing upper and lower airway disease. Animal models and human observation concur with this theory. Preliminary prevention studies with oral antihistamines provide evidence that early intervention might slow the atopic march.
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            Atopic dermatitis.

            Atopic dermatitis is a highly pruritic chronic inflammatory skin disorder affecting 10-20% of children worldwide. Symptoms can persist or begin in adulthood. It is also the most common cause of occupational skin disease in adults. This disease results from an interaction between susceptibility genes, the host's environment, pharmacological abnormalities, skin barrier defects, and immunological factors. New management approaches have evolved from advances in our understanding of the pathobiology of this common skin disorder.
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              Null mutations in the filaggrin gene (FLG) determine major susceptibility to early-onset atopic dermatitis that persists into adulthood.

              Atopic dermatitis (AD) is a common disease with a complex etiology in childhood and adult life. A significant proportion of childhood AD is transient, but in many cases it persists into adulthood. We have recently shown that null mutations in the filaggrin gene (FLG) are an important predisposing factor for childhood eczema and eczema-associated asthma, but persistence to adulthood has not been analyzed. Here we studied a cohort of adult patients with persistent AD, which had been present since early childhood. In this cohort, the combined allele frequency of the two common FLG null variants was 0.270 (cf. population frequency 0.046). This represents an odds ratio of 7.7 with 95% confidence interval of 5.3-10.9 and a chi2 P-value of 1.7 x 10(-53). Our data conclusively demonstrate that identification of FLG null alleles is an indicator of a poor prognosis in AD, predisposing to a form of eczema that starts in early infancy and persists into adulthood. This study helps to further define the nature of the AD phenotype associated with FLG null alleles.
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                Author and article information

                Journal
                J Korean Med Sci
                JKMS
                Journal of Korean Medical Science
                The Korean Academy of Medical Sciences
                1011-8934
                1598-6357
                July 2011
                20 June 2011
                : 26
                : 7
                : 870-874
                Affiliations
                [1 ]Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Korea.
                [2 ]Department of Laboratory Medicine, Chung-Ang University College of Medicine, Seoul, Korea.
                Author notes
                Address for Correspondence: Seong Jun Seo, MD. Department of Dermatology, Chung Ang University Hospital, 102 Heukseok-ro, Dongjak-gu, Seoul 156-755, Korea. Tel: +82.2-6299-1525, Fax: +82.2-823-1049, drseo@ 123456hanafos.com
                Article
                10.3346/jkms.2011.26.7.870
                3124715
                21738338
                98bd2968-50bf-40f8-9c25-c07a9428e2d3
                © 2011 The Korean Academy of Medical Sciences.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 January 2011
                : 08 April 2011
                Categories
                Original Article
                Immunology, Allergic Disorders & Rheumatology

                Medicine
                fcεriβ polymorphism,immunoglobulin e,fcεriα polymorphism,atopic dermatitis
                Medicine
                fcεriβ polymorphism, immunoglobulin e, fcεriα polymorphism, atopic dermatitis

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