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• W4247682368 abstract "There are remarkable differences in the diagnostic and therapeutic management of atopic dermatitis practiced by dermatologists and pediatricians in different countries. Therefore, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams who were given the task of finding a consensus to serve as a guideline for clinical practice in Europe as well as in North America. The consensus report is part of the PRACTALL initiative, which is endorsed by both academies. There are remarkable differences in the diagnostic and therapeutic management of atopic dermatitis practiced by dermatologists and pediatricians in different countries. Therefore, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams who were given the task of finding a consensus to serve as a guideline for clinical practice in Europe as well as in North America. The consensus report is part of the PRACTALL initiative, which is endorsed by both academies. Atopic dermatitis (AD) is a chronic inflammatory pruritic skin disease that affects a large number of children and adults in industrialized countries. The 12-month prevalence in 11-year-old children, as studied in the Global International Study of Asthma and Allergies in Childhood trial, ranged from 1% to 20%, with the highest prevalence typically found in Northern Europe.1Anonymous Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee.Lancet. 1998; 351: 1225-1232Abstract Full Text Full Text PDF PubMed Scopus (2459) Google Scholar In 45% of children, the onset of AD occurs during the first 6 months of life, during the first year of life in 60%, and before the age of 5 years in at least 85% of affected individuals.2Kay J. Gawkrodger D.J. Mortimer M.J. Jaron A.G. The prevalence of childhood atopic eczema in a general population.J Am Acad Dermatol. 1994; 30: 35-39Abstract Full Text PDF PubMed Google Scholar In those children with onset before the age of 2 years, 20% will have persisting manifestations of the disease, and an additional 17% will have intermittent symptoms by the age of 7 years (Fig 1).3Illi S. von Mutius E. Lau S. Nickel R. Gruber C. Niggemann B. et al.The natural course of atopic dermatitis from birth to age 7 years and the association with asthma.J Allergy Clin Immunol. 2004; 113: 925-931Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar In adults with AD, only 16.8% had onset after adolescence.4Williams H.C. Strachan D.P. The natural history of childhood eczema: observations from the British 1958 birth cohort study.Br J Dermatol. 1998; 139: 834-839Crossref PubMed Scopus (79) Google Scholar, 5Ozkaya E. Adult-onset atopic dermatitis.J Am Acad Dermatol. 2005; 52: 579-582Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar The clinical pattern of AD varies with age. Infants typically present with erythematous papules and vesicles on the cheeks, forehead, or scalp, which are intensely pruritic. The childhood phase typically occurs from 2 years of age to puberty. Children are less likely to have the exudative lesions of infancy and instead exhibit more lichenified papules and plaques representing the more chronic disease and involving the hands, feet, wrists, ankles, and antecubital and popliteal regions. The adult phase of AD begins at puberty and frequently continues into adulthood. Predominant areas of involvement include the flexural folds, the face and neck, the upper arms and back, and the dorsa of the hands, feet, fingers, and toes. The eruption is characterized by dry, scaling erythematous papules and plaques and the formation of large lichenified plaques from lesional chronicity. Parental atopy, in particular AD, is significantly associated with the manifestation and severity of early AD in children. The circumstance by which the genetics of AD might play a role in the level of natural history and development has been reflected in 2 forms of genetic studies:•genome-wide screens that identify broad regions of the genome linked with AD and•candidate gene studies that examine a presumed contribution of genetic variants of disease-process genes in case-control association studies. Both approaches highlight the search for disease-specific AD alleles, as well as identifying overlapping genes associated with other allergic characteristics and disorders. This process has been recently reviewed.6Hoffjan S. Epplen J.T. The genetics of atopic dermatitis: recent findings and future options.J Mol Med. 2005; 83: 682-692Crossref PubMed Scopus (73) Google Scholar A European study of about 200 families with affected sibs looked at phenotypes for AD, as well as allergic sensitization, and found a region of highest linkage at human chromosome 3q21.7Lee Y.A. Wahn U. Kehrt R. Tarani L. Businco L. Gustafsson D. et al.A major susceptibility locus for atopic dermatitis maps to chromosome 3q21.Nat Genet. 2000; 26: 470-473Crossref PubMed Scopus (196) Google Scholar Another study of 148 nuclear families in which AD, as well as other intermediate phenotypes, including asthma phenotype and total serum IgE level, were examined identified association with 5 regions, including 1q21, 17q25, 20p, 16q, and 5q31.8Cookson W.O. Ubhi B. Lawrence R. Abecasis G.R. Walley A.J. Cox H.E. et al.Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci.Nat Genet. 2001; 27: 372-373Crossref PubMed Scopus (272) Google Scholar A Swedish study of 197 affected sib pairs identified 4 phenotypes, as well as 11 locations, associated with all of the different phenotypes that ranged from severity of AD, specific IgE, and direct diagnosis of AD.9Bradley M. Soderhall C. Luthman H. Wahlgren C.F. Kockum I. Nordenskjold M. Susceptibility loci for atopic dermatitis on chromosomes 3, 13, 15, 17 and 18 in a Swedish population.Hum Mol Genet. 2002; 11: 1539-1548Crossref PubMed Google Scholar Finally, a Danish study looked at a small number of affected sib pairs and found association with 3 locations within the genome.10Haagerup A. Bjerke T. Schiotz P.O. Dahl R. Binderup H.G. Tan Q. et al.Atopic dermatitis—a total genome-scan for susceptibility genes.Acta Derm Venereol. 2004; 84: 346-352Crossref PubMed Scopus (52) Google Scholar Not all of these locations are highly robust, and most of these associations from genome-wide screens might not yield effective identification of specific genes when examined in more detail; these are summarized in Table I.7Lee Y.A. Wahn U. Kehrt R. Tarani L. Businco L. Gustafsson D. et al.A major susceptibility locus for atopic dermatitis maps to chromosome 3q21.Nat Genet. 2000; 26: 470-473Crossref PubMed Scopus (196) Google Scholar, 8Cookson W.O. Ubhi B. Lawrence R. Abecasis G.R. Walley A.J. Cox H.E. et al.Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci.Nat Genet. 2001; 27: 372-373Crossref PubMed Scopus (272) Google Scholar, 9Bradley M. Soderhall C. Luthman H. Wahlgren C.F. Kockum I. Nordenskjold M. Susceptibility loci for atopic dermatitis on chromosomes 3, 13, 15, 17 and 18 in a Swedish population.Hum Mol Genet. 2002; 11: 1539-1548Crossref PubMed Google Scholar, 10Haagerup A. Bjerke T. Schiotz P.O. Dahl R. Binderup H.G. Tan Q. et al.Atopic dermatitis—a total genome-scan for susceptibility genes.Acta Derm Venereol. 2004; 84: 346-352Crossref PubMed Scopus (52) Google Scholar Table II11Novak N. Kruse S. Potreck J. Weidinger S. Fimmers R. Bieber T. Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema.J Allergy Clin Immunol. 2005; 115: 828-833Abstract Full Text Full Text PDF PubMed Scopus (69) Google Scholar, 12Weidinger S. Klopp N. Rümmler L. Wagenpfeil S. Novak N. Baurecht H.J. et al.Association of NOD1 polymorphisms with atopic eczema and related phenotypes.J Allergy Clin Immunol. 2005; 116: 177-184Abstract Full Text Full Text PDF PubMed Scopus (106) Google Scholar, 13Weidinger S. Rümmler L. Klopp N. Wagenpfeil S. Baurecht H.J. Fischer G. et al.Association study of mast cell chymase polymorphisms with atopy.Allergy. 2005; 60: 1256-1261Crossref PubMed Scopus (31) Google Scholar summarizes the findings of candidate gene studies and their association with atopy and asthma.Table IGenome-wide screens of ADReferenceStudy populationSamplePhenotypesRegions of highest linkageLee et al,7Lee Y.A. Wahn U. Kehrt R. Tarani L. Businco L. Gustafsson D. et al.A major susceptibility locus for atopic dermatitis maps to chromosome 3q21.Nat Genet. 2000; 26: 470-473Crossref PubMed Scopus (196) Google Scholar 2000European199 families with 2 affected siblingsAD3q21Allergic sensitization3q21Cookson et al,8Cookson W.O. Ubhi B. Lawrence R. Abecasis G.R. Walley A.J. Cox H.E. et al.Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci.Nat Genet. 2001; 27: 372-373Crossref PubMed Scopus (272) Google Scholar 2001British148 nuclear families recruited through children with active ADAD1q2117q25AD plus asthma20pSerum IgE16q-tel5q31Bradley et al,9Bradley M. Soderhall C. Luthman H. Wahlgren C.F. Kockum I. Nordenskjold M. Susceptibility loci for atopic dermatitis on chromosomes 3, 13, 15, 17 and 18 in a Swedish population.Hum Mol Genet. 2002; 11: 1539-1548Crossref PubMed Google Scholar 2002Swedish109 families (197 affected full sib pairs, 9 affected half sib pairs)AD3p24-225p136q1610p13-12AD plus specific IgE18q214q24-266p1p32Extreme AD18p21q217p14Severity score of AD13q1415q14-1517q213q14Haagerup et al,10Haagerup A. Bjerke T. Schiotz P.O. Dahl R. Binderup H.G. Tan Q. et al.Atopic dermatitis—a total genome-scan for susceptibility genes.Acta Derm Venereol. 2004; 84: 346-352Crossref PubMed Scopus (52) Google Scholar 2004Danish23 affected sib-pair familiesAD plus specific IgE3p26-244p15-1418q11-12 Open table in a new tab Table IICandidate gene studies in ADGeneGene nameLocationVariantPhenotypePopulationAssociationTLR2Toll-like receptor 24q32Arg753GlnSevere ADGermanYesADGermanNoIRF2Interferon regulatory factor 24q35−467 G/AADJapaneseYesCSF2Colony-stimulating factor 25q31−677 A/CADBritishYes3606 T/C, 3928 C/TAD at 12 and 24 moCanadianYesIL4IL-45q31−590 C/TADJapaneseYesExtrinsic ADGermanYesADAustralianNoIntrinsic ADJapaneseNoIL13IL-135q31Arg130GlnADCanadianYesADJapaneseYesADGermanYes−111 C/TADDutchYesADJapaneseNoIL5IL-55q31−703 C/TBlood eosinophilia in ADJapaneseIL1811Novak N. Kruse S. Potreck J. Weidinger S. Fimmers R. Bieber T. Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema.J Allergy Clin Immunol. 2005; 115: 828-833Abstract Full Text Full Text PDF PubMed Scopus (69) Google ScholarIL-1811q22−137 G/C, −133 C/GADGermanYes113 T/G, 127 G/TCARD412Weidinger S. Klopp N. Rümmler L. Wagenpfeil S. Novak N. Baurecht H.J. et al.Association of NOD1 polymorphisms with atopic eczema and related phenotypes.J Allergy Clin Immunol. 2005; 116: 177-184Abstract Full Text Full Text PDF PubMed Scopus (106) Google ScholarCaspase recruitment domain-containing protein 47p14-p15-rs2736726ADGermanYesrs2075817rs2975632rs2075822rs2907749rs2907748CD14Monocyte differentiation antigen CD145q31−159 C/TAD (interaction with dog ownership)AmericanYesADGermanNoIL12BIL-12B5q31-331188 A/CAD, psoriasisJapaneseYesSPINK5Serine protease inhibitor, Kazal-type 5Glu420LysADBritishYesADJapaneseYesADJapaneseYesAsthma with ADGermanYesDisease severity and food allergy in ADJapaneseYesFCER1BHigh-affinity IgE receptor β chain11q13RsaIin2, RsaIex7ADBritishYesGSTP1Glutathione-S-transferase, PI11q13Ile105ValADRussianYesHaplotypesADRussianYesPHF11Plant homeodomain zinc finger 11 protein13q14T/C intron3, G/A 3 UTRChildhood ADAustralianYesCMA1Mast cell chymase14q11BstXIADJapaneseYesADJapaneseYesADJapaneseNoADItalianNo−1903 G/AIgE levels in ADBritishYesADGerman13Weidinger S. Rümmler L. Klopp N. Wagenpfeil S. Baurecht H.J. Fischer G. et al.Association study of mast cell chymase polymorphisms with atopy.Allergy. 2005; 60: 1256-1261Crossref PubMed Scopus (31) Google ScholarYesIL4RAIL-4 Receptor chain16p12Gln551ArgSevere ADAmericanYesAdult ADJapaneseYesAd (interaction with infection)BritishYesIntrinsic ADJapaneseNo−3223 C/TExtrinsic ADGermanYesADJapaneseYesCARD15Caspase recruitment domain-containing protein 1516q122722 G/CADGermanYesADGerman11Novak N. Kruse S. Potreck J. Weidinger S. Fimmers R. Bieber T. Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema.J Allergy Clin Immunol. 2005; 115: 828-833Abstract Full Text Full Text PDF PubMed Scopus (69) Google ScholarYesRANTESRegulated on activation, normally T cell expressed plus secreted17q11-q12−403 A/GADGermanYesADHungarianNoEOTAXINEotaxin17q21−426 C/T, −384 A/GIgE levels in ADJapaneseYesTGFβ1TGF-β119q13.1Arg25ProADBritishYesSCCEStratum corneum chymotryptic enzyme19q13AACCinsADBritishYes Open table in a new tab Among nongenetic determinants for the development of AD, the role of infantile feeding has been investigated.14Laubereau B. Brockow I. Zirngibl A. Koletzko S. Gruebl A. von Berg A. et al.Effect of breast-feeding on the development of atopic dermatitis during the first 3 years of life—results from the GINI-birth cohort study.J Pediatr. 2004; 144: 602-607Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar A recent meta-analysis suggests that the incidence of infantile AD is reduced by breast-feeding for a least 4 months,15Schafer T. [Prevention of atopic eczema. Evidence based guidelines].Hautarzt. 2005; 56: 232-240Crossref PubMed Scopus (7) Google Scholar but this effect is most probably transient and tends to disappear after 3 years of age. Environmental factors also play a role in the development of AD. In contrast to asthma, the role of passive tobacco smoke exposure in AD is inconclusive. However, exposure to aeroallergens (pets, mites, and pollen) has been clearly shown to increase the risk factors for AD and AD severity.16Capristo C. Romei I. Boner A.L. Environmental prevention in atopic eczema dermatitis syndrome (AEDS) and asthma: avoidance of indoor allergens.Allergy. 2004; 59: 53-60Crossref PubMed Google Scholar, 17Purvis D.J. Thompson J.M. Clark P.M. Robinson E. Black P.N. Wild C.J. et al.Risk factors for atopic dermatitis in New Zealand children at 3.5 years of age.Br J Dermatol. 2005; 152: 742-749Crossref PubMed Scopus (79) Google Scholar, 18Schafer T. Heinrich J. Wjst M. Adam H. Ring J. Wichmann H.E. Association between severity of atopic eczema and degree of sensitization to aeroallergens in schoolchildren.J Allergy Clin Immunol. 1999; 104: 1280-1284Abstract Full Text Full Text PDF PubMed Google Scholar In addition, aeroallergens are a trigger for exacerbations in adult AD. Sensitization to food allergens (cow's milk and hen's eggs) is associated with infantile AD and related to disease severity. Food allergen sensitization is also predictive for persistence of symptoms throughout childhood.3Illi S. von Mutius E. Lau S. Nickel R. Gruber C. Niggemann B. et al.The natural course of atopic dermatitis from birth to age 7 years and the association with asthma.J Allergy Clin Immunol. 2004; 113: 925-931Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar Only in a minority of those with food sensitization (up to 33% of patients with moderate-to-severe disease of all age groups) are food allergens of clinical relevance, as demonstrated by food challenge studies.19Eigenmann P.A. Sicherer S.H. Borkowski T.A. Cohen B.A. Sampson H.A. Prevalence of IgE-mediated food allergy among children with atopic dermatitis.Pediatrics. 1998; 101: e8Crossref PubMed Google Scholar Another risk factor for persistent AD symptoms is the severity of disease in infancy. Children with AD are at high risk of allergic asthma and allergic rhinitis. Of those with AD during the first 2 years of life, 50% will have asthma during subsequent years.20Warner J.O. ETAC Study Group A double-blinded, randomized, placebo-controlled trial of cetirizine in preventing the onset of asthma in children with atopic dermatitis: 18 months' treatment and 18 months' posttreatment follow-up.J Allergy Clin Immunol. 2001; 108: 929-937Abstract Full Text Full Text PDF PubMed Scopus (193) Google Scholar The severity of AD, including early sensitization to food, increases the risk of asthma and allergic rhinitis.3Illi S. von Mutius E. Lau S. Nickel R. Gruber C. Niggemann B. et al.The natural course of atopic dermatitis from birth to age 7 years and the association with asthma.J Allergy Clin Immunol. 2004; 113: 925-931Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar, 21Gustafsson D. Sjoberg O. Foucard T. Development of allergies and asthma in infants and young children with atopic dermatitis—a prospective follow-up to 7 years of age.Allergy. 2000; 55: 240-245Crossref PubMed Scopus (193) Google Scholar The exact mechanism for the progression of the disease in children with AD is unknown; however, it appears to be a complex interaction of genetics, environmental exposure, and sensitization. For children with a family history of atopy, early AD, and sensitization, almost all are expected to have asthma. In murine models of AD, epicutaneous sensitization leads to systemic allergic responses, increased IgE levels, airway eosinophilia, airway sensitization, and airway hyperresponsiveness similar to that seen in human asthma and allergy.22Spergel J.M. Mizoguchi E. Brewer J.P. Martin T.R. Bhan A.K. Geha R.S. Epicutaneous sensitization with protein antigen induces localized allergic dermatitis and hyperresponsiveness to methacholine after single exposure to aerosolized antigen in mice.J Clin Invest. 1998; 101: 1614-1622Crossref PubMed Google Scholar In human subjects a recent report suggests that in selected individuals sensitization to peanut allergen might occur through the skin.23Lack G. Fox D. Northstone K. Golding J. Avon Longitudinal Study of Parents and Children Study Team Factors associated with the development of peanut allergy in childhood.N Engl J Med. 2003; 348: 977-985Crossref PubMed Scopus (390) Google Scholar The pathophysiology of AD is the product of a complex interaction between various susceptibility genes, host environments, infectious agents, defects in skin barrier function, and immunologic responses.24Novak N. Bieber T. Leung D.Y. Immune mechanisms leading to atopic dermatitis.J Allergy Clin Immunol. 2003; 112: S128-S139Abstract Full Text Full Text PDF PubMed Scopus (198) Google Scholar Activation of T lymphocytes, dendritic cells (DCs), macrophages, keratinocytes, mast cells, and eosinophils are characteristic of AD skin inflammatory responses. Clinically unaffected skin in AD is not normal. It is frequently dry and has a greater irritant skin response than normal healthy skin. Microscopic studies reveal a sparse perivascular T-cell infiltrate in unaffected AD skin that is not seen in normal healthy skin (Fig 2).25Leung D.Y.M. Bhan A.K. Schneeberger E.E. Geha R.S. Characterization of the mononuclear cell infiltrate in atopic dermatitis using monoclonal antibodies.J Allergy Clin Immunol. 1983; 71: 47-56Abstract Full Text PDF PubMed Google Scholar Acute AD skin lesions present to the physician as intensely pruritic, erythematous papules associated with excoriation and serous exudation. There is a marked infiltration of CD4+ activated memory T cells in acute AD. Antigen-presenting cells (eg, Langerhans cells [LCs], inflammatory dendritic epidermal cells [IDECs], and macrophages) in lesional and, to a lesser extent, in nonlesional skin bear IgE molecules.26Novak N. Kraft S. Bieber T. IgE receptors.Curr Opin Immunol. 2001; 13: 721-726Crossref PubMed Scopus (65) Google Scholar Mast cell degranulation can be observed. Chronic AD skin lesions have undergone tissue remodeling caused by chronic inflammation. These skin lesions are associated with thickened plaques with increased skin markings (lichenification), increased collagen deposition in the dermis, and dry fibrotic papules. Macrophages dominate the dermal mononuclear cell infiltrate. Eosinophils also contribute to the inflammatory response, and T cells remain present, although in smaller numbers than seen in acute AD. AD skin lesions are orchestrated by the local tissue expression of proinflammatory cytokines and chemokines.27Leung D.Y. Boguniewicz M. Howell M.D. Nomura I. Hamid Q.A. New insights into atopic dermatitis.J Clin Invest. 2004; 113: 651-657Crossref PubMed Google Scholar Cytokines, such as TNF-α and IL-1 from resident cells (keratinocytes, mast cells, and DCs), binds to receptors on the vascular endothelium, activating cellular signaling, including the nuclear factor (NF) κB pathway, and inducing expression of vascular endothelial cell adhesion molecules. These events initiate the process of tethering, activation, and adhesion to the endothelium, followed by extravasation of inflammatory cells. Once the inflammatory cells have infiltrated into the tissue, they respond to chemotactic gradients established by chemoattractant cytokines and chemokines, which emanate from sites of injury or infection. These molecules play a central role in defining the nature of the inflammatory infiltrate in AD. The onset of acute AD is strongly associated with the production of TH2-produced cytokines, notably IL-4 and IL-13, levels of which are significantly higher in AD individuals compared with control subjects.28Hamid Q. Boguniewicz M. Leung D.Y. Differential in situ cytokine gene expression in acute versus chronic dermatitis.J Clin Invest. 1994; 94: 870-876Crossref PubMed Google Scholar Mediating isotype switching to IgE synthesis and upregulating expression of adhesion molecules on endothelial cells, IL-4 and IL-13 are implicated in the initial phase of tissue inflammation, whereas the TH2 cytokine IL-5, which is involved in eosinophil development and survival, predominates in the chronic form of the disease.28Hamid Q. Boguniewicz M. Leung D.Y. Differential in situ cytokine gene expression in acute versus chronic dermatitis.J Clin Invest. 1994; 94: 870-876Crossref PubMed Google Scholar Increased production of GM-CSF in patients with AD is reported to inhibit apoptosis of monocytes, thereby contributing to the chronicity of this condition.29Bratton D.L. Hamid Q. Boguniewicz M. Doherty D.E. Kailey J.M. Leung D.Y. Granulocyte macrophage colony-stimulating factor contributes to enhanced monocyte survival in chronic atopic dermatitis.J Clin Invest. 1995; 95: 211-218Crossref PubMed Google Scholar The maintenance of chronic AD also involves production of the TH1-like cytokines IL-12 and IL-18, as well as several remodeling-associated cytokines, such as IL-11 and TGF-β1, which are expressed preferentially in chronic forms of the disease.30Toda M. Leung D.Y. Molet S. Boguniewicz M. Taha R. Christodoulopoulos P. et al.Polarized in vivo expression of IL-11 and Il-17 between acute and chronic skin lesions.J Allergy Clin Immunol. 2003; 111: 875-881Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar Increased expression of C-C chemokines (monocyte chemoattractant protein 4, eotaxin, and RANTES) contributes to infiltration of macrophages, eosinophils, and T cells into acute and chronic AD skin lesions.31Taha R.A. Minshall E.M. Leung D.Y. Boguniewicz M. Luster A. et al.Evidence for increased expression of eotaxin and monocyte chemotactic protein-4 in atopic dermatitis.J Allergy Clin Immunol. 2000; 105: 1002-1007Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar Cutaneous T cell–attracting chemokine (CCL27) is highly upregulated in AD and preferentially attracts cutaneous lymphocyte antigen–positive T cells into the skin. Finally, selective recruitment of CCR4-expressing TH2 cells is mediated by macrophage-derived chemokine and thymus and activation-regulated cytokine, levels of which are increased in patients with AD.27Leung D.Y. Boguniewicz M. Howell M.D. Nomura I. Hamid Q.A. New insights into atopic dermatitis.J Clin Invest. 2004; 113: 651-657Crossref PubMed Google Scholar Severity of AD has been linked to magnitude of thymus and activation-regulated cytokine levels.32Hijnen D. De Bruin-Weller M. Oosting B. Lebre C. De Jong E. Bruijnzeel-Koomen C. 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: 334-340Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar In addition, chemokines, such as fractalkine,33Echigo T. Hasegawa M. Shimada Y. Takehara K. Sato S. Expression of fractalkine and its receptor, CX3CR1, in atopic dermatitis: possible contribution to skin inflammation.J Allergy Clin Immunol. 2004; 113: 940-948Abstract Full Text Full Text PDF PubMed Scopus (41) Google Scholar IFN-γ–inducible protein 10, monokine induced by IFN-γ, and IFN-γ–inducible α chemoattractant, are strongly upregulated in keratinocytes34Klunker S. Trautmann A. Akdis M. Verhagen J. Schmid-Grendelmeier P. Blaser K. et al.A second step of chemotaxis after transendothelial migration: keratinocytes undergoing apoptosis release IFN-gamma-inducible protein 10, monokine induced by IFN-gamma, and IFN-gamma-inducible alpha-chemoattractant for T cell chemotaxis toward epidermis in atopic dermatitis.J Immunol. 2003; 171: 1078-1084PubMed Google Scholar and contribute to TH1 cell migration toward the epidermis. In about 80% of adult patients with AD, the disease is associated with increased serum IgE levels (>150 kU/L), sensitization against aeroallergens and food allergens, and/or concomitant allergic rhinitis and asthma.35Novak N. Bieber T. Allergic and nonallergic forms of atopic diseases.J Allergy Clin Immunol. 2003; 112: 252-262Abstract Full Text Full Text PDF PubMed Scopus (221) Google Scholar, 36Schmid-Grendelmeier P. Simon D. Simon H.U. Akdis C.A. Wuthrich B. Epidemiology, clinical features, and immunology of the “intrinsic” (non-IgE-mediated) type of atopic dermatitis (constitutional dermatitis).Allergy. 2001; 56: 841-849Crossref PubMed Scopus (159) Google Scholar In contrast, 20% of adult patients with AD have normal serum IgE levels. This subtype of AD often has a late onset (>20 years of life) and a lack of IgE sensitization against inhalant or food allergens.35Novak N. Bieber T. Allergic and nonallergic forms of atopic diseases.J Allergy Clin Immunol. 2003; 112: 252-262Abstract Full Text Full Text PDF PubMed Scopus (221) Google Scholar, 36Schmid-Grendelmeier P. Simon D. Simon H.U. Akdis C.A. Wuthrich B. Epidemiology, clinical features, and immunology of the “intrinsic” (non-IgE-mediated) type of atopic dermatitis (constitutional dermatitis).Allergy. 2001; 56: 841-849Crossref PubMed Scopus (159) Google Scholar However, some of these patients might have IgE sensitization against microbial antigens, such as Staphylococcus aureus enterotoxins and Candida albicans or Malassezia sympodialis (formally known as Pityrosporum ovale).37Scheynius A. Johansson C. Buentke E. Zagari A. Linder M.T. Atopic eczema/dermatitis syndrome and Malassezia.Int Arch Allergy Immunol. 2002; 127: 161-169Crossref PubMed Scopus (73) Google Scholar, 38Novak N. Allam J.P. Bieber T. Allergic hyperreactivity to microbial components: a trigger factor of “intrinsic” atopic dermatitis?.J Allergy Clin Immunol. 2003; 112: 215-216Abstract Full Text Full Text PDF PubMed Google Scholar In addition, some of these patients have positive reactions on the atopy patch test (APT).39Kerschenlohr K. Decard S. Darsow U. Ollert M. Wollenberg A. Clinical and immunologic reactivity to aeroallergens in “intrinsic” atopic dermatitis patients.J Allergy Clin Immunol. 2003; 111: 195-197Abstract Full Text Full Text PDF PubMed Google Scholar In children a transient form of AD with low IgE serum levels and without any detectable sensitizations has been shown, which develops into the extrinsic variant of AD with increasing IgE serum levels and developing sensitizations against aeroallergens and food allergens later in life.40Novembre E. Cianferoni A. Lombardi E. Bernardini R. Pucci N. Vierucci A. Natural history of “intrinsic” atopic dermatitis.Allergy. 2001; 56: 452-453Crossref PubMed Scopus (75) Google Scholar Expression of IgE receptors (ie, the high-affinity receptor for IgE [FcεRI]) can be found in the epidermal skin lesions of patients with AD. The reason for a higher IgE-binding capacity of DCs in the skin and in the peripheral blood of patients with AD is that FcεRI is regulated distinctly on DCs of atopic and nonatopic subjects.41Novak N. Tepel C. Koch S. Brix K. Bieber T. Kraft S. Evidence for a differential expression of the FcepsilonRIgamma chain in dendritic cells of atopic and nonatopic donors.J Clin Invest. 2003; 111: 1047-1056Crossref PubMed Scopus (77) Google Scholar AD is characterized by dry skin, even involving nonlesional skin and increased transepidermal water loss. In particular, ceramides serve as the major water-retaining molecules in the extracellular space of the cornified envelope, and the barrier function of these complex structures is provided by a matrix of structural proteins, which are bound to ceramides.42Sator P.G. Schmidt J.B. Honigsmann H. Comparison of epidermal hydration and skin surface lipids in healthy individuals and in patients with atopic dermatitis.J Am Acad Dermatol. 2003; 48: 352-358Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar, 43Arikawa J. Ishibashi M. Kawashima M. Takagi Y. Ichikawa Y. Imokawa G. Decreased levels of sphingosine, a natural antimicrobial agent, may be associated with vulnerability of the stratum corneum from patients with atopic dermatitis to colonization by Staphylococcus aureus.J Invest Der" @default.
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• W4247682368 title "Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report" @default.
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