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Thymic stromal lymphopoietin variation, filaggrin loss of function, and the persistence of atopic dermatitis
Journal article   Open access   Peer reviewed

Thymic stromal lymphopoietin variation, filaggrin loss of function, and the persistence of atopic dermatitis

David J Margolis, Brian Kim, Andrea J Apter, Jayanta Gupta, Ole Hoffstad, Maryte Papadopoulos and Nandita Mitra
JAMA dermatology (Chicago, Ill.), Vol.150(3), pp.254-259
03-2014
PMCID: PMC4414492
PMID: 24401911

Abstract

Child Child, Preschool Cohort Studies Confidence Intervals Cytokines - genetics Dermatitis, Atopic - epidemiology Dermatitis, Atopic - genetics Dermatitis, Atopic - physiopathology Female Genetic Predisposition to Disease Humans Intermediate Filament Proteins - genetics Male Mutation Odds Ratio Polymorphism, Single Nucleotide Prevalence Prognosis Prospective Studies Recurrence Registries Risk Assessment Severity of Illness Index
Atopic dermatitis (AD) is a common chronic illness of childhood. To evaluate the association between thymic stromal lymphopoietin (TSLP) variation and the persistence of skin symptoms of AD. A prospective cohort study was conducted in the general community. Participants included 796 children enrolled in the Pediatric Eczema Elective Registry. EXPOSURE Evaluation of TSLP variation. Self-reported outcome of whether a child's skin had no symptoms of AD and required no medications for 6 months at 6-month intervals. We evaluated 14 variants of TSLP. The variant rs1898671 was significantly associated with the outcome in white children (P = .01). As measured by overlapping CIs, similar odds ratios (ORs) were noted among whites (OR, 1.72; 95% CI, 1.11-2.66) and African Americans (1.33; 0.52-3.45). Further within the subcohort of individuals with a filaggrin protein (FLG) loss-of-function mutation, those with TSLP variation were more likely to have less-persistent disease (OR, 4.92; 95% CI, 2.04-11.86). The TSLP variation is associated with less persistent AD. Therefore, TSLP may be a potential therapeutic target for the treatment of AD, especially in individuals with diminished barrier function due to FLG mutations. This is an attractive hypothesis that can be tested in clinical trials.
url
https://doi.org/10.1001/jamadermatol.2013.7954View
Published (Version of record) Open

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