dc.contributor.author | IRVINE, ALAN | en |
dc.date.accessioned | 2015-11-05T15:26:24Z | |
dc.date.available | 2015-11-05T15:26:24Z | |
dc.date.issued | 2015 | en |
dc.date.submitted | 2015 | en |
dc.identifier.citation | Kelleher M, Dunn-Galvin A, Hourihane JO, Murray D, Campbell LE, McLean WH, Irvine AD, Skin barrier dysfunction measured by transepidermal water loss at 2 days and 2 months predates and predicts atopic dermatitis at 1 year., The Journal of allergy and clinical immunology, 135, 4, 2015, 930-5.e1 | en |
dc.identifier.issn | 0091-6749 | en |
dc.identifier.other | Y | en |
dc.identifier.uri | http://hdl.handle.net/2262/74851 | |
dc.description | PUBLISHED | en |
dc.description.abstract | Loss-of-function mutations in the skin barrier protein filaggrin (FLG) are a major risk for atopic dermatitis (AD). The pathogenic sequence of disturbances in skin barrier function before or during the early development of AD is not fully understood. A more detailed understanding of these events is needed to develop a clearer picture of disease pathogenesis. A robust, noninvasive test to identify babies at high risk of AD would be important in planning early intervention and/or prevention studies.
OBJECTIVES:
To ascertain whether a noninvasive measurement of skin barrier function at day 2 after birth and at 2 months predicts the development of AD at 1 year. Furthermore, to determine whether increases in transepidermal water loss (TEWL) predate the development of clinical AD.
METHODS:
A total of 1903 infants were enrolled in the Cork Babies After Scope: Evaluating the Longitudinal Impact Using Neurological and Nutritional Endpoints Birth Cohort study from July 2009 to October 2011. Measurements of TEWL were made at birth (day 2) and at 2 and 6 months. The presence of AD was ascertained at 6 and 12 months, and disease severity was assessed by using the SCORing Atopic Dermatitis clinical tool at 6 months and by using both the SCORing Atopic Dermatitis clinical tool and Nottingham Severity Score at 12 months. A total of 1300 infants were genotyped for FLG mutations.
RESULTS:
At 6 months, 18.7% of the children had AD, and at 12 months, 15.53%. In a logistic regression model, day 2 upper quartile TEWL measurement was significantly predictive of AD at 12 months (area under the receiver operating characteristic curve, 0.81; P < .05). Lowest quartile day 2 TEWL was protective against AD at 12 months. An upper quartile 2 month TEWL was also strongly predictive of AD at 12 months (area under the receiver operating characteristic curve, 0.84; P < .05). At both ages, this effect was independent of parental atopy, FLG status, or report of an itchy flexural rash at 2 months. Associations were increased when parental atopy status or child FLG mutation status was added into the linear regression model.
CONCLUSIONS:
Impairment of skin barrier function at birth and at 2 months precedes clinical AD. In addition to providing important mechanistic insights into disease pathogenesis, these findings have implications for the optimal timing of interventions for the prevention of AD | en |
dc.format.extent | 930-5.e1 | en |
dc.relation.ispartofseries | The Journal of allergy and clinical immunology | en |
dc.relation.ispartofseries | 135 | en |
dc.relation.ispartofseries | 4 | en |
dc.rights | Y | en |
dc.subject | Infant | en |
dc.subject | skin barrier | en |
dc.subject | TEWL | en |
dc.subject | atopic dermatitis | en |
dc.subject | filaggrin | en |
dc.subject | predictor | en |
dc.subject | biomarker | en |
dc.title | Skin barrier dysfunction measured by transepidermal water loss at 2 days and 2 months predates and predicts atopic dermatitis at 1 year. | en |
dc.type | Journal Article | en |
dc.type.supercollection | scholarly_publications | en |
dc.type.supercollection | refereed_publications | en |
dc.identifier.peoplefinderurl | http://people.tcd.ie/irvinea | en |
dc.identifier.rssinternalid | 107262 | en |
dc.identifier.doi | http://dx.doi.org/10.1016/j.jaci.2014.12.013 | en |
dc.rights.ecaccessrights | openAccess | |
dc.identifier.orcid_id | 0000-0002-9048-2044 | en |