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Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/29107
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dc.contributor.authorHarris M.en
dc.contributor.authorThomson R.L.en
dc.contributor.authorVuillermin P.J.en
dc.contributor.authorWentworth J.M.en
dc.contributor.authorHarrison L.C.en
dc.contributor.authorCouper J.J.en
dc.contributor.authorSoldatos G.en
dc.contributor.authorPenno M.A.S.en
dc.contributor.authorOakey H.en
dc.contributor.authorAugustine P.en
dc.contributor.authorTaranto M.en
dc.contributor.authorBarry S.C.en
dc.contributor.authorColman P.G.en
dc.contributor.authorCraig M.E.en
dc.contributor.authorDavis E.A.en
dc.contributor.authorGiles L.C.en
dc.contributor.authorHaynes A.en
dc.contributor.authorMcGorm K.en
dc.contributor.authorMorahan G.en
dc.contributor.authorMorbey C.en
dc.contributor.authorRawlinson W.D.en
dc.contributor.authorSinnott R.O.en
dc.date.accessioned2021-05-14T09:49:23Zen
dc.date.available2021-05-14T09:49:23Zen
dc.date.copyright2020en
dc.date.created20200928en
dc.date.issued2020-09-28en
dc.identifier.citationPediatric Diabetes. 21 (6) (pp 945-949), 2020. Date of Publication: 01 Sep 2020.en
dc.identifier.issn1399-543Xen
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/29107en
dc.description.abstractBackgrounds: We aimed to monitor pancreatic exocrine function longitudinally in relation to the development of islet autoimmunity (IA) and type 1 diabetes (T1D) in at-risk children with a first-degree relative with T1D, who were followed prospectively in the Environmental Determinants of Islet Autoimmunity (ENDIA) study. Method(s): Fecal elastase-1 (FE-1) concentration was measured longitudinally in 85 ENDIA children from median age 1.0 (IQR 0.7,1.3) year. Twenty-eight of 85 children (progressors) developed persistent islet autoantibodies at median age of 1.5 (IQR 1.1,2.5) years, of whom 11 went on to develop clinical diabetes. The other 57 islet autoantibody-negative children (non-progressors) followed similarly were age and gender-matched with the progressors. An adjusted linear mixed model compared FE-1 concentrations in progressors and non-progressors. Result(s): Baseline FE-1 did not differ between progressors and non-progressors, or by HLA DR type or proband status. FE-1 decreased over time in progressors in comparison to non-progressors (Wald statistic 5.46, P =.02); in some progressors the fall in FE-1 preceded the onset of IA. Conclusion(s): Pancreatic exocrine function decreases in the majority of young at-risk children who progress to IA and T1D.Copyright © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltden
dc.languageEnglishen
dc.languageenen
dc.publisherBlackwell Publishing Ltd (E-mail: info@royensoc.co.uk)en
dc.relation.ispartofPediatric Diabetesen
dc.subject.meshinsulin dependent diabetes mellitus-
dc.subject.meshpancreas function-
dc.subject.meshpancreas islet-
dc.subject.meshpatient monitoring-
dc.subject.meshpediatric patient-
dc.subject.meshhigh risk-
dc.subject.meshstatistical-
dc.subject.meshenzyme linked immunosorbent assay-
dc.subject.meshfeces level-
dc.subject.meshfirst-degree relative-
dc.subject.meshgender-
dc.subject.meshautoantibody-
dc.subject.meshglutamate decarboxylase antibody-
dc.subject.meshHLA DR antigen-
dc.subject.meshinsulin antibody-
dc.subject.meshpancreatic elastase-
dc.subject.meshELISA kit-
dc.subject.meshlinear mixed-
dc.subject.meshtyrosine phosphatase related islet antigen 2 antibody-
dc.subject.meshzinc transporter 8 antibody-
dc.subject.meshautoimmunity-
dc.titleChanges in pancreatic exocrine function in young at-risk children followed to islet autoimmunity and type 1 diabetes in the ENDIA study.en
dc.typeArticleen
dc.identifier.affiliationDiabetes and Vascular Medicine-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1111/pedi.13056-
dc.publisher.placeUnited Kingdomen
dc.identifier.pubmedid32430977 [http://www.ncbi.nlm.nih.gov/pubmed/?term=32430977]en
dc.identifier.source2005193675en
dc.identifier.institution(Penno, Oakey, Barry, McGorm, Thomson, Couper) Robinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia (Augustine, Couper) Department of Diabetes and Endocrinology, Women's and Children's Hospital, Adelaide, SA, Australia (Taranto) PathWest Laboratories, Fiona Stanley Hospital Network, Murdoch, WA, Australia (Colman, Wentworth) Department of Diabetes and Endocrinology, Royal Melbourne Hospital, Melbourne, VIC, Australia (Craig) School of Women's and Children's Health, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia (Craig) Institute of Endocrinology and Diabetes, The Children's Hospital at Westmead, Sydney, NSW, Australia (Davis, Haynes) Telethon Institute for Child Health Research, Centre for Child Health Research, The University of Western Australia, Perth, WA, Australia (Giles) Robinson Research Institute, School of Public Health, University of Adelaide, Adelaide, SA, Australia (Harris) The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, QLD, Australia (Harris) Endocrinology Department, Queensland Children's Hospital, South Brisbane, QLD, Australia (Morahan) Centre for Diabetes Research, Harry Perkins Institute of Medical Research, The University of Western Australia, Perth, WA, Australia (Morbey) Hunter Diabetes Centre, Newcastle, NSW, Australia (Rawlinson) Virology Research Laboratory, Serology and Virology Division, South Eastern Area Laboratory Services Microbiology, Prince of Wales Hospital, Sydney, NSW, Australia (Rawlinson) School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia (Sinnott) Melbourne eResearch Group, School of Computing and Information Services, University of Melbourne, Melbourne, VIC, Australia (Soldatos) Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia (Soldatos) Diabetes and Vascular Medicine Unit, Monash Health, Melbourne, VIC, Australia (Vuillermin) Faculty of Health, School of Medicine, Deakin University, Geelong, VIC, Australia (Vuillermin) Child Health Research Unit, Barwon Health, Geelong, VIC, Australia (Wentworth, Harrison) Population Health and Immunity Division, Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australiaen
dc.description.addressJ.J. Couper, Robinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia. E-mail: jennifer.couper@adelaide.edu.au J.J. Couper, Department of Diabetes and Endocrinology, Women's and Children's Hospital, Adelaide, SA, Australia. E-mail: jennifer.couper@adelaide.edu.auen
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2020 Elsevier B.V., All rights reserved.en
dc.subect.keywordschildren exocrine pancreas fecal elastase islet autoimmunity type 1 diabetesen
dc.identifier.authoremailCouper J.J.; jennifer.couper@adelaide.edu.auen
dc.description.grantOrganization: (JDRF) *Juvenile Diabetes Research Foundation United States of America* Organization No: 100008871 Country: United States Organization: (NHMRC) *National Health and Medical Research Council* Organization No: 501100000925 Country: Australia Organization: *Juvenile Diabetes Research Foundation Australia* Organization No: 501100001067 Country: Australia Organization: *Leona M. and Harry B. Helmsley Charitable Trust* Organization No: 100007028 Country: United Statesen
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.openairetypeArticle-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptOncology-
crisitem.author.deptEndocrinology-
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