부산대학교 도서관

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1399-5448.2007.00349.x Byline: Maria Elfving (a), Bengt Lindberg (b), Kristian Lynch (c), Majvi Mansson (b), Goran Sundkvist (d), Ake Lernmark (c,e), Sten A Ivarsson (b) Keywords: cord blood; HLA; islet autoantibodies; type 1 (insulin-dependent) diabetes mellitus Abstract: Objective: Cord blood islet autoantibodies in children born to mothers with type 1 diabetes may be associated with a reduced risk of islet autoimmunity and diabetes. The aim of this study was to investigate in children with type 1 diabetes but born to non-diabetic mothers whether islet autoantibodies at birth affected their presence at diagnosis. Patients and methods: Serum samples at birth and at diagnosis were available from 141 children who developed type 1 diabetes between 1 and 19 yr of age (median 9.0 yr; male/female ratio 83/58). The samples were tested for autoantibodies against glutamic acid decarboxylase, insulinoma-associated antigen 2, and insulin as well as for islet cell antibodies. The human leukocyte antigen genotype was also determined. Results: The frequency of islet autoantibodies in the umbilical cord blood was 11% compared with 91% at diagnosis. Children with fewer islet autoantibodies at diagnosis were more likely to have had autoantibodies at birth (p = 0.02). Autoantibodies present in cord blood at birth were observed in 25% (3/12) of children with no islet autoantibodies at diagnosis, in 17% (7/42) of children with one or two antibodies at diagnosis, and in only 5% (4/86) of children with more than two antibodies, demonstrating an inverse relationship between autoantibodies at birth and at diagnosis (test for trend, p < 0.001). Conclusions: Our preliminary data suggest that exposure to cord blood islet autoantibodies may influence the presence of islet autoantibodies at the time of diagnosis of type 1 diabetes and explain why some type 1 diabetes children are islet autoantibody negative at clinical diagnosis. Author Affiliation: (a)Department of Clinical Sciences, Pediatric Unit, Lund University Hospital, Lund University, Lund, Sweden (b)Department of Clinical Sciences, Pediatric Unit, Malmo University Hospital, Lund University, Malmo, Sweden (c)Department of Clinical Sciences, Diabetes and Celiac Disease Unit, Malmo University Hospital, Lund University, Malmo, Sweden (d)Department of Clinical Sciences, Diabetes Epidemiology and Neuropathy Unit, Malmo University Hospital, Lund University, Malmo, Sweden (e)Department of Medicine, University of Washington, Seattle, WA, USA Article History: Submitted 22 July 2007. Accepted for publication 8 October 2007 Article note: Maria Elfving, MD, Department of Clinical Sciences, Pediatric Unit, Lund University Hospital, Lund University, Lund SE-221 85, Sweden., Tel: +46-46-171000; fax: +46-46-178035; e-mail: maria.elfving@skane.se