title: Genetic and perinatal factors as risk for childhood type 1 diabetes.
abstract: The mechanisms by which gestational infections, blood incompatibility, birth weight, mother's age and other prenatal or neonatal events increase the risk for type 1 diabetes are not understood. Studies so far have been retrospective, and there is a lack of population-based prospective studies. The possibility of identifying children at type 1 diabetes risk among first-degree relatives has resulted in prospective studies aimed at identifying postnatal events associated with the appearance of autoantibody markers for type 1 diabetes and a possible later onset of diabetes. However, the majority (85%) of new onset type 1 diabetes children do not have a first-degree relative with the disease. Population-based studies are therefore designed to prospectively analyse pregnant mothers and their offspring. One such study is DiPiS (Diabetes Prediction in Skåne), which is examining a total of about 10,000 pregnancies expected every year in the Skåne (Scania) region of Sweden that has 1.1 million inhabitants. Blood samples from all mothers in this region are obtained during pregnancy and at the time of delivery. Cord blood is analysed for HLA high-risk alleles and for autoantibodies against the 65 kD isoform of glutamic acid decarboxylase (GADA), the protein tyrosine phosphatase-related IA-2 antigen (IA-2A) and insulin (IAA) as a measure of prenatal autoimmune exposure. Identifying high-risk children by genetic, autoimmune and gestational risk factors followed by prospective analyses will make it possible to test the hypothesis that gestational events may trigger beta cell autoimmunity as a prerequisite for childhood type 1 diabetes.
authors.affiliation: Department of Paediatrics, Kristianstad Hospital, Kristianstad, Sweden. karin.larsson@litcon.se
authors.forename: Karin
authors.initials: K
authors.lastname: Larsson
authors.forename: Helena
authors.initials: H
authors.lastname: Elding-Larsson
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Cederwall
authors.forename: Karin
authors.initials: K
authors.lastname: Kockum
authors.forename: Jan
authors.initials: J
authors.lastname: Neiderud
authors.forename: Sture
authors.initials: S
authors.lastname: Sjöblad
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindberg
authors.forename: Barbro
authors.initials: B
authors.lastname: Lernmark
authors.forename: Corrado
authors.initials: C
authors.lastname: Cilio
authors.forename: Sten-A
authors.initials: SA
authors.lastname: Ivarsson
authors.forename: Ake
authors.initials: A
authors.lastname: Lernmark
mesh_terms: D015551:Autoimmunity; D001787:Blood Group Incompatibility / Q000150:complications*; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000503:physiopathology; D007239:Infections / Q000150:complications*; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D011248:Pregnancy Complications; D012307:Risk Factors