Seroconversion to islet autoantibodies between early pregnancy and delivery in non-diabetic mothers.
Islet autoantibodies are currently used to classify type 1 diabetes at diagnosis as they reflect the autoimmune pathogenesis of the disease. The presence of maternal autoantibodies reactive with pancreatic islet antigens is thought to increase the risk for type 1 diabetes in the offspring. The objective of this study was to determine seroconversion to islet autoantibodies in non-diabetic mothers during pregnancy. Screening of 33,682 mothers between September 2000 and August 2004 in the Diabetes Prediction in Skåne (DiPiS) study showed that at delivery, 242 non-diabetic mothers had increased titers of islet autoantibodies reactive with glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A) or insulin (IAA), alone or in combination. Control mothers (n=1419), who were islet autoantibody negative at delivery, were randomly selected and matched by age, parity and pregnancy sampling date. Mothers positive for GADA (92%), IA-2A (84%) or IAA (65%) at delivery had increased titers already evident in early pregnancy. Titers declined for GADA (p<0.0001), IA-2A (p<0.0001) and IAA (p<0.0001). Seroconversion during pregnancy was observed for GADA in 10 (8%), IA-2A in 3 (16%) and IAA in 37 (35%) mothers. It is concluded that non-diabetic mothers with islet autoantibodies at delivery had significantly higher titers during early pregnancy than at delivery. As the statistical power in the seroconverting mothers was insufficient, further studies are needed to determine if the risk for type 1 diabetes in the offspring differs between mothers who already had increased titers of islet autoantibodies during early pregnancy or acquired them during pregnancy.
Department of Clinical Sciences, Diabetes and Celiac Disease Unit, Lund University/CRC, Skåne University Hospital SUS, 20502 Malmö, Sweden. sabina.lindehammer@med.lu.se
Sabina Resic
SR
Lindehammer
Ida
I
Hansson
Bo
B
Midberg
Sten Anders
SA
Ivarsson
Kristian Francis
KF
Lynch
Joakim
J
Dillner
Ake
A
Lernmark
D001323:Autoantibodies / Q000097:blood* / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000276:immunology; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D005865:Gestational Age; D005968:Glutamate Decarboxylase / Q000097:blood / Q000276:immunology*; D006801:Humans; D007328:Insulin / Q000097:blood / Q000276:immunology*; D007330:Insulin Antibodies / Q000097:blood; D007515:Islets of Langerhans / Q000276:immunology*; D036801:Parturition / Q000276:immunology; D011247:Pregnancy; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8 / Q000097:blood / Q000276:immunology*
D001323:Autoantibodies; D007328:Insulin; D007330:Insulin Antibodies; C516862:PTPRN protein, human; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase