title: [Prevalence of ICA antibodies, anti-GAD and antylA-2 in women with gestational diabetes treated with diet].
abstract: Gestational diabetes is considered an important factor complicating foetal development. Furthermore it might potentate the risk of type I maternal diabetes after delivery. Nowadays, on the basis of a detection of antibodies against islet cells (ICA, anti GAD, IA-2 IAA), we can recognize autoimmune disorders typical for the type I diabetes. Therefore, the aim of our study was to estimate the prevalence of islet cells autoantibodies in women with a history of gestational diabetes and to assess, if they might be a risk factor for foetus development and gestation outcome. Our investigations were carried out in 156 patients with the history of gestational diabetes (treated with diet), 6 weeks after delivery. ICA, anti GAD, IA-2, HbA1c and lipid profiles were estimated. Then IVGTT was performed to measure the first phase of insulin secretion. The number of previous abortions per number of pregnancies and birth weight of children were also assessed. In the population studied the most frequently detected antibodies were anti-GAD--7.0% and ICA--5.1%, less frequently--IA-2--3.2%. The prevalence of Abs was higher than in the healthy population but lower than observed among women with family history of type I diabetes. The presence of 2 types of antibodies was found in 3.8% of patients. In the group with the autoimmune disorders, significantly higher birth weights and more frequent failures of previous pregnancies were found.
  
  
  CONCLUSIONS
  the foregoing data suggest that the detection of antibodies against the beta cells in women with gestational diabetes might be a serious risk factor and a possible indication for early insulin treatment. As a result the better prognosis of gestation outcome is expected. However, we believe that the further prospective studies are required to verify our statement.
authors.affiliation: Zakładu Patofizjologii Ciazy Instytutu Połoznictwa i Chorób Kobiecych, Akademii Medycznej w Białymstoku.
authors.forename: M
authors.initials: M
authors.lastname: Kinalski
authors.forename: A
authors.initials: A
authors.lastname: Kretowski
authors.forename: B
authors.initials: B
authors.lastname: Telejko
authors.forename: I
authors.initials: I
authors.lastname: Kowalska
authors.forename: P
authors.initials: P
authors.lastname: Bingley
authors.forename: I
authors.initials: I
authors.lastname: Kinalska
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D016640:Diabetes, Gestational / Q000178:diet therapy* / Q000276:immunology*; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D005260:Female; D018698:Glutamic Acid / Q000276:immunology; D006801:Humans; D007328:Insulin / Q000276:immunology; D007515:Islets of Langerhans / Q000276:immunology*; D011247:Pregnancy; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000276:immunology; D011863:Radioimmunoassay
chemical_list: D001323:Autoantibodies; D004040:Dietary Carbohydrates; D007328:Insulin; D018698:Glutamic Acid; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases