title: Fibrinolytic dysfunction after gestation is associated to components of insulin resistance and early type 2 diabetes in latino women with previous gestational diabetes.
abstract: Among patients with metabolic syndrome (MS), atherosclerosis and abnormal fibrinolytic function are frequently present, mostly owing to an increase in plasminogen activator inhibitor-1(PAI-1). We analyze PAI-1 in pregnant women, both normal and with gestational diabetes (GDM) and postpartum regarding its correlation to MS surrogates. Clinical characteristics, glucose tolerance (100g-OGTT), lipids, PAI-1 antigen, insulin sensitivity (HOMA-S), and pancreatic beta-cell function (HOMA-B) were investigated in 34 women. Eleven had normal glucose tolerance (NGT) during pregnancy and 23 had GDM (all GAD antibodies-negative). All patients were studied at 28-34 weeks of gestation and 16-24 weeks after delivery (75 g-OGTT). Parameters of interest were determined using commercial test systems. During pregnancy, PAI-1 was not statistically different between NGT and GDM (47+/-25 ng/ml versus 47+/-28 ng/ml, p=0.9). After gestation, 19 (56%) women had NGT (11 of them from previous NGT group) and 15 (44%) had impaired glucose tolerance (IGT) or DM. The IGT (IGT+DM) group had higher PAI-1 (p=0.01), which did not decreased after delivery NGT-NGT before and after delivery (47+/-25 ng/ml versus 6+/-5 ng/ml; p<0.001), GDM-NGT (62+/-36 ng/ml versus 14+/-15 ng/ml; p=0.001) and GDM-IGT (39+/-20 ng/ml versus 27+/-23 ng/ml; p=0.15). PAI-1 levels were positively correlated (p<0.05) to total cholesterol (r(s)=0.37), triglycerides (r(s)=0.48), fasting plasma glucose (r(s)=0.52), 2-h plasma glucose in the OGTT (r(s)=0.58) and were negatively correlated (p<0.05) with HOMA-S (r(s)=-0.42) and HOMA-B (r(s)=-0.38). Fibrinolytic dysfunction is still present in GDM women and is associated with early development of IGT or T2DM. PAI correlated with surrogate markers of MS levels and may identify a group of women at risk for macroangiopathy.
authors.affiliation: Diabetes Center of Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Lilian K
authors.initials: LK
authors.lastname: Morimitsu
authors.forename: Annunciata S
authors.initials: AS
authors.lastname: Fusaro
authors.forename: Victor H
authors.initials: VH
authors.lastname: Sanchez
authors.forename: Cristiane C F
authors.initials: CC
authors.lastname: Hagemann
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Bertini
authors.forename: Sergio A
authors.initials: SA
authors.lastname: Dib
mesh_terms: D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D016640:Diabetes, Gestational / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology*; D007558:Italy; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D049590:Postpartum Period / Q000502:physiology; D011247:Pregnancy; D012016:Reference Values
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1