title: Subclinical inflammation and vascular dysfunction in women with previous gestational diabetes mellitus.
abstract: BACKGROUND
  A history of gestational diabetes (GDM) significantly increases the risk of developing type 2 diabetes, an independent risk factor for cardiovascular disease (CVD). It is not known whether nondiabetic women with prior GDM are also at increased risk of CVD.
  
  
  OBJECTIVE
  The aim of this study was to compare biochemical and hemodynamic surrogate markers of CVD in nondiabetic women with and without a history of GDM who were at least 1 yr post delivery.
  
  
  METHODS
  This was a single center cross-sectional study.
  
  
  METHODS
  The study was performed in an academic referral center.
  
  
  METHODS
  Forty-eight premenopausal healthy women with a history of GDM (n = 25) or a history of normal pregnancy (n = 23) were studied in the follicular phase of the menstrual cycle.
  
  
  METHODS
  The main outcome measures were: 1) inflammatory markers associated with CVD including C-reactive protein, IL-6, and plasminogen activator inhibitor-1; 2) the adipokine adiponectin; and 3) conduit vessel stiffness.
  
  
  RESULTS
  When compared to normal controls, women with prior GDM had higher mean levels of C-reactive protein (3.58 +/- 3.86 vs. 0.52 +/- 0.16 mg/liter; P < 0.001), IL-6 (1.81 +/- 1.04 vs. 0.99 +/- 0.52 pg/ml; P = 0.001), plasminogen activator inhibitor-1 (29.6 +/- 17.6 vs. 16.5 +/- 14.0 ng/ml; P = 0.001), and lower levels of adiponectin (8.9 +/- 3.9 vs. 15.9 +/- 7.3 microg/ml; P = 0.001). Women with prior GDM also had significantly (P </= 0.04) increased peripheral vascular resistance (1658 +/- 290 vs. 1462 +/- 340 dyne.sec/cm(5)), decreased stroke volume (65 +/- 13 vs. 75 +/- 14 ml/beat), and decreased cardiac output (70 +/- 12 vs. 74 +/- 13 ml/sec) when compared to controls, after adjusting for body mass index.
  
  
  CONCLUSIONS
  Nondiabetic women with prior GDM have evidence of subclinical inflammation, hypoadiponectinemia, and early vascular dysfunction; this population may be at increased risk of developing CVD.
authors.affiliation: Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. sheitritter@partners.org.
authors.forename: Shannon M
authors.initials: SM
authors.lastname: Heitritter
authors.forename: Caren G
authors.initials: CG
authors.lastname: Solomon
authors.forename: Gary F
authors.initials: GF
authors.lastname: Mitchell
authors.forename: Nadia
authors.initials: N
authors.lastname: Skali-Ounis
authors.forename: Ellen W
authors.initials: EW
authors.lastname: Seely
mesh_terms: D052242:Adiponectin; D000328:Adult; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology*; D003430:Cross-Sectional Studies; D016640:Diabetes, Gestational / Q000150:complications* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011247:Pregnancy; D014655:Vascular Resistance
chemical_list: D052242:Adiponectin; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D002097:C-Reactive Protein