title: Maternal hyperinsulinism and glycaemic status in the first trimester of pregnancy are associated with the development of pregnancy-induced hypertension and gestational diabetes.
abstract: OBJECTIVE
  To evaluate the relationships across a range of glucose and insulin measures at 12 weeks of gestation with the development of pregnancy-induced hypertension (PIH), gestational diabetes mellitus (GDM) and birth size.
  
  
  METHODS
  Prospective study of pregnant women booking before 15th week of gestation. At the first antenatal visit, standard measures of height, weight, blood pressure (BP) and social status were recorded, and blood sample was drawn for measurements of fasting glucose and plasma insulin. Oral glucose tolerance test with 75  g glucose load was performed after overnight fast. Odds ratios (ORs) with 95% CI were calculated to determine the risk of developing PIH or GDM depending on quartiles of blood glucose or tertiles of plasma insulin levels.
  
  
  RESULTS
  One thousand six hundred and fifty pregnant women were included in the study. Of them, 1484 delivered a live infant of whom 70 were preterm, 166 did not complete the study, 155 mothers developed PIH (10.4%), 18 were diagnosed with GDM (1.2%) and four had both PIH and GDM. At 12 weeks of gestation, women who became hypertensive were heavier (P<0.001), with higher BMI (P<0.001) than controls. Both systolic (P<0.001) and diastolic BPs (P<0.001) were already higher in women who developed PIH. Fasting insulin concentrations were higher in PIH group (P<0.002). Fasting glucose level >6.8 mmol/l was associated with the likelihood of delivering a macrosomic baby (OR 3.1 (95% CI: 1.21-8.0); P=0.02); the effect was heightened in multiparous mothers (OR 4.0 (95% CI: 1.4-11.1); P=0.01). Fasting plasma insulin had, however, no effect on size at birth in this study.
  
  
  CONCLUSIONS
  Our data suggest that women who develop PIH may be metabolically challenged at early stages of pregnancy with hyperinsulinism, insulin insensitivity and slightly higher BP.
authors.affiliation: Developmental Endocrinology Research Group, Clinical and Molecular Genetics Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK.
authors.forename: Simon
authors.initials: S
authors.lastname: Kayemba-Kay's
authors.forename: Catherine
authors.initials: C
authors.lastname: Peters
authors.forename: Michael P P
authors.initials: MP
authors.lastname: Geary
authors.forename: Nathan R
authors.initials: NR
authors.lastname: Hill
authors.forename: David R
authors.initials: DR
authors.lastname: Mathews
authors.forename: Peter C
authors.initials: PC
authors.lastname: Hindmarsh
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015331:Cohort Studies; D016640:Diabetes, Gestational / Q000453:epidemiology / Q000209:etiology*; D005260:Female; D005500:Follow-Up Studies; D006785:Hospitals, University; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D046110:Hypertension, Pregnancy-Induced / Q000453:epidemiology / Q000209:etiology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008131:London / Q000453:epidemiology; D010044:Outpatient Clinics, Hospital; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D011261:Pregnancy Trimester, First; D047928:Premature Birth / Q000453:epidemiology / Q000209:etiology; D015995:Prevalence; D011446:Prospective Studies
chemical_list: D001786:Blood Glucose; D007328:Insulin