title: Relationship of fetal macrosomia to maternal postprandial glucose control during pregnancy.
abstract: OBJECTIVE
  To determine the gestational ages at which maternal hyperglycemia is most closely related to fetal macrosomia; to determine whether macrosomia is related to elevations of fasting glucose, postprandial glucose, or both; and to assess the relationship of macrosomia to maternal insulin dose and caloric intake.
  
  
  METHODS
  One hundred eleven consecutive pregnant women with Class B through RF diabetes were studied longitudinally from 13 to 36 wk gestation. Macrosomia was defined by birthweight greater than 90th percentile for gestational age based on California norms. Women who delivered macrosomic infants were compared with those without macrosomic infants on pre- and postprandial blood glucose, GHb, insulin dose, macronutrient intake, and several other maternal variables.
  
  
  RESULTS
  Macrosomia occurred in 32 (29%) cases, although several measures indicated reasonable glycemic control throughout pregnancy. Women delivering macrosomic infants did not differ from those without macrosomic infants in maternal age, prepregnant weight, duration of diabetes, White class, macronutrient intake, GHb, or fasting glucose. Macrosomia was associated with higher postprandial glucose levels up to 32 wk gestation and lower insulin doses from 29 to 36 wk gestation. In multiple logistic regression, macrosomia was significantly associated with postprandial glucose only between 29 and 32 wk gestation. Postprandial glucose values less than 7.3 mM (less than 130 mg/dl) were associated with a higher risk of small-for-gestational-age infants (18%) compared with values above this level (1%).
  
  
  CONCLUSIONS
  Because macrosomia was related to postprandial glucose but not fasting glucose, we conclude that postprandial glucose measurement should be a part of routine care for diabetes in pregnancy. A target 1-h postprandial glucose value of 7.3 mM (130 mg/dl) may be the level that optimally reduces the incidence of macrosomia without increasing the incidence of small-for-gestational-age infants.
authors.affiliation: Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco.
authors.forename: C A
authors.initials: CA
authors.lastname: Combs
authors.forename: E
authors.initials: E
authors.lastname: Gunderson
authors.forename: J L
authors.initials: JL
authors.lastname: Kitzmiller
authors.forename: L A
authors.initials: LA
authors.lastname: Gavin
authors.forename: E K
authors.initials: EK
authors.lastname: Main
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001724:Birth Weight; D001786:Blood Glucose / Q000378:metabolism*; D003927:Diet, Diabetic; D004435:Eating; D002149:Energy Intake; D005260:Female; D005320:Fetal Macrosomia / Q000453:epidemiology / Q000209:etiology*; D005865:Gestational Age; D006801:Humans; D015994:Incidence; D007231:Infant, Newborn; D007328:Insulin / Q000627:therapeutic use; D008423:Maternal Age; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D007328:Insulin