title: Metabolic control and progression of retinopathy. The Diabetes in Early Pregnancy Study. National Institute of Child Health and Human Development Diabetes in Early Pregnancy Study.
abstract: OBJECTIVE
  To evaluate the role of metabolic control in the progression of diabetic retinopathy during pregnancy.
  
  
  METHODS
  We conducted a prospective cohort study of 155 diabetic women in the Diabetes in Early Pregnancy Study followed from the periconceptional period to 1 month postpartum. Fundus photographs were obtained shortly after conception (95% within 5 weeks of conception) and within 1 month postpartum. Glycosylated hemoglobin was measured weekly during the 1st trimester and monthly thereafter.
  
  
  RESULTS
  In the 140 patients who did not have proliferative retinopathy at baseline, progression of retinopathy was seen in 10.3, 21.1, 18.8, and 54.8% of patients with no retinopathy, microaneurysms only, mild nonproliferative retinopathy, and moderate-to-severe nonproliferative retinopathy at baseline, respectively. Proliferative retinopathy developed in 6.3% with mild and 29% with moderate-to-severe baseline retinopathy. Elevated glycosylated hemoglobin at baseline and the magnitude of improvement of glucose control through week 14 were associated with a higher risk of progression of retinopathy (adjusted odds ratio for progression in those with glycohemoglobin > or = 6 SD above the control mean versus those within 2 SD was 2.7; 95% confidence interval was 1.1-7.2; P = 0.039).
  
  
  CONCLUSIONS
  The risk for progression of diabetic retinopathy was increased by initial glycosylated hemoglobin elevations as low as 6 SD above the control mean. This increased risk may be due to suboptimal control itself or to the rapid improvement in metabolic control that occurred in early pregnancy. Excellent metabolic control before conception may be required to avoid this increase in risk. Those with moderate-to-severe retinopathy at conception need more careful ophthalmic monitoring, particularly if their diabetes was suboptimally controlled at conception.
authors.affiliation: Division of Biometry and Epidemiology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-2510, USA.
authors.forename: E Y
authors.initials: EY
authors.lastname: Chew
authors.forename: J L
authors.initials: JL
authors.lastname: Mills
authors.forename: B E
authors.initials: BE
authors.lastname: Metzger
authors.forename: N A
authors.initials: NA
authors.lastname: Remaley
authors.forename: L
authors.initials: L
authors.lastname: Jovanovic-Peterson
authors.forename: R H
authors.initials: RH
authors.lastname: Knopp
authors.forename: M
authors.initials: M
authors.lastname: Conley
authors.forename: L
authors.initials: L
authors.lastname: Rand
authors.forename: J L
authors.initials: JL
authors.lastname: Simpson
authors.forename: L B
authors.initials: LB
authors.lastname: Holmes
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D015331:Cohort Studies; D016001:Confidence Intervals; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D005313:Fetal Death / Q000453:epidemiology; D005451:Fluorescein Angiography; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D011254:Pregnancy in Diabetics / Q000097:blood / Q000503:physiopathology*; D011446:Prospective Studies; D011644:Puerperal Disorders / Q000503:physiopathology; D012016:Reference Values
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin