Original Article

Journal of Perinatology (2005) 25, 134–138. doi:10.1038/sj.jp.7211222 Published online 4 November 2004

Prothrombotic Risk Factors in Infants of Diabetic Mothers

The project was supported by a fellowship research grant from the Department of Neonatology, University of Connecticut.

Presented, in part, as a poster at the Society for Pediatric Research meeting, Baltimore, MD, May, 2002.

Shikha Sarkar MD1, Nathan J Hagstrom MD2, Charles J Ingardia MD4,5, Trudy Lerer MS3 and Victor C Herson MD1

  1. 1Department of Pediatrics, Divisions of Neonatology (S.S., V.C.H.), Connecticut Children's Medical Center, Hartford, CT, USA
  2. 2Department of Pediatrics, Division of Hematology-Oncology (N.J.H.), Connecticut Children's Medical Center, Hartford, CT, USA
  3. 3Department of Pediatrics, Division of Research (T.L.), Connecticut Children's Medical Center, Hartford, CT, USA
  4. 4Department of Obstetrics and Gynecology (C.J.I.), Hartford Hospital, Hartford, CT, USA
  5. 5University of Connecticut School of Medicine (C.J.I.), Farmington, CT, USA

Correspondence: Victor Herson, MD, Department of Pediatrics, Division of Neonatology, Connecticut Children's Medical Center, 282 Washington Street, Hartford, CT 06106, USA

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Abstract

BACKGROUND:

 

Infants of diabetic mothers (IDMs) are at an increased risk for thromboembolic disease. The mechanism(s) to explain this association is unclear. We hypothesized that the pathophysiology of thrombosis in IDMs is multifactorial and likely involves interactions among genetic and acquired factors affecting the procoagulant, anticoagulant and fibrinolytic pathways.

OBJECTIVE:

 

To compare the prevalence of common prothrombotic risk factors in a cohort of IDMs to a matched control group.

PATIENTS/METHODS:

 

Full-term infants born to mothers with diet controlled (A1-IDM) (N=17), insulin requiring diabetes (ID-IDM) (N=20) and healthy term infants (controls) (N=20) matched for mode of delivery had cord blood collected at delivery. Samples were analyzed for the following: factor V Leiden (FVL), prothrombin 20210A (P20210A), methylenetetrahydrofolate reductase C677 T (MTHFR), Factor VIII (FVIII), Protein C (PC), Lipoprotein(a) (Lp(a)) and plasminogen activator inhibitor-1 (PAI-1).

RESULTS:

 

None of the infants had a clinically apparent thrombotic event. IDM mothers and their infants were clinically similar to controls except for a higher prevalence of hypoglycemia (30 vs 0%; p=0.005). There was no significant difference in the prevalence of the common genetic risk factors (FVL, P20210A, MTHFR) FVIII, or PAI-1 levels. Elevated Lp(a) levels were seen more frequently in IDMs than Controls (40 vs 20%) but this difference was not statistically significant. The PC activity (%) was significantly decreased in the IDM group compared to controls, 35plusminus12 vs 44plusminus9 (p<0.005). A1-IDM had lower PC activity compared to ID-IDM (p=0.05) and controls (p=0.001).

CONCLUSIONS:

 

PC deficiency is likely one mechanism to explain thrombosis in IDMs.

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