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Lipoprotein (a): its role in childhood thromboembolism

U Nowak-Göttl1, O Debus, M Findeisen

  • 1Department of Paediatrics, University Hospital, Münster, Germany.

Pediatrics
|June 1, 1997
PubMed

Insights

Elevated lipoprotein (a) levels are linked to childhood thrombosis. This study investigated lipoprotein (a) in children with arterial or venous clots, finding it a significant risk factor.

Area of Science:

  • Pediatric Thrombosis Research
  • Cardiovascular Risk Factors
  • Lipoprotein Metabolism

Background:

  • Elevated lipoprotein (a) [Lp (a)] is an independent risk factor for coronary heart disease and stroke in young adults.
  • The role of Lp (a) in childhood thromboembolism requires further clarification.
  • Thromboembolism in children necessitates understanding underlying risk factors.

Purpose of the Study:

  • To investigate the role of elevated lipoprotein (a) concentrations in pediatric thromboembolism.
  • To measure Lp (a) levels in children diagnosed with arterial or venous thrombosis.
  • To assess the association between Lp (a) and other thrombotic risk factors in children.

Main Methods:

  • Lp (a) levels were measured in 72 children with thromboembolism (36 arterial, 36 venous).
  • Investigated defects in the protein C anticoagulant system, antithrombin, and antiphospholipid antibodies.
  • Assessed the prevalence of factor V Leiden mutation and protein C deficiency.

Main Results:

  • Elevated Lp (a) (>50 mg/dL) was found in 8/36 children with arterial and 5/36 with venous thrombosis.
  • Factor V Leiden mutation was present in 25 children, protein C deficiency in 10, antithrombin deficiency in 2, and antiphospholipid syndrome in 4.
  • Three children with high Lp (a) had factor V Leiden mutation; one also had protein C deficiency.

Conclusions:

  • Increased concentrations of lipoprotein (a) are implicated as a significant factor in childhood thrombosis.
  • Lp (a) may contribute to the pathogenesis of thromboembolic events in pediatric populations.
  • Further research is warranted to elucidate the precise mechanisms linking Lp (a) to childhood thrombosis.
Abstract

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