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Heparin cofactor II in adults and infants with thrombosis and DIC
A Chuansumrit1, M J Manco-Johnson, W E Hathaway
1Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.
Insights
Heparin cofactor II (HC II) levels are lower in preterm and term infants due to immature liver function. Significantly reduced HC II activity was observed in infants with disseminated intravascular coagulation.
Area of Science:
- Biochemistry
- Pediatric Hematology
- Coagulation Science
Background:
- Heparin cofactor II (HC II) is a key inhibitor of thrombin.
- Understanding HC II levels in neonates is crucial for assessing coagulation status.
Purpose of the Study:
- To measure Heparin cofactor II (HC II) activity in preterm infants, full-term infants, and adults.
- To investigate factors influencing HC II levels in different pediatric populations.
Main Methods:
- Chromogenic activity assay was used to quantify HC II levels.
- Study included normal preterm infants, normal full-term infants, and normal adults.
- HC II activity was also assessed in specific patient groups, including those with thrombosis history, protein C/S deficiency, and disseminated intravascular coagulation.
Main Results:
- Preterm infants (29%) and full-term infants (49%) showed lower HC II activity compared to adults (101%).
- Children reached adult HC II levels by 5-7 months of age.
- Significantly lower HC II activity was found in infants with disseminated intravascular coagulation.
Conclusions:
- Lower HC II levels in neonates are likely due to immature liver function.
- HC II activity is not significantly reduced in individuals with thrombosis history or protein C/S deficiency.
- Disseminated intravascular coagulation is associated with markedly decreased HC II activity in infants.
Abstract:
Heparin cofactor II (HC II) was measured by a chromogenic activity assay in normal preterm infants (gestational age, 28-36 weeks; n = 17; 29% +/- 11.5 [mean +/- 1 SD], range 11-51), normal full-term infants (n = 18; 49% +/- 6.6 [mean +/- 1 SD], range 36-58), and normal adults (n = 38; 101% +/- 14 [mean +/- 1 SD], range 73-130). Normal children attained adult levels at approximately 5 to 7 months of age. The lower values in preterm and term infants most likely reflect immature liver function. Neither adults and children with a history of thrombosis with prior negative evaluation (n = 74), patients with documented protein C and protein S deficiency (n = 4), nor sick infants without evidence of consumptive coagulopathy (n = 15) had significantly lower levels of HC II activity. Infants with disseminated intravascular coagulation (n = 2) had strikingly lower levels of HC II activity.