Factor V Leiden, protein C, and lipoprotein (a) in catheter-related thrombosis in childhood: A prospective study☆,☆☆
Section snippets
Methods
Over a 2-year period, 163 consecutively admitted infants and children, ranging in age from neonate to 18 years, were enrolled in the study. In addition, to compare the prevalence of familial thrombophilia, 155 age-matched, healthy children undergoing elective minor surgery (S) were investigated in the same fashion.
One hundred forty children (C) without previously diagnosed thromboembolism underwent diagnostic percutaneous venous cardiac catheterization, and in 105 of these 140 children, central
Results
No difference was seen in the prevalence of familial thrombophilia in the two age-matched populations studied: heterozygous factor V Leiden mutation was diagnosed in 20 of the 318 subjects (C: n = 5; B: n = 4; S: n = 11), homozygous factor V Leiden mutation was found in two subjects (C: n = 1; S: n = 1), protein C deficiency type I was diagnosed in nine subjects (C: n = 4; B: n = 1; S: n = 4), and five of the 318 subjects showed increased plasma concentrations of Lp (a) (C: n = 3; S: n = 2).
Discussion
Data from this prospective study demonstrate, both clinically and sonographically, 8, 9, 12 an 11% overall incidence of catheter-related thrombus formation in children with indwelling central lines, which was in most cases associated with genetic risk factors for familial thrombophilia. The factor V Leiden mutation, also stated to be a genetic risk factor for childhood thromboembolism, 15, 21, 22, 23 plays the major role in catheter-related thrombosis in the population studied. Deficiencies of
Acknowledgements
We thank Susan Griesbach for editing this manuscript.
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Reprint requests: Ulrike Nowak-Göttl, MD, Westfälische Wilhelms-Universität, Pediatric Hematology and Oncology, Albert-Schweitzer-Str. 33, D-48149 Münster, Germany.
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