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5. Resistance to activated protein C (APCR) in children with acute lymphoblastic leukaemia???the need for a prospective multicentre study

Author

Nowak-G??ttl, U., primary, Aschka, I., additional, Koch, H. G., additional, Boos, J., additional, Dockhorn-Dworniczak, B., additional, Deufel, T., additional, J??rgens, H., additional, Kohlhase, B., additional, Kuhn, N., additional, Laupert, A., additional, Rath, B., additional, Wolff, J. E. A., additional, and Schneppenheim, R., additional

Published
1995
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9. Thromboembolism and resistance to activated protein C in children with underlying cardiac disease

Author

Kohlhase, B., Vielhaber, H., Kehl, H.G., Kececioglu, D., Koch, H.G., and Nowak-Gottl, U.

Abstract

OBJECTIVES: In the majority of cases, resistance to activated protein C is caused by the point mutation Arg^5^0^6 to Gln in the factor V gene and has emerged as the most important hereditary cause of thromboembolism. METHODS: To determine to what extent resistance to activated protein C was present in children with thromboembolism and underlying cardiac disease, its occurrence was retrospectively investigated. By using a method based on activated partial thromboplastin time, with DNA technique derived from the polymerase chain reaction, we investigated nine children with underlying cardiac disease in whom thromboembolism had previously occurred. RESULTS: Heterozygous Arg^5^0^6-to-Gln mutation in the factor V gene was diagnosed in five of the nine children investigated. In addition, protein C type I deficiency w as found in three patients, and two of the nine children showed increased lipoprotein (a) plasma values. Risk factors were present in all children with symptoms. CONCLUSIONS: These data indicate that deficiencies in the protein C anticoagulant pathway are likely to play an important role in the early manifestation of thromboembolism in children with underlying cardiac disease. (J Pediatr 1996;129:677-9)

Published
1996
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10. Resistance to activated protein C (APCR) in children with acute lymphoblastic leukaemia--the need for a prospective multicentre study.

Author

Nowak-Göttl U, Aschka I, Koch HG, Boos J, Dockhorn-Dworniczak B, Deufel T, Jürgens H, Kohlhase B, Kuhn N, and Laupert A

Subjects
Adolescent, Antithrombin III metabolism, Child, Child, Preschool, Factor V metabolism, Female, Humans, Infant, Male, Prospective Studies, Protein S metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma physiopathology, Protein C metabolism
Abstract

Activated protein C resistance (APCR), usually due to the Arg506-->Gln point mutation of the factor V gene, has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT based method in the presence of APC, together with a DNA technique based on the polymerase chain reaction, we investigated 65 leukaemic children and 65 age-matched healthy controls for the presence of this mutation. In both groups three children showed APCR. All six children showed the common factor V gene mutation, Arg506-->Gln. Although no child in the control group presented with thrombosis, all three children with acute lymphoblastic leukaemia had thromboembolic events. Whether the poor anticoagulant response to activated protein C in leukaemic children treated with prednisone, vincristine, daunorubicin and asparaginase affects the risk of thrombotic events requires a more extensive multicentre study.

Published
1995
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