Report on a disease-adapted treatment in a patient with severe factor X deficiency resulting from a homozygous factor X gene mutation

Thromb Haemost 2008; 99(01): 238-239
DOI: 10.1160/TH07-08-0486

Letters to the Editor

Schattauer GmbH

Andrea Gerhardt

¹Department of Hemostasis and Transfusion Medicine, Heinrich-Heine University Medical Center, Düsseldorf, Germany

,

Fatima Araba

¹Department of Hemostasis and Transfusion Medicine, Heinrich-Heine University Medical Center, Düsseldorf, Germany

,

Rüdiger E Scharf

¹Department of Hemostasis and Transfusion Medicine, Heinrich-Heine University Medical Center, Düsseldorf, Germany

,

Rainer B Zotz

¹Department of Hemostasis and Transfusion Medicine, Heinrich-Heine University Medical Center, Düsseldorf, Germany

References
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2 Dewerchin M, Liang Z, Moons L. et al. Blood coagulation factor X deficiency causes partial embryonic lethality and fatal neonatal bleeding in mice. Thromb Haemost 2000; 83: 185-190.
3 Al-Hilal A, Wulff K, Abdel-Razeq H. et al. Analysis of the novel factor X gene mutation Glu51Lys in two families with factor X-Riyad anomaly. Thromb Haemost 2007; 97: 542-545.
4 Peyvandi F, Menegatti M, Santagostino E. et al. Gene mutations and three-dimensional structural analysis in 13 families with severe Factor X deficiency. Br J Haematol 2002; 117: 685-692.
5 Todd T, Perry DJ, Hayman E. et al. Severe factor X deficiency due to a homozygous mutation (Cys364Arg) that disrupts a disulphide bond in the catalytic domain. Haemophilia 2006; 12: 621-624.
6 Kohler M. Thrombogenicity of prothrombin complex concentrates. Thromb Res 1999; 95: S13-17.