An 81-year-old man was referred to our department because of suspected factor VII (FVII) deficiency. His FVII activity was under 1%, whereas the FVII activity levels of his son and granddaughter were 65 and 109%, respectively. The nucleotide at position 3886 of his FVII gene
was homozygous for G. A single T to G substitution results in the replacement of wild-type Cys at residue 22 by Gly. His son was heterozygous for G and T at position 3886, whereas his granddaughter was homozygous for wild-type T. These results suggest that he was homozygous for FVII Cys22Gly.
He underwent radiofrequency ablation (RFA) for hepatocellular carcinoma, receiving 20 μg/kg of recombinant FVIIa prior to RFA and 10 μg/kg of recombinant FVIIa twice after RFA. He showed no bleeding tendency; however, a myocardial infarction was diagnosed and percutaneous coronary
intervention was performed.
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factor VII deficiency;
factor VII mutation;
recombinant factor VIIa
Document Type: Research Article
Department of Hematology
Department of Cardiovascular Medicine
Department of Gastroenterology, Tokushima Prefectural Central Hospital
Department of Medicine and Bioregulatory Sciences
Department of Medical Education, Graduated School of Health Biosciences, The University of Tokushima, Tokushima, Japan
December 1, 2015