Factor X deficiency (also called Stuart-Prower factor deficiency) is an autosomal recessive disorder that manifests with prolonged nasal and mucosal hemorrhage, menorrhagia, hematuria, and occasionally hemarthrosis (bleeding in the joints). The disorder gets its original name from the names of the first two individuals identified with this form of bleeding disorder, Mr. Stuart and Miss Prower. Deficiency of factor X in females can be particularly troublesome as it will result adverse fetal outcomes such as recurrent spontaneous abortions, placental abruptions, and premature births.
The factor X protein is synthesized in the liver as a single polypeptide but is processed into a heavy chain and a light chain held together by disulfide bonds. As might be expected, due to the dependence of its serine protease activity on vitamin K-dependent carboxylation, factor X shows a high degree of homology to the other vitamin K-dependent factors of coagulation.
The factor X gene (symbol F10) is located on chromosome 13q34 spanning 25 kbp and is composed of 8 exons encoding a 488 amino acid preproprotein. Exon 1 encodes the leader peptide, exon 2 encodes the proprotein region cleaved by the "tenase complex" as well as the gla-residue-rich domain, exons 4 and 5 encode epidermal growth factor (EGF)-like domains, exon 6 encodes the activation domain, and exons 7 and 8 encode the catalytic domain.