[Genetic analysis and clinical features of a pedigree affected with hereditary coagulation factor Ⅶ deficiency caused by compound heterozygotic mutations]

Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2019 Oct 10;36(10):1006-1009. doi: 10.3760/cma.j.issn.1003-9406.2019.10.014.
[Article in Chinese]

Abstract

Objective: To detect potential mutations of the coagulation factor Ⅶ (F7) gene in a pedigree affected with hereditary FⅦ deficiency and explore its molecular pathogenesis.

Methods: The FⅦ antigen (FⅦ:Ag) was analyzed by an enzyme-linked immunosorbent assay (ELISA) method. Prothrombin time (PT), FⅦ activity (FⅦ:C) and other coagulant parameters were quantified with an one-stage clotting assay. The F7 gene was amplified by PCR and sequenced. Mutational sites were confirmed by reverse sequencing. Impact of amino acid substitution was assessed using SIFT and PolyPhen-2 software. Structure of the mutant protein was analyzed using Swiss-pdb Viewer software based on the three-dimensional structure in the Protein Data Bank.

Results: The propositus had prolonged PT (36.3 s), with FⅦ:C and FⅦ:Ag significantly reduced to 2% and 44%, respectively. Her father, mother, younger sister and daughter had slightly prolonged PT and reduced FⅦ:C (86%-120%). The FⅦ:Ag of her father and younger sister were also reduced. DNA sequencing revealed that the propositus has carried compound heterozygous mutations (Lys341Glu and IVS6-1G>A) of the F7 gene. Her father and younger sister were heterozygous for the IVS6-1G>A mutation, while her mother and daughter were heterozygous for the Lys341Glu mutation. Bioinformatics analysis indicated that Lys341Glu mutation may affect the stability and function of the FⅦ protein.

Conclusion: The Lys341Glu and IVS6-1G>A mutations probably underlie the reduced activity of FⅦ in this pedigree.

MeSH terms

  • Factor VII / genetics*
  • Factor VII Deficiency / genetics*
  • Female
  • Genetic Testing
  • Heterozygote
  • Humans
  • Male
  • Mutation
  • Pedigree

Substances

  • Factor VII