ArticleNagoya journal of medical science2021
The prevalence of Factor V Leiden (Arg506Gln) mutation in King Khalid University Hospital patients, 2017-2019.
Article in Nagoya journal of medical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
- Influence of Factor V Leiden Mutation and Protein C and Protein S Deficiencies on Preeclampsia Among Sudanese Women.Cureus · 2025Article
- Efficacy and safety of anti-Xa direct oral anticoagulants vs. warfarin in patients homozygous for Factor V Leiden and prothrombin G20210A mutations.Journal of thrombosis and thrombolysis · 2025Article
- Complications of Mesenteric Vein Thrombosis: Heterozygous Factor V Leiden Mutation Leads to Pulmonary Embolism in a Patient With Post-Bowel Resection Surgery.Clinical case reports · 2025Article
- Independent case-control study inSaudi journal of biological sciences · 2022Article
- Clinical Impact of Inherited Thrombophilia in Patients With Thrombosis: Evaluating the Real Risk of FVL, PTG20210A, and MTHFR Mutations in the Kurdistan Region of Iraq.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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11 authors at 1 institution in 1 country.
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Abstract
Arg506Gln mutation is responsible for one of the procoagulant factors and most common inherited thrombophilia in the Factor V Leiden (FVL) family. The replacement of the missense mutation for Arg506Gln / R506Q is at 1691st position from Guanine to Adenine with the modification of the amino acid from arginine to glutamine. The aim of this study was to investigate the current prevalence of the G1691A mutation in the FVL gene in the capital city's King Khalid University Hospitals (KKUH). Since 2017-2019 we have recruited 482 patients in these cross-sectional studies to test the G1691A mutation in KKUH's FVL gene. DNA was extracted using 2mL of the EDTA blood and genotyping was performed with polymerase chain reaction and the data was analyzed using Sanger sequencing. In this study, 4.4% of the G1691A mutation was found to be positive (combined heterozygous-GA and homozygous-AA variants) and 95.6% of them with negative, i.e., homozygous normal-GG genotypes. Our study concludes that with the advances in genetic testing and their recent availability, early mutation detection could approve the genotype risks for many patients and this mutation is not as rare as previously believed in the Saudi region as our study has established with a 4.4 percent prevalence.
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