The relationship between FV Leiden and pulmonary embolism

Hooper, W. Craig; Staercke, Christine De

doi:10.1186/rr180

Cited by 12 publications

(4 citation statements)

References 26 publications

(28 reference statements)

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“…The PADUA model involves deficiencies in proteins C, S, and antithrombin III, as well as factors like Factor V Leiden(FVL) and prothrombin G20210A mutation. It is noteworthy that genetic susceptibility can potentially hold equal significance as environmental and clinical factors in terms of the risk factor for PE [ 42 ]. According to previous reports, deficiencies in proteins C and S have been linked to an increased risk of PE compared to that in the general population [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Validation of a pulmonary embolism risk assessment model in gynecological inpatients

Jin,

Li,

et al. 2024

Thrombosis J

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Objective To compare the predictive efficacy of the PADUA and Caprini models for pulmonary embolism (PE) in gynecological inpatients, analyze the risk factors for PE, and validate whether both models can effectively predict mortality rates. Methods A total of 355 gynecological inpatients who underwent computed tomography pulmonary angiography (CTPA) were included in the retrospective analysis. The comparative assessment of the predictive capabilities for PE between the PADUA and Caprini was carried out using receiver operating characteristic (ROC) curves. Logistic regression analysis was used to identify risk factors associated with PE. Additionally, Kaplan–Meier survival analysis plots were generated to validate the predictive efficacy for mortality rates. Results Among 355 patients, the PADUA and Caprini demonstrated the area under the curve (AUC) values of 0.757 and 0.756, respectively. There was no statistically significant difference in the AUC between the two models (P = 0.9542). Multivariate logistic analysis revealed immobility (P < 0.001), history of venous thromboembolism (VTE) (P = 0.002), thrombophilia (P < 0.001), hormonal treatment (P = 0.022), and obesity (P = 0.019) as independent risk factors for PE. Kaplan–Meier survival analysis demonstrated the reliable predictive efficacy of both the Caprini (P = 0.00051) and PADUA (P = 0.00031) for mortality. ROC for the three- and six-month follow-ups suggested that the Caprini model exhibited superior predictive efficacy for mortality. Conclusions The PADUA model can serve as a simple and effective tool for stratifying high-risk gynecological inpatients before undergoing CTPA. The Caprini model demonstrated superior predictive efficacy for mortality rates.

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Section: Discussionmentioning

confidence: 99%

Validation of a pulmonary embolism risk assessment model in gynecological inpatients

Jin,

Li,

et al. 2024

Thrombosis J

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“…Factor V Leiden occurs due to a single point mutation of G-to-A transition at nucleotide 1691 in the factor V gene that leads to the amino acid substitution of arginine to glutamine [6]. As a result of the single amino acid substitution, procoagulant Factor Va becomes resistant to Activated Protein C (APC).…”

Section: Discussionmentioning

confidence: 99%

Treating Venous Thromboembolism Post Intracranial Hemorrhage: A Case Report

Ajmeri

Zaheer

McCorkle

et al. 2020

Cureus

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Venous thromboembolism (VTE) is a significant issue occurring due to genetic, acquired and circumstantial risk factors. Treatment is according to the clinical situation and judgment for long term anticoagulation based on individual risk. Anticoagulation after a history of a hemorrhagic stroke poses a therapeutic dilemma. We present a case of a 68-year-old male who presented with right-sided chest pain and shortness of breath. Workup included a CT that was positive for multiple right-sided pulmonary emboli (PE). The patient has a past medical history of Factor V Leiden Mutation, recurrent PE, and deep vein thrombosis (DVT). Two months prior he was diagnosed with a 1.3-cm intracranial hemorrhage (ICH) from multiple cavernous angiomas. At that time his warfarin was discontinued and an inferior vena cave (IVC) filter was placed. Facing the recent ICH and now multiple and recurrent PE, it was decided to resume anticoagulation based on ICH location. ICH from a deep source is likely a better characteristic that favors a resumption of anticoagulation. Our case will highlight that IVC filters cannot be solely relied upon in patients that are at high risk for thrombotic events with underlying genetic thrombophilia.

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“…The importance of genetic thrombophilia factors in developing VTE has been increasingly recognized. Inherited gene disorders related to the haemostatic system have been documented as risk factors in different studies 2 3 4 5 .…”

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confidence: 99%

“…Factor V Leiden ( FV 1691G/A, rs6025), prothrombin gene mutation G20210A ( FII 20210G/A), the variant 677C/T of methylene tetrahydrofolate reductase (MTHFR 677C/T, rs1801133) and polymorphism A2 ( PLA2 ) in platelet glycoprotein GPIIb/IIIa ( GpIIIa 1565T/C, rs5918) are among main inherited risk factors. The prevalence of these polymorphisms is different according to ethnicity in normal population and VTE patients 2 3 4 . Whether these abnormalities may impact differently PE and DVT is not well defined, and the available data are controversial.…”

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confidence: 99%

A preliminary study of inherited thrombophilic risk factors in different clinical manifestations of venous thromboembolism in central Iran

Karimi¹,

Abolhasani²,

Chaleshtori³

et al. 2015

Indian J Med Res

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Background & objectives:Inherited thrombophilia is known to be an important risk factor for developing venous thromboembolism. Whether such abnormalities may impact the development of deep vein thrombosis (DVT) and pulmonary embolism (PE) differently is not well defined. This preliminary study was undertaken to compare thrombophilic polymorphism in patients with DVT and PE.Methods:A total of 35 DVT, 23 DVT/PE, and 37 PE patients admitted to the Hajar Hospital, Shahrekord, Iran, between October 2009 and February 2011 were included in the study and 306 healthy volunteers matched by age and sex from the same geographical area with no history of venous or arterial diseases were included as control group. Factor V Leiden (FV 1691G/A, rs6025), prothrombin (FII 20210G/A), methylene tetrahydrofulate reductase (MTHFR 677C/T, rs1801133), and PLA2 polymorphisms of platelet glycoprotein IIb/IIIa (GpIIIa 1565T/C, rs5918) were investigated by polymerase chain reaction-restriction fragment length polymorphism.Results:The number of patients with the investigated polymorphisms and homozygous carriers was significantly different among the groups (P<0.05). No significant difference was observed in the presence of FV 1691G/A and FII 20210G/A between any of the patients groups and the control group. GpIIIa 1565T/C and homozygous MTHFR 677C/T polymorphisms were higher in DVT patients compared with the control group (OR=6.65, 95% CI=3.09-14.30 and OR=4.08, 95% CI=1.35-12.38, respectively).Interpretation & conclusions:As none of the investigated polymorphisms were associated with PE, other thrombophilia polymorphisms may have a role in the pathogenesis of PE in these patients and should be investigated. Because of different prognostic risk factors among different types of patients, the treatment approach could be different.

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The relationship between FV Leiden and pulmonary embolism

Cited by 12 publications

References 26 publications

Validation of a pulmonary embolism risk assessment model in gynecological inpatients

Validation of a pulmonary embolism risk assessment model in gynecological inpatients

Treating Venous Thromboembolism Post Intracranial Hemorrhage: A Case Report

A preliminary study of inherited thrombophilic risk factors in different clinical manifestations of venous thromboembolism in central Iran

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