Postoperative Pulmonary Embolism in a Young Female Accompanying with Factor V Leiden Mutation and Hereditary Sypherocytosis

2004 ◽  
Vol 17 (3) ◽  
pp. 213-217 ◽  
Author(s):  
Demet Karnak ◽  
Sumru Beder ◽  
Oya Kayacan ◽  
Özlem Berk
Keyword(s):  
Pulmonary Embolism ◽  
Factor V Leiden ◽  
Young Female ◽  
Factor V ◽  
Factor V Leiden Mutation

scholarly journals Lipoprotein(a) a Risk Factor for Venous Thrombosis and Pulmonary Embolism in Patients Younger Than 50 Years of Age

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5055-5055
Author(s):  
Sonha Nguyen ◽  
Lynette Ilano ◽  
Nneka Oluoha ◽  
Zahra Pakbaz
Keyword(s):  
Pulmonary Embolism ◽  
Elevated Serum ◽  
Factor V Leiden ◽  
Serum Lipoprotein ◽  
Convincing Evidence ◽  
Factor V ◽  
Data Set ◽  
Factor V Leiden Mutation ◽  
Lipoprotein A ◽  
Lipid Panel

Abstract Introduction: Despite convincing evidence toward causal role of Lipoprotein(a) in occlusive arterial disease, the data is conflicting when it comes to venous thromboembolism (VTE) and pulmonary embolism (PE). Also it is not known if intervention to normalize Lipoprotein(a) will decrease risk of recurrent VTE and PE eliminating the need for life long anticoagulation. To our knowledge this isfirst data set report focusing on evaluating association between Lipoprotein(a) and VTE in patients younger than 50 years old. Methods: Inthis retrospective study, chart review was completed for twenty-six consecutive patients referred to hematology clinic with diagnosis of deep vein thrombosis (DVT) or PE in year 2017-2018 . Four patients older than 50 years old at the time of acute events were excluded. Lipoprotein(a) had only been measured in patients who had negative hypercoagulable work up with normal lipid panel but had obesity . Protein C, S and anti-thrombin were not measured if patients were already on anticoagulation. Serum level of Lipoprotein(a) greater than 75 nmol/L was considered to be elevated. Results: Total of 22 patients (18 females) were included in the data analysis. Nine patients had DVT, 5 patients had PE, and 8 patients had both DVT and PE. Median age was 34 (12-47). Lipoprotein(a) level was not checked on eight patients who had SLE (n=1), surgery (n=1), Factor V Leiden mutation (n=1), protein S deficiency (n=1), anti-phospholipid syndrome (n=2), prothrombin gene mutation (n=1), and one patient who had lost follow up. The median Lipoprotein(a) level was 107 (8-276). Serum Lipoprotein(a) was elevated in 8 out of the 14 screened patients (57%) with the median of 135 (107-276). Out of 8 patients with elevated Lipoprotein(a), only 1 patient had additional clinical risk factors for thrombosis (history of smoking, alcohol abuse, hypertriglyceridemia and elevated LDL). In an attempt to normalize Lipoprotein(a) level, 3 patients were started on niacin but only one tolerated maximum 1000 mg niacin daily which resulted in decrease in level but did not achieve normalization. Conclusion: This data suggests that elevated serum Lipoprotein(a) in females younger than 50 years old is associated with DVT/PE events. Further investigation is required to confirm this finding. At this time it is not known if attempt to normalize Lipoprotein(a) will prevent recurrent PE/DVT and eliminate need for long life anticoagulation in patients with unprovoked VTE who have elevated lipoprotein(a). Disclosures Pakbaz: Novartis: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.

Varicella Infection May Cause Thrombosis: A Case Report

2018 ◽  
Vol 3 (3) ◽  
Keyword(s):  
Pulmonary Embolism ◽  
Anticoagulant Therapy ◽  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Skin Lesions ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor V Leiden Mutation ◽  
Varicella Zoster

This case was presented due to development of DVT and pulmonary embolism after VZV infection and determination of Factor V Leiden mutation and activated protein C resistance. A 19-year old male patient presented with fever at the 10th day of varicella zoster virus (VZV) infection, and pruritic vesicopustular skin lesions and increased leukocyte and CRP levels. Acyclovir and ampicillin-sulbactam therapy were started. On the fourth day of hospitalization, left leg DVT and pulmonary embolism developed. Anticoagulant therapy was started. Tests revealed activated protein C resistance and Factor V Leiden mutation. The patient was discharged after the relief of symptoms with anticoagulant therapy. Thrombosis rarely develops in the course of VZV infection. It is essential to investigate the factors contributing to predisposition to thrombosis in patients with thrombosis.

scholarly journals Risk Factor Profiles in Patients with Different Clinical Manifestations of Venous Thromboembolism: A Focus on the Factor V Leiden Mutation

1996 ◽  
Vol 76 (04) ◽  
pp. 510-513 ◽  
Author(s):  
Bert Manten ◽  
Rudi G J Westendorp ◽  
Ted Koster ◽  
Pieter H Reitsma ◽  
Frits R Rosendaal
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Venous Thromboembolism ◽  
Clinical Manifestations ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis ◽  
Increased Risk ◽  
Deep Vein

Summary Background. Patients with venous thromboembolic disease may present with different clinical manifestations. Factor V Leiden mutation leading to resistance to activated protein C is associated with a sevenfold increased risk for presenting with deep-vein thrombosis. It is not yet established whether carriers of the mutation have a similarly increased risk for manifesting with pulmonary embolism. Methods. From an Anticoagulation Clinic monitoring coumarin therapy, a consecutive series of patients with a first thromboembolic event (objectively proven by current radiological methods) were enrolled. All patients were interviewed and blood was drawn for geno-typing. From the hospital charts and the personal interview, information was obtained on acquired risk factors and the signs and symptoms on hospital admission. Results. 45 patients presented with symptoms of pulmonary embolism only, 211 had only symptoms of deep-vein thrombosis whereas 23 had clinical features of both. In about half of the patients acquired risk factors for venous thromboembolism were present which did not differ between the three groups of patients. Recent surgery had been performed more often in patients presenting with pulmonary embolism than in other patients (33.3% vs. 18.5%, p <0,05). Factor V Leiden was present in 9% of the patients presenting with pulmonary embolism (relative risk: 3.3 95% Cl: 1.0-10.6) and 17% of the patients presenting with deep-vein thrombosis (relative risk: 6.9 95% Cl: 3.6-12.8). The prevalence of factor V Leiden was intermediate in patients with both clinical characteristics. Conclusion. These data suggest that patients with venous thromboembolism have different clinical presentation depending on the risk factor profile. Factor V Leiden may preferentially lead to manifest deep-vein thrombosis. Differences in structure of venous thrombi could underlie differences in embolic tendency.

scholarly journals Factor V Leiden Thrombophilia in a Female Collegiate Soccer Athlete: A Case Report

2013 ◽  
Vol 48 (3) ◽  
pp. 431-435 ◽  
Author(s):  
Kendra Erickson ◽  
Michael E. Powers
Keyword(s):  
Emergency Department ◽  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Anticoagulant Therapy ◽  
Athletic Trainers ◽  
Factor V Leiden ◽  
Genetic Mutation ◽  
Factor V ◽  
Care Providers ◽  
Factor V Leiden Mutation

Objective: To raise awareness among health care providers caring for an active population to an uncommon genetic mutation that increases the risk for a potentially fatal venous thromboembolism. Background: A 19-year-old previously healthy female collegiate soccer athlete complained of coughing and progressively decreased exercise tolerance, which were attributed to a recent illness and lack of sleep. Later that evening, she complained of dyspnea and pleuritic pain and was referred to the emergency department. Bilateral pulmonary emboli were identified with computed tomography, and a hypercoagulable panel revealed that the patient was heterozygous for the factor V Leiden mutation. Differential Diagnosis: Pneumonia, pneumothorax, pericarditis, pleuritis, gastroesophageal reflux disease, pulmonary embolism. Treatment: Intravenous heparin therapy was initiated immediately in the emergency department. This was followed by inpatient anticoagulant therapy for 5 days and outpatient anticoagulant therapy for an additional 12 months. During this time, the patient was unable to participate in soccer drills or return to competition and was limited to conditioning activities due to the risk of increased bleeding time. Uniqueness: Documented cases of pulmonary embolism in a young athletic population are rare and are usually associated with genetic risk factors. Factor V Leiden is a relatively uncommon genetic mutation that dramatically increases the risk for venous thromboembolism. Although the fatality rate in this population is low, fatality is preventable if the condition is recognized early and managed properly. Conclusions: Athletes should be encouraged to communicate with their athletic trainers regarding any changes in health status or medication usage. When an athlete presents with nonspecific symptoms such as dyspnea and chest pain, athletic trainers should consider the possibility of pulmonary embolism. A high degree of suspicion results in early diagnosis and treatment and may prevent a fatal event.

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