scholarly journals HELLP Syndrome and Cerebral Venous Sinus Thrombosis Associated with Factor V Leiden Mutation during Pregnancy

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Zeynep Ozcan Dag ◽  
Yuksel Işik ◽  
Yavuz Simsek ◽  
Ozlem Banu Tulmac ◽  
Demet Demiray
Keyword(s):  
Hellp Syndrome ◽  
Sinus Thrombosis ◽  
Factor V Leiden ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Factor V ◽  
Hormonal Changes ◽  
Factor V Leiden Mutation ◽  
Venous Sinus Thrombosis ◽  
Increased Risk

Preeclampsia is a leading cause of maternal mortality and morbidity worldwide. The neurological complications of preeclampsia and eclampsia are responsible for a major proportion of the morbidity and mortality for women and their infants alike. Hormonal changes during pregnancy and the puerperium carry an increased risk of venous thromboembolism including cerebral venous sinus thrombosis (CVST). Factor 5 leiden (FVL) is a procoagulant mutation associated primarily with venous thrombosis and pregnancy complications. We report a patient with FVL mutation who presented with CVST at 24th week of pregnancy and was diagnosed as HELLP syndrome at 34th week of pregnancy.

Fatal Cerebral Venous Sinus Thrombosis Associated with the Factor V Leiden Mutation and the Use of Oral Contraceptives

1995 ◽  
Vol 74 (05) ◽  
pp. 1382-1382 ◽  
Author(s):  
Françoise Bridey ◽  
Michel Wolff ◽  
Jean Pierre Laissy ◽  
Véronique Morin ◽  
Martine Lefebvre ◽  
...  
Keyword(s):  
Oral Contraceptives ◽  
Sinus Thrombosis ◽  
Factor V Leiden ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Venous Sinus Thrombosis

Cerebral venous sinus thrombosis in a neonate due to factor V Leiden deficiency

2007 ◽  
Vol 91 (2) ◽  
pp. 243-245 ◽  
Author(s):  
M Abrantes ◽  
AF Lacerda ◽  
CR Abreu ◽  
A Levy ◽  
A Azevedo ◽  
...  
Keyword(s):  
Sinus Thrombosis ◽  
Factor V Leiden ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Factor V ◽  
Venous Sinus Thrombosis

scholarly journals A Lady with Systemic Lupus Erythematosus Complicated with Central Venous Sinus Thrombosis: A Case Report

2020 ◽  
Vol 20 (01) ◽  
pp. 42-46
Author(s):  
Alexandra Hoi Yan Ng ◽  
Daniel Kam Hung Ng
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Antiphospholipid Antibodies ◽  
Sinus Thrombosis ◽  
Rare Condition ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Systemic Lupus ◽  
Venous Sinus Thrombosis ◽  
Increased Risk

Systemic lupus erythematosus (SLE) is associated with an increased risk of venous thromboses and cerebrovascular diseases. Herein, we discuss the case of a young 38-year-old Asian lady who was presented with cerebral venous sinus thrombosis (CVST) shortly after she was diagnosed with SLE. She developed headache, right hemiparesis and sustained an episode of seizure on the first presentation. CVST was diagnosed with plain computed tomography (CT) of the brain and CT venogram. With prompt administration of anticoagulation and immunosuppressant treatment for SLE, she had an excellent neurological recovery. There are many different risk factors for developing CVST in SLE patients. It has been reported in literature that CVST is usually associated with antiphospholipid antibodies but only around 40% of them would have positive antiphospholipid antibodies indicating that there are also other mechanisms contributing to the process [1]. As CVST in SLE is a rare condition, no standardized treatment strategy has been delineated. The main cornerstone of treatment would be anticoagulation and appropriate treatment for SLE as these patients are commonly associated with underlying active SLE. With timely management, the prognosis for CVST in SLE patients is generally favourable.

scholarly journals Cerebral Venous Sinus Thrombosis in a Patient with Ulcerative Colitis Flare

2018 ◽  
Vol 2018 ◽  
pp. 1-7
Author(s):  
L. M. Conners ◽  
R. Ahad ◽  
P. H. Janda ◽  
Z. Mudasir
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Sinus Thrombosis ◽  
Rare Complication ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Venous Sinus Thrombosis ◽  
Increased Risk ◽  
Inflammatory Bowel

Inflammatory bowel disease is characterized by a chronic inflammatory state and is therefore associated with abnormalities in coagulation and a hypercoagulable state. Cerebral venous sinus thrombosis is a rare complication of inflammatory bowel disease yet contributes significant morbidity and mortality to those affected. Early diagnosis is critical, as a delay in diagnosis portends a worse prognosis. This paper seeks to highlight the increased risk of venous sinus thrombosis in patients with inflammatory bowel disease. We start by discussing the case of a seventeen-year-old female who presented with ulcerative colitis flare and developed new-onset seizures, found to be caused by a large venous sinus thrombosis.

scholarly journals Management of a decompensated acute-on-chronic intracranial venous sinus thrombosis

2019 ◽  
Vol 12 ◽  
pp. 175628641989515 ◽  
Author(s):  
Carmen Serna Candel ◽  
Victoria Hellstern ◽  
Tania Beitlich ◽  
Marta Aguilar Pérez ◽  
Hansjörg Bäzner ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Endovascular Treatment ◽  
Sinus Thrombosis ◽  
Vasogenic Edema ◽  
Factor V Leiden ◽  
Venous Sinus ◽  
Venous Stasis ◽  
Left Frontal Lobe ◽  
Factor V Leiden Mutation ◽  
Venous Sinus Thrombosis

A 34-year-old female patient presented during the 10th week of her second gravidity with headache, nausea and vomiting 2 weeks before admission. Her medical history was remarkable for a heterozygous factor V Leiden mutation, elevated lipoprotein A, and a cerebral venous thrombosis (CVT) after oral contraceptive intake 15 years before. Magnetic resonance imaging (MRI) suggested acute and massive intracranial sinus thrombosis. Despite full-dose anticoagulation, the patient deteriorated clinically and eventually became comatose. Now, MRI/magnetic resonance angiography revealed vasogenic edema of both thalami, of the left frontal lobe, and of the head of the caudate nucleus, with venous stasis and frontal petechial hemorrhage. She was referred for endovascular treatment. Diagnostic angiography confirmed a complete superficial and deep venous sinus occlusion. Endovascular access to the straight and superior sagittal sinus was possible, but neither rheolysis nor balloon angioplasty resulted in recanalization of the venous sinuses. Monitored heparinization was continued and antiaggregation was initiated. The patient remained comatose for another 5 days and MRI showed progress of the cytotoxic edema. On day 6, infusion of eptifibatide at body-weight-adapted dosage was started. The following day, the patient improved and slowly regained consciousness. MRI confirmed regression of the edema. The eptifibatide infusion was continued for a total of 14 days. Thereafter two doses of 180 mg ticagrelor per os (PO) daily were started. The patient remained on acetylsalicylic acid (ASA), ticagrelor, and enoxaparin on an unchanged dosage regimen. She was discharged home 26 days after the endovascular treatment without serious neurological deficit, with the pregnancy intact. At the 30th week of pregnancy the dosage of ASA was reduced to 300 mg once PO daily. Cesarian delivery was carried out at the 38th week of pregnancy. The newborn was completely healthy. Ultima ratio therapeutic options for severe intracranial venous sinus thrombosis refractory to anticoagulation are discussed, with an emphasis on platelet-function inhibition.

scholarly journals Genetic Aspects of Preeclampsia and the HELLP Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Kjell Haram ◽  
Jan Helge Mortensen ◽  
Bálint Nagy
Keyword(s):  
Hellp Syndrome ◽  
Genetic Diseases ◽  
Factor V Leiden ◽  
Mthfr C677t ◽  
Envelope Gene ◽  
Factor V ◽  
Vegf Mrna ◽  
Factor V Leiden Mutation ◽  
Blood Flows ◽  
Increased Risk

Both preeclampsia and the HELLP syndrome have their origin in the placenta. The aim of this study is to review genetic factors involved in development of preeclampsia and the HELLP syndrome using literature search in PubMed. A familial cohort links chromosomes 2q, 5q, and 13q to preeclampsia. The chromosome 12q is coupled with the HELLP syndrome. TheSTOX1gene, theERAP1and 2 genes, the syncytin envelope gene, and the−670 Fasreceptor polymorphisms are involved in the development of preeclampsia. TheACVR2Agene on chromosome 2q22 is also implicated. The toll-like receptor-4 (TLR-4) and factor V Leiden mutation participate both in development of preeclampsia and the HELLP syndrome. Carriers of the TT and the CC genotype of theMTHFR C677Tpolymorphism seem to have an increased risk of the HELLP syndrome. The placental levels of VEGF mRNA are reduced both in women with preeclampsia and in women with the HELLP syndrome. The BclI polymorphism is engaged in development of the HELLP syndrome but not in development of severe preeclampsia. TheACE I/Dpolymorphism affects uteroplacental and umbilical artery blood flows in women with preeclampsia. In women with preeclampsia and the HELLP syndrome several genes in the placenta are deregulated. Preeclampsia and the HELLP syndrome are multiplex genetic diseases.

scholarly journals Cerebral Venous Sinus Thrombosis (CVST) in a Middle-Aged Female with Clustering of Risk Factors

2021 ◽  
Vol 10 (34) ◽  
pp. 2960-2963
Author(s):  
Maria Prothasis ◽  
Yash Gupte ◽  
Sourya Acharya ◽  
Samarth Shukla ◽  
Neema Acharya
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Sinus Thrombosis ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Factor V ◽  
Venous Sinus Thrombosis

Thrombosis of cerebral venous channel is a known complication of hypercoagulable states. Hyperhomocysteinaemia is a known hypercoagulable state. Obesity is a modern-day global epidemic. Disorders such as myocardial infarction (MI), stroke, and venous thromboembolism are on the rising trend and its increased morbidity and mortality is being associated with obesity. To date, however, the knowledge about the association between obesity and adult cerebral venous thrombosis (CVT) is sparse. We report a 44-year-old young morbidly obese metabolically unhealthy female who presented with headache, nausea, vomiting and giddiness. On evaluation, magnetic resonance venogram showed cerebral venous sinus thrombosis. On investigations, she had concomitant hyperhomocysteinaemia and metabolic syndrome. Cerebral venous sinus thrombosis causing stroke in young adults is uncommon with various conditions precipitating it.1,2,3 Severe headache (70 - 90 %), focal lateralized signs (25 % - 75 %), seizures (30 – 40 %) as well as behavioural symptoms such as delirium, amnesia, and disturbances in consciousness are the various associated clinical symptoms. The known inherited hypercoagulable risk factors that cause CVST are gain of function mutations in the genes encoding factor V (factor V Leiden) and prothrombin, Protein C, S and antithrombin III deficiency. Hyperhomocysteinaemia, is a known risk factor for causing venous thrombosis of the lower limbs. However, till date there is no data available showing its role in causing cerebral venous thrombosis. The interaction between genetic and acquired determinants result in high plasma levels of total homocysteine (tHcy).4,5,6 Vitamins such as folic acid, pyridoxine, and cobalamin are involved in the metabolic pathways of homocysteine and its deficiencies represent the acquired determinants. Venous thromboembolism (VTE) comprises of deep vein thrombosis of the leg and pulmonary embolism and obesity is now being recognised as one of the risk factors causing it. The risk of VTE is approximately increased to 2-fold in an individual with a body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) of 30 or more compared with a normal BMI (< 25), and higher BMIs increase more risk with approximately 3 times higher risk in individuals with a BMI greater than 40.7, 8,9 Again obesity as a risk factor for CVST is less known.

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