scholarly journals Retinopathy Revealing Cerebral Venous Thrombosis in Sickle Cell Disease in Niger

2019 ◽  
Vol 09 (03) ◽  
pp. 134-140
Author(s):  
Nouhou Diori Adam ◽  
Yacoubou Soumana ◽  
Saley Ali ◽  
Amadou Moussa Salia ◽  
Saley Idrissa
Author(s):  
Athena Sharifi Razavi ◽  
Narges Karimi

Background: The most common symptom of the novel Coronavirus Disease 2019 (COVID-19) infection is fever and dyspnea that leads to hypoxia in severe cases. Some COVID-19 patients experience neurological symptoms, including ischemic stroke and intracerebral hemorrhage. Sickle Cell Disease (SCD) is a hypercoagulable state, however, it has not been approved as a significant cause of Cerebral Venous Thrombosis (CVT). Case presentation: In this case report, we described CVT in an SCD patient who had COVID-19, as well. We reported a 32-year-old man with a history of sickle cell anemia presented with left hemiparesis, headache, and seizure. After evaluation of the patient, CVT accompanied by COVID-19 infection was diagnosed. He was treated with intravenous unsaturated heparin, antiepileptic drugs, and antiviral agents with a favorable outcome. Based on our knowledge, this is the first case study to describe an association between CVT and COVID-19 infection in a patient with SCD. Conclusion: During the recent pandemic, vaso-occlusive attacks in SCD patients can be evaluated for COVID-19 as an etiological factor.


Blood ◽  
2017 ◽  
Vol 130 (16) ◽  
pp. 1795-1799 ◽  
Author(s):  
James R. Byrnes ◽  
Alisa S. Wolberg

Abstract Red blood cells (RBCs) have historically been considered passive bystanders in thrombosis. However, clinical and epidemiological studies have associated quantitative and qualitative abnormalities in RBCs, including altered hematocrit, sickle cell disease, thalassemia, hemolytic anemias, and malaria, with both arterial and venous thrombosis. A growing body of mechanistic studies suggests that RBCs can promote thrombus formation and enhance thrombus stability. These findings suggest that RBCs may contribute to thrombosis pathophysiology and reveal potential strategies for therapeutically targeting RBCs to reduce thrombosis.


2020 ◽  
Vol 21 (15) ◽  
pp. 5279
Author(s):  
Maria A. Lizarralde-Iragorri ◽  
Arun S. Shet

Venous thromboembolism (VTE) is an important cause of vascular morbidity and mortality. Many risk factors have been identified for venous thrombosis that lead to alterations in blood flow, activate the vascular endothelium, and increase the propensity for blood coagulation. However, the precise molecular and cellular mechanisms that cause blood clots in the venous vasculature have not been fully elucidated. Patients with sickle cell disease (SCD) demonstrate all the risk factors for venous stasis, activated endothelium, and blood hypercoagulability, making them particularly vulnerable to VTE. In this review, we will discuss how mouse models have elucidated the complex vascular pathobiology of SCD. We review the dysregulated pathways of inflammation and coagulation in SCD and how the resultant hypercoagulable state can potentiate thrombosis through down-regulation of vascular anticoagulants. Studies of VTE pathogenesis using SCD mouse models may provide insight into the intersection between the cellular and molecular processes involving inflammation and coagulation and help to identify novel mechanistic pathways.


2006 ◽  
Vol 119 (10) ◽  
pp. 897.e7-897.e11 ◽  
Author(s):  
Paul D. Stein ◽  
Afzal Beemath ◽  
Frederick A. Meyers ◽  
Elias Skaf ◽  
Ronald E. Olson

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 4913-4913
Author(s):  
Salam Alkindi ◽  
Anwaar Al-Ghadani ◽  
Samah Al-zeheimi ◽  
Anil Pathare

Abstract Background and Purpose: Venous thromboembolism (VTE) is common in patients with sickle cell disease (SCD). Traditional risk factors such as central venous catheters, frequent hospitalization, orthopedic surgeries for avascular necrosis, and pregnancy often leads to an increased incidence of VTE in the SCD. In addition, SCD itself appears to be a hypercoagulable state with many SCD-specific factors such as genotype, splenectomy and thrombophilia modifying the risk of VTE. This study aims to assess the clinical and pathological characteristics of VTE amongst a cohort of patients with SCD at the Sultan Qaboos University Hospital and determine its relation to morbidity and mortality. Methodology: In this retrospective case control study, medical details of all patients with SCD who developed thromboembolic complications over the past decade were retrieved from the hospital information system. SCD patients matched for age and gender (2:1 ratio) who did not have thromboembolic complications but had a thrombophilia screen performed served as controls. The study was approved by the local Medical Research and Ethics Committee. Results & Discussion: A total of 53 SCD patients were enrolled [34 cases, 19 controls] in this study. Amongst the 34 cases (mean age-30 yrs.), 18 had pulmonary embolism, eight had deep venous thrombosis, whereas, three each had cerebral venous thrombosis and portal venous thrombosis and one each had cerebral arterial thrombosis and VTE. A higher incidence of autosplenectomy(69.7% v/s 52.6%) and central venous catheters(42.4% v/s 5.3%) were significantly associated with thrombosis (p<0.05, Chi Square test). High LDH levels, WBC and Platelet counts were significant risk factors(p<0.05) for VTE. 21 patients [63.6%] amongst the cases developed acute chest syndrome, where 3[9%] had cerebrovascular accident. Mortality was seen in seven cases [21%]. Conclusions: The study shows that thromboembolic complications in SCD has a high impact on the morbidity and mortality. It confirms PE as the leading cause for VTE in SCD with asplenia, central venous catheter, high LDH, WBC and Platelet counts being significant risk factors. Disclosures No relevant conflicts of interest to declare.


2015 ◽  
Vol 62 (5) ◽  
pp. 838-841 ◽  
Author(s):  
Tiago de Oliveira Boechat ◽  
Emilia Matos do Nascimento ◽  
Clarisse Lopes de Castro Lobo ◽  
Samir K. Ballas

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