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Published on: November 5, 2019
Atherosclerosis in sickle cell disease - a review
Mohamed A Elsharawy1, Khaled M Moghazy, Mohamed A Shawarby
1Departments of Surgery;
Insights
Sickle cell disease (SCD) patients experience atherosclerosis due to endothelial dysfunction, homocysteine, and platelets. This review covers its pathogenesis, sites, assessment, and treatments.
Area of Science:
- Cardiovascular Science
- Hematology
- Pathology
Background:
- Sickle cell disease (SCD) is characterized by acute vaso-occlusive crises.
- Atherosclerosis development is increasingly recognized in SCD patients.
Purpose of the Study:
- To review the pathogenesis of atherosclerosis in SCD.
- To describe common and uncommon sites of atherosclerosis.
- To discuss radiological assessment and therapeutic strategies.
Main Methods:
- Review of current literature on SCD and atherosclerosis.
- Analysis of the roles of endothelial dysfunction, homocysteine, and platelets.
- Evaluation of radiological findings and treatment options.
Main Results:
- Endothelial dysfunction, elevated homocysteine, and platelet activation are key contributors to atherosclerosis in SCD.
- Atherosclerosis affects various vascular beds in SCD patients.
- Radiological assessment aids in identifying and monitoring atherosclerosis.
Conclusions:
- Understanding atherosclerosis pathogenesis in SCD is crucial for management.
- Targeting endothelial dysfunction, homocysteine, and platelets may offer therapeutic benefits.
- Multifaceted approaches are needed for treating atherosclerosis in SCD patients.
Abstract:
Acute, vaso-occlusive crises are the most common and earliest clinical manifestations of sickle cell disease. Recent thoughts about development of atherosclerosis as a result of this disease are presented. Current insights into the pathogenesis of atherosclerosis in sickle cell disease are reviewed, in particular the role of endothelial dysfunction, homocysteine and platelets. Common and uncommon sites of atherosclerosis are described. Radiological assessment and potential therapeutic agents to slow the progression of atherosclerosis are discussed. Finally, treatment of atherosclerosis in certain sites is evaluated and reviewed.
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