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Published on: April 1, 2015
Platelet aggregation and physiological anticoagulants in sickle-cell disease
L A M Bashawri1, A A Al-Mulhim, M A Ahmed
1College of Applied Medical Sciences, King Faisal University, Dammam, Saudi Arabia. laylabashawri@yahoo.com
Sickle-cell anaemia patients show lower levels of key blood proteins (antithrombin III, protein C, protein S) and altered platelet aggregation compared to healthy adults. These levels remain low during both crisis and steady states.
Area of Science:
- Hematology
- Clinical Biochemistry
Background:
- Sickle-cell anaemia is a genetic blood disorder characterized by abnormal hemoglobin.
- Vaso-occlusive crisis is a common and painful complication of sickle-cell anaemia.
- Coagulation factors and platelet function are implicated in sickle-cell pathophysiology.
Purpose of the Study:
- To investigate levels of antithrombin III, protein C, and protein S in sickle-cell anaemia patients.
- To assess platelet aggregation in sickle-cell anaemia patients during vaso-occlusive crisis and steady state.
- To compare these parameters with healthy adult controls.
Main Methods:
- Prospective study of 30 sickle-cell anaemia patients (January 2002-December 2004).
- Measurement of antithrombin III, protein C, and protein S levels.
- Platelet aggregation studies were performed.
- Comparison with 36 healthy adult controls.
Main Results:
- Control group exhibited significantly higher levels of protein C, protein S, and antithrombin III compared to patients (P < 0.001).
- Significant differences in platelet aggregation factors (except adrenaline) were observed between controls and patients.
- No significant differences in protein C, protein S, antithrombin III, or platelet aggregation were found between patients in steady state and those in vaso-occlusive crisis.
Conclusions:
- Sickle-cell anaemia patients have depleted levels of key anticoagulant proteins and altered platelet function.
- These hemostatic abnormalities are present regardless of disease state (crisis vs. steady state).
- Findings suggest a potential role for these factors in the thrombotic complications of sickle-cell anaemia.
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