Red Cell Distribution Width and Mean Platelet Volume in Amyloidosis.
ABSTRACT We aimed to determine whether red cell distribution width (RDW) and mean platelet volume (MPV) values differ between patients with reactive amyloid A (AA) amyloidosis due to chronic inflammatory disease and in healthy participants. In this study, 33 patients with AA amyloidosis and 40 age- and sex-matched healthy controls were enrolled. Erythrocyte sedimentation rate (ESR), RDW, platelet count (PLT), and MPV levels were retrospectively obtained from our computerized patient database. We found RDW, ESR, and PLT levels to be significantly higher in patients with AA amyloidosis compared with the controls (P < .0001). Mean platelet volume was significantly lower in patients with amyloidosis (P < .0001). Inflammatory diseases such as AA amyloidosis may demonstrate low MPV and high RDW levels.
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ABSTRACT: Familial Mediterranean fever (FMF) is an inflammatory disorder that is leading cause of secondary amyloidosis (AA). This study was designed to investigate the level of mean platelet volume (MPV) in AA. Seventy-four FMF, 29 AA patients and 180 healthy controls, were included. There was no significant difference between the cases in terms of sex and age. MPV levels were measured in all groups. In the FMF group, MPV level was significantly higher when compared to the control group. MPV level was significantly lower in AA group in comparison with the FMF and healthy control groups. In summary, our present study showed low MPV values in AA due to FMF.Rheumatology International 05/2013; · 2.21 Impact Factor
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ABSTRACT: Thrombosis is a major contributor to cardiovascular disease, which can lead to myocardial infarction and stroke. Thrombosis may form in tortuous microvessels, which are often seen throughout the human body, but the microscale mechanisms and processes are not well understood. In straight vessels, the presence of red blood cells (RBCs) is known to push platelets toward walls, which may affect platelet aggregation and thrombus formation. However in tortuous vessels, the effects of RBC interactions with platelets in thrombosis are largely unknown. Accordingly, the objective of this work was to determine the physical effects of RBCs, platelet size, and vessel tortuosity on platelet activation and thrombus formation in tortuous arterioles. A discrete element computational model was used to simulate the transport, collision, adhesion, aggregation, and shear-induced platelet activation of hundreds of individual platelets and RBCs in thrombus formation in tortuous arterioles. Results showed that high shear stress near the inner sides of curved arteriole walls activated platelets to initiate thrombosis. RBCs initially promoted platelet activation, but then collisions of RBCs with mural thrombi reduced the amount of mural thrombus and the size of emboli. In the absence of RBCs, mural thrombus mass was smaller in a highly tortuous arteriole compared to a less tortuous arteriole. In the presence of RBCs however, mural thrombus mass was larger in the highly tortuous arteriole compared to the less tortuous arteriole. As well, smaller platelet size yielded less mural thrombus mass and smaller emboli, either with or without RBCs. This study shed light on microscopic interactions of RBCs and platelets in tortuous microvessels, which have implications in various pathologies associated with thrombosis and bleeding.Frontiers in Bioengineering and Biotechnology 01/2013; 1:18.