Red Blood Cells and Relation to Thrombosis

Blood coagulation and thrombin generation are primarily a function of platelets, coagulation factors, and endothelial cells. Red blood cells (RBCs) have generally been viewed as innocent bystanders in the clotting process. However, there has been a steadily growing clinical data revealing the active roles of erythrocytes in hemostasis. RBCs may contribute to thrombosis in several ways. In polycythemia, RBCs increase blood viscosity and marginate platelets toward the endothelium. The increased incidence of thrombosis is also associated with hemolytic anemia, especially with sickle cell disease and paroxysmal nocturnal hemoglobinuria. RBCs express phosphatidylserine and microparticles, supporting thrombin generation. They interact with platelets, endothelial cells, and fibrinogen, and these interactions lead their incorporation into the thrombi. The presence of RBCs in clots suppresses plasmin generation and reduces clot dissolution. Decreasing thrombus RBC content would accelerate thrombus resolution. In conclusion, RBCs are important complements of the complex reactions of clot formation

Blood Groups

Blood groups, erythrocyte antigens, and transfusion are fundamental areas of medicine and are related to many disciplines of science like hematology, immunology, surgery, and genetics. This book is a collection of information related to blood groups and transfusion, and a practical resource for all concerned physicians. The book is divided into two sections. The first section includes chapters on blood transfusion reactions and hemolytic disease of the fetus. The second section includes information for the future perspectives of blood group antigens. This book will be a stepping stone for scientists who are rapidly advancing their science journey

Receptor Activator of Nuclear Factor kappa-Beta Ligand/Osteoprotegerin Axis in Adults with Hb S/beta-Thalassemia and beta-Thalassemia Trait

There is not enough data about osteoporosis and the role of receptor activator of nuclear factor kappa-Beta ligand (RANKL)/serum osteoprotegerin (OPG) system in patients with double heterozygosity for sickle cell disease and beta-thalassemia [Hb S (HBB: c.20A>T)/beta-thal] and beta-thal trait. Aim of the study was to investigate bone mineral densities (BMD) and the role of RANKL/OPG system in these cases. We studied 58 adults with Hb S/beta-thal, 52 adults with beta-thal trait, 34 healthy subjects as a control group. The BMD was determined by dual-energy X-ray absorptiometry (DEXA). Biochemical markers of bone metabolism (serum calcium, phosphorus, alkaline phosphatase, osteocalcin) parameters that affect bone metabolism (serum parathyroid hormone, thyroid-stimulating hormone, 25-hydroxyvitamin D, OPG, soluble RANKL [sRANKL]) were studied. Femoral neck Z-scores of 93.2% for beta-thal trait, 83.0% for Hb S/beta-thal patients were within the expected range. Lumbar spine Z-scores of 89.1% for beta-thal, 90.2% for Hb S/beta-thal patients were above -2.0 SD. Z-scores of the control group were within the expected range. Median serum sRANKL level was 2.80, 4.52, 5.79 pmol/L in Hb S/beta-thal, beta-thal trait, control groups, respectively (p = 0.010). Median serum OPG level was 1.07, 0.86, 0.86 pmol/L in Hb S/beta-thal, beta-thal trait, control groups, respectively (p < 0.001). beta-Thalassemia trait alone is not a risk factor for osteopenia/osteoporosis and osteoporosis does not develop in premenopausal women and men younger than 50 years with Hb S/beta-thal. However, as we determined lower levels of osteocalcin, compensatory decrease of sRANKL with compensatory increase of OPG, more severe osteoporosis may develop in advanced ages in these patient populations.Mersin UniversityMersin University [BAP-TF DTB (AT) 2010-3]This study was supported by the Mersin University Scientific Research Projects [BAP-TF DTB (AT) 2010-3 code].WOS:0005649855000012-s2.0-85090149538PubMed: 3287308