Erythrocyte–Platelet Interaction in Uncomplicated Pregnancy

Abstract

Maternal and fetal requirements during uncomplicated pregnancy are associated with changes in the hematopoietic system. Platelets and erythrocytes [red blood cells (RBCs)], and especially their membranes, are involved in coagulation, and their interactions may provide reasons for the changed hematopoietic system during uncomplicated pregnancy. We review literature regarding RBC and platelet membrane structure and interactions during hypercoagulability and hormonal changes. We then study interactions between RBCs and platelets in uncomplicated pregnancy, as their interactions may be one of the reasons for increased hypercoagulability during uncomplicated pregnancy. Scanning electron microscopy was used to study whole blood smears from 90 pregnant females in different phases of pregnancy. Pregnancy-specific interaction was seen between RBCs and platelets. Typically, one or more platelets interacted through platelet spreading and pseudopodia formation with a single RBC. However, multiple interactions with RBCs were also shown for a single platelet. Specific RBC-platelet interaction seen during uncomplicated pregnancy may be caused by increased estrogen and/or increased fibrinogen concentrations. This interaction may contribute to the hypercoagulable state associated with healthy and uncomplicated pregnancy and may also play a fundamental role in gestational thrombocytopenia.

An Evaluation of the Accuracy of the Subtraction Method Used for Determining Platelet Counts in Advanced Platelet-Rich Fibrin and Concentrated Growth Factor Preparations

“…Owing to their deformability and Fe 2+ -dependent high specific gravity, although smaller in size than large WBCs, RBCs spin-down faster. Specific binding and mechanical interaction, to some extent, cause RBCs to bring platelets into the RBC fractions, as demonstrated in previous studies [ 14 , 15 ]. WBCs and platelets spin-down essentially depending on their size.…”

Pathological Clotting and Deep Vein Thrombosis in Patients with HIV

“…The interaction of activated platelets with RBCs therefore has a positive feedback on the coagulation system. 45 Fibrinogen expresses binding sites for the membrane receptors of cells involved in inflammation, and enhances adhesion of the RBCs, by binding to the RBC membrane. 45 RBC aggregation thereby increases in the localized presence of fibrinogen.…”

“…45 Fibrinogen expresses binding sites for the membrane receptors of cells involved in inflammation, and enhances adhesion of the RBCs, by binding to the RBC membrane. 45 RBC aggregation thereby increases in the localized presence of fibrinogen. Fibrinogen, arguably one of the most important circulating plasma proteins, is a large centrosymmetric glycoprotein.…”

“…49 Hormonal changes, such as an increase in estrogen, also cause a granular fibrin network. 45 Fibrin clot proteolysis in hypercoagulable conditions may be inhibited or delayed. The delayed/inhibited breakdown of the fibrin clot may be due to inflammatory cellular elements that are trapped in the fibrin network that stimulates a firm clot formation resistant to antithrombotic agents.…”

Evaluation of Immunological Parameters in Pregnant Women: Low Levels of B and NK Cells

“…The total blood volume (red and white blood cell [WBC] mass) increases, while platelet counts decrease, especially in the 3 rd trimester. 3,4 Alterations may occur in the maternal peripheral blood, in the composition of cellular subsets of the immune system and in the maternalfetal interface at the endometrial uterine wall. 1,3 Invasion of allogenic fetal cells, vascularization (especially spiral arteries), and the formation of the placenta may cause inflammation at the maternal-fetal interface.…”