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Related Concept Videos

Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Formation of the Platelet Plug01:22

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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

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Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
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Updated: Jun 18, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Complement activation on platelets correlates with a decrease in circulating immature platelets in patients with

Ellinor I B Peerschke1, Biree Andemariam, Wei Yin

  • 1Weill-Cornell Medical College of Cornell University, New York, NY, USA. ellinor.peerschke@mountsinai.org

British Journal of Haematology
|November 21, 2009
PubMed
Summary
This summary is machine-generated.

The complement system may drive immune thrombocytopenic purpura (ITP) by activating on platelets. This complement activation/fixation capacity (CAC) was elevated in ITP patients, correlating with lower platelet counts and immature platelet fractions.

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Area of Science:

  • Immunology
  • Hematology

Background:

  • The complement system's role in immune thrombocytopenic purpura (ITP) remains unclear.
  • ITP is characterized by autoantibodies against platelets, leading to their destruction.

Purpose of the Study:

  • To investigate the complement activation/fixation capacity (CAC) in patients with ITP.
  • To determine if CAC correlates with clinical parameters and treatment responses in ITP.

Main Methods:

  • Plasma samples from 79 ITP patients, 50 healthy volunteers, and 25 patients with non-immune thrombocytopenia were analyzed.
  • Complement activation/fixation capacity (CAC) was measured using immobilized heterologous platelets.
  • Deposition of C1q and C4d was assessed for stricter analysis.

Main Results:

  • Enhanced CAC was observed in 59% of ITP patients, but not in non-immune thrombocytopenia patients.
  • Elevated CAC in ITP correlated with lower absolute immature platelet fraction (A-IPF) and thrombocytopenia.
  • Strictly defined CAC (C1q/C4d deposition) showed 100% specificity and positive predictive value for low A-IPF.
  • A trend towards better response to splenectomy was noted with enhanced CAC.

Conclusions:

  • Complement fixation may contribute to thrombocytopenia in ITP through enhanced platelet clearance or direct damage.
  • CAC, particularly C1q/C4d deposition, could serve as a biomarker for ITP severity and platelet destruction mechanisms.