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Secondary cold agglutinin syndrome occurs when autoantibodies bind to red blood cells, rendering them subject to attack by the complement system. [17] It is a result of an underlying condition potentially associated with either monoclonal cold-reacting autoantibodies or polyclonal cold-reacting autoantibodies [16] predominantly caused by infection or lymphoproliferative disorders. [16]
The syndrome is caused by antiphospholipid antibodies that target a group of proteins in the body that are associated with phospholipids. These antibodies activate endothelial cells, platelets, and immune cells, ultimately causing a large inflammatory immune response and widespread clotting. [1] CAPS was first described by Ronald Asherson in 1992.
21-hydroxylase antibodies Confirmed 0.93-1.4 per 10,000 [72] Autoimmune oophoritis: Ovaries: Anti-ovarian antibodies Probable Rare [73] Autoimmune orchitis: Testes: Anti-sperm antibodies Probable Rare [74] Autoimmune pancreatitis: Pancreas: IgG4, Anti-CA2 antibodies Confirmed 0.82-1.3 per 100,000 [75] Autoimmune polyendocrine syndrome type 1 (APS1)
Antiphospholipid syndrome is known for causing arterial or venous blood clots, in any organ system, and pregnancy-related complications.While blood clots and pregnancy complications are the most common and diagnostic symptoms associated with APS, other organs and body parts may be affected like platelet levels, heart, kidneys, brain, and skin.
For example, a PI of 25,000 platelets/μL, a BSA of 1.8m 2 and a PD of 4x10 11 gives a CCI of 11,250 platelets*m 2 /10 11 μL At 1 hour post-transfusion a CCI greater than 7500 indicates a sufficient post-transfusion increment, whereas a CCI less than 7500 is considered diagnostic of platelet refractoriness. [ 10 ]
Cold agglutinins are antibodies, typically immunoglobulin M (), that are acquainted with and then binding the antigens on red blood cells, typically antigens "I" or "i" on the RBC surface, [1] in the environment in which the temperatures are lower than normal core body temperature and, thus, ends up leading to agglutinations of the red blood cells and hemolysis reaction occurring outside the ...
These can stimulate production of alloantibodies (that is, antibodies against other people's antigens) in recipients of transfused platelets from donors with different HPAs. These antibodies cause neonatal alloimmune thrombocytopenia, post-transfusion purpura, and some cases of platelet transfusion refractoriness to infusion of donor platelets. [1]
In biochemistry and medicine, glycoprotein IIb/IIIa (GPIIb/IIIa, also known as integrin α IIb β 3) is an integrin complex found on platelets. It is a transmembrane receptor for fibrinogen [1] and von Willebrand factor, and aids platelet activation. The complex is formed via calcium-dependent association of gpIIb and gpIIIa, a required step in ...