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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.
In a suspected antiphospholipid syndrome, lupus anticoagulant is generally tested in conjunction with anti-apolipoprotein antibodies and anti-cardiolipin antibodies, and diagnostic criteria require one clinical event (i.e. thrombosis or pregnancy complication) and two positive blood test results spaced at least three months apart that detect at ...
Schematic representation of antibody. Anti-cardiolipin antibodies (ACA) are antibodies often directed against cardiolipin and found in several diseases, including syphilis, [1] antiphospholipid syndrome, livedoid vasculitis, vertebrobasilar insufficiency, Behçet's syndrome, [2] idiopathic spontaneous abortion, [3] and systemic lupus erythematosus (SLE). [4]
Antiphospholipid syndrome was described in full in the 1980s, after various previous reports of specific antibodies in people with systemic lupus erythematosus and thrombosis. [18] [49] The syndrome is often attributed to the British rheumatologist Graham R.V. Hughes, and is often referred to as Hughes syndrome for that reason. [50]
Catastrophic antiphospholipid syndrome (CAPS), also known as Asherson's syndrome, is a rare autoimmune disease in which widespread, intravascular clotting causes multi-organ failure. [1] The syndrome is caused by antiphospholipid antibodies that target a group of proteins in the body that are associated with phospholipids .
3.3 per 100,000 (adults), 50 per 100,000 (children) [90] Thrombotic thrombocytopenic purpura: ADAMTS13 autoantibodies Confirmed 1-2 per million [91] Antiphospholipid syndrome: Antiphospholipid antibodies Confirmed 40-50 per 100,000 [92] Paroxysmal nocturnal hemoglobinuria: None specific, mutation causes self-cells to become susceptible to ...
Human Chr 3. In terms of the cause of protein S deficiency it can be in inherited via autosomal dominance.A mutation in the PROS1 gene triggers the condition. The cytogenetic location of the gene in question is chromosome 3, specifically 3q11.1 [6] [7] Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver disease, kidney disease, chemotherapy ...
Reportedly, less than 5% of all TTP cases are due to Upshaw–Schulman syndrome. [21] People with this syndrome generally have 5–10% of normal ADAMTS-13 activity. [22] [23] A 2024 study suggested that hereditary TTP is underdiagnosed and should be considered in cases of unexplained stroke, neonatal jaundice, and severe pre-eclampsia. [24]