• clinical
  • This thesis has aimed to investigate the frequency of protein C pathway defects in patients with aPA and to study clinical correlates examine the mechanisms of antiphospholipid interference in the protein C pathway and to assess activated protein C (APC) resistance in patients with aPA in terms of thrombin generation. (bl.uk)
  • The current classification criteria for antiphospholipid syndrome include both laboratory criteria and clinical criteria. (endocrinologyadvisor.com)
  • cardiolipin
  • It was previously thought that these antibodies bound to the phospholipid known as cardiolipin. (endocrinologyadvisor.com)
  • These antibodies are identified by detecting their binding to beta-2 glycoprotein 1 in association with cardiolipin. (endocrinologyadvisor.com)
  • This is in contrast to rheumatoid arthritis with systemic sclerosis (scleroderma) because anti-cardiolipin antibodies are present in both conditions, and therefore may tie the two conditions together. (wikipedia.org)
  • Anti-cardiolipin antibodies can be classified in two ways: As IgM, IgG or IgA As β2-glycoprotein dependent or independent In autoimmune disease ACA are beta-2 glycoprotein dependent syphilis ACA are beta-2 glycoprotein independent and can be assayed using the Venereal Disease Research Laboratory test β2-glycoprotein I has been identified as Apolipoprotein H and is required for the recognition of ACA in autoimmune disease. (wikipedia.org)
  • Some (but not all) studies have shown an association between (migraine) headaches in SLE and associated Raynaud's phenomenon and/or anti-cardiolipin antibodies. (wikipedia.org)
  • Heparin
  • Heparin, which acts as a pro-survival factor in human trophoblast, attenuated the anti-beta(2)GPI antibody-mediated cell death, and also the pro-inflammatory response, but only at high concentrations. (nih.gov)
  • syndrome include
  • Nonthrombotic manifestations of antiphospholipid syndrome include a host of cardiovascular diseases, neurologic disorders, hematologic disorders, renal dysfunction, and cutaneous changes. (endocrinologyadvisor.com)
  • Risk factors for developing antiphospholipid syndrome include:[citation needed] Primary APS genetic marker HLA-DR7 Secondary APS SLE or other autoimmune disorders Genetic markers: HLA-B8, HLA-DR2, HLA-DR3 Race: Blacks, Hispanics, Asians, and Native Americans There is an additional elevated risk of adrenal gland bleeds leading to Waterhouse-Friderichsen syndrome (Neisseria meningitidis caused primary adrenal insufficiency). (wikipedia.org)
  • trophoblast
  • Antiphospholipid antibodies induce a pro-inflammatory response in first trimester trophoblast via the TLR4/MyD88 pathway. (nih.gov)
  • First trimester trophoblast cells were treated with anti-beta(2)GPI monoclonal antibodies and patient-derived aPL, after which cell survival and function was evaluated. (nih.gov)
  • We report that anti-beta(2)GPI antibodies trigger an inflammatory response in trophoblast, characterized by increased secretion of interleukin (IL)-8, MCP-1, GRO-alpha, and IL-1beta, and that this occurs in a TLR-4/MyD88-dependent manner. (nih.gov)
  • proteins
  • VP1-proteins are incorporated into the capsid structure in a non-stochiometrical relation (based on antibody-binding analysis and X-ray structural analysis the VP1-unique region is assumed to be exposed at the surface of the virus particle. (wikipedia.org)
  • presence
  • The presence of prolonged clotting times on a routine plasma test often triggers functional testing of the blood clotting function, as well as serological testing to identify common autoantibodies such as antiphospholipid antibodies. (wikipedia.org)