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10.1007/s10067-021-05790-9 http://scihub22266oqcxt.onion/10.1007/s10067-021-05790-9 34109491!8189705!34109491     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Rheumatol 2021 ; 40 (12): 4807-4815 Nephropedia Template TP {{tp|p=34109491|t=2021. Mechanisms of thrombosis in ANCA-associated vasculitis |pdf=|usr=}}{{34109491}} gab.com Text Mechanisms of thrombosis in ANCA-associated vasculitis JO: Clin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=34109491 #FOAvip Patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) have a two- to threefold greater risk of developing venous as well as arterial thrombotic events. Although such thrombotic events are more commonly seen during phases of active AAV, they are also recognized to occur during AAV in remission. Endothelial injury is a key pathogenic event in AAV. Endothelial injury can be caused by neutrophil activation and release of thrombogenic tissue factor into the circulation. Neutrophil activation further results in the formation of neutrophil extracellular traps (NETs). NETs contribute to thrombosis by expressing tissue factor. NETs have also been detected in cutaneous thrombi from patients with AAV induced by hydralazine. Activated neutrophils in AAV patients release thrombogenic microparticles loaded with tissue factor which further enhances clotting of blood. Antiphospholipid antibodies (APLs) have been detected in up to a third of AAV and might also be induced by drugs such as cocaine adulterated with levamisole and propylthiouracil, which are known to trigger AAV. Such APLs further drive the thrombosis in AAV. Once thrombogenesis occurs, the homeostatic mechanisms resulting in clot dissolution are further impaired in AAV due to anti-plasminogen antibodies. The ongoing pandemic of coronavirus disease 2019 (COVID-19) is associated with endothelial injury and NETosis, mechanisms which are in common with AAV. Reports of new-onset AAV following COVID-19 have been described in the literature, and there could be shared mechanisms driving these processes that require further evaluation. Twit Text FOAVip Mechanisms of thrombosis in ANCA-associated vasculitis ????Clin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=34109491 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34109491 #FOAvip English Wikipedia <ref>{{Cite pmid|34109491}}</ref> Mechanisms of thrombosis in ANCA-associated vasculitis #MMPMID34109491 Misra DP; Thomas KN; Gasparyan AY; Zimba O Clin Rheumatol 2021[Dec]; 40 (12): 4807-4815 PMID34109491show ga Patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) have a two- to threefold greater risk of developing venous as well as arterial thrombotic events. Although such thrombotic events are more commonly seen during phases of active AAV, they are also recognized to occur during AAV in remission. Endothelial injury is a key pathogenic event in AAV. Endothelial injury can be caused by neutrophil activation and release of thrombogenic tissue factor into the circulation. Neutrophil activation further results in the formation of neutrophil extracellular traps (NETs). NETs contribute to thrombosis by expressing tissue factor. NETs have also been detected in cutaneous thrombi from patients with AAV induced by hydralazine. Activated neutrophils in AAV patients release thrombogenic microparticles loaded with tissue factor which further enhances clotting of blood. Antiphospholipid antibodies (APLs) have been detected in up to a third of AAV and might also be induced by drugs such as cocaine adulterated with levamisole and propylthiouracil, which are known to trigger AAV. Such APLs further drive the thrombosis in AAV. Once thrombogenesis occurs, the homeostatic mechanisms resulting in clot dissolution are further impaired in AAV due to anti-plasminogen antibodies. The ongoing pandemic of coronavirus disease 2019 (COVID-19) is associated with endothelial injury and NETosis, mechanisms which are in common with AAV. Reports of new-onset AAV following COVID-19 have been described in the literature, and there could be shared mechanisms driving these processes that require further evaluation. |*Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/complications[MESH] |*COVID-19[MESH] |*Extracellular Traps[MESH] |*Thrombosis[MESH] |Antibodies, Antineutrophil Cytoplasmic[MESH] |Humans[MESH] |Neutrophils[MESH]Mechanisms of thrombosis in ANCA-associated vasculitis (epmc).pdf DeepDyve Pubget Overpricing