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10.1016/S2665-9913(20)30121-1 http://scihub22266oqcxt.onion/10.1016/S2665-9913(20)30121-1 C7252093!7252093!32835247     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Lancet+Rheumatol 2020 ; 2 (7): e437-45 Nephropedia Template TP {{tp|p=32835247|t=2020. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia |pdf=|usr=}}{{32835247}} gab.com Text Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia JO: Lancet Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=32835247 #FOAvip The lung pathology seen in patients with coronavirus disease 2019 (COVID-19) shows marked microvascular thrombosis and haemorrhage linked to extensive alveolar and interstitial inflammation that shares features with macrophage activation syndrome (MAS). We have termed the lung-restricted vascular immunopathology associated with COVID-19 as diffuse pulmonary intravascular coagulopathy, which in its early stages is distinct from disseminated intravascular coagulation. Increased circulating D-dimer concentrations (reflecting pulmonary vascular bed thrombosis with fibrinolysis) and elevated cardiac enzyme concentrations (reflecting emergent ventricular stress induced by pulmonary hypertension) in the face of normal fibrinogen and platelet levels are key early features of severe pulmonary intravascular coagulopathy related to COVID-19. Extensive immunothrombosis over a wide pulmonary vascular territory without confirmation of COVID-19 viraemia in early disease best explains the adverse impact of male sex, hypertension, obesity, and diabetes on the prognosis of patients with COVID-19. The immune mechanism underlying diffuse alveolar and pulmonary interstitial inflammation in COVID-19 involves a MAS-like state that triggers extensive immunothrombosis, which might unmask subclinical cardiovascular disease and is distinct from the MAS and disseminated intravascular coagulation that is more familiar to rheumatologists. Twit Text FOAVip Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia ????Lancet Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=32835247 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32835247 #FOAvip English Wikipedia <ref>{{Cite pmid|32835247}}</ref> Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia #MMPMID32835247 McGonagle D; O'Donnell JS; Sharif K; Emery P; Bridgewood C Lancet Rheumatol 2020[Jul]; 2 (7): e437-45 PMID32835247show ga The lung pathology seen in patients with coronavirus disease 2019 (COVID-19) shows marked microvascular thrombosis and haemorrhage linked to extensive alveolar and interstitial inflammation that shares features with macrophage activation syndrome (MAS). We have termed the lung-restricted vascular immunopathology associated with COVID-19 as diffuse pulmonary intravascular coagulopathy, which in its early stages is distinct from disseminated intravascular coagulation. Increased circulating D-dimer concentrations (reflecting pulmonary vascular bed thrombosis with fibrinolysis) and elevated cardiac enzyme concentrations (reflecting emergent ventricular stress induced by pulmonary hypertension) in the face of normal fibrinogen and platelet levels are key early features of severe pulmonary intravascular coagulopathy related to COVID-19. Extensive immunothrombosis over a wide pulmonary vascular territory without confirmation of COVID-19 viraemia in early disease best explains the adverse impact of male sex, hypertension, obesity, and diabetes on the prognosis of patients with COVID-19. The immune mechanism underlying diffuse alveolar and pulmonary interstitial inflammation in COVID-19 involves a MAS-like state that triggers extensive immunothrombosis, which might unmask subclinical cardiovascular disease and is distinct from the MAS and disseminated intravascular coagulation that is more familiar to rheumatologists. äImmune mechanisms of pulmonary intravascular coagulopathy in COVID-19 (epmc).pdf DeepDyve Pubget Overpricing