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10.3390/biomedicines9080899 http://scihub22266oqcxt.onion/10.3390/biomedicines9080899 34440103!8389622!34440103     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34440103&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Biomedicines 2021 ; 9 (8): ? Nephropedia Template TP {{tp|p=34440103|t=2021. Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a Supporting Actor |pdf=|usr=}}{{34440103}} gab.com Text Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a Supporting Actor JO: Biomedicines http://www.kidney.de/pget.php?&tw=1&pmid=34440103 #FOAvip BACKGROUND: COVID-19 clinical features include a hypercoagulable state that resembles the antiphospholipid syndrome (APS), a disease characterized by thrombosis and presence of antiphospholipid antibodies (aPL). The relationship between aPL-presence and the appearance of thrombi as well as the transience or permanence of aPL in COVID-19 patients is not sufficiently clear. METHODS: A group of 360 COVID-19 patients were followed-up for 6 months. Classic aPL, anti-B2GPI IgA, anti-phosphatidylserine/prothrombin IgG/M and anti-SARS-CoV-2 antibodies were determined at acute phase and >12 weeks later. The reference group included 143 healthy volunteers of the same age-range distribution. RESULTS: aPL prevalence was similar in COVID-19 patients and the reference population. aPL presence in both determinations was significantly associated with thrombosis (OR: 2.33 and 3.71), strong agreement being found for classic aPL and anti-B2GPI IgA (Weighted kappa: 0.85-0.91). Thrombosis-associated aPL occurred a median of 17 days after hospital admission (IQR: 6-28) vs. 4 days for the rest (IQR: 3-7). Although anti-SARS-CoV-2 antibodies levels increased during convalescence, aPL hardly changed. CONCLUSIONS: Most COVID-19 patients would carry these aPL before the infection. At least two mechanisms could be behind thrombosis, early immune-dysregulation-mediated thrombosis after infection and belated-aPL-mediated thrombosis, with SARS-CoV-2 behaving as a second hit. Twit Text FOAVip Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a Supporting Actor ????Biomedicines http://www.kidney.de/pget.php?&tw=1&pmid=34440103 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34440103 #FOAvip English Wikipedia <ref>{{Cite pmid|34440103}}</ref> Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a Supporting Actor #MMPMID34440103 Gil-Etayo FJ; Garcinuno S; Lalueza A; Diaz-Simon R; Garcia-Reyne A; Pleguezuelo DE; Cabrera-Marante O; Rodriguez-Frias EA; Perez-Rivilla A; Serrano M; Serrano A Biomedicines 2021[Jul]; 9 (8): ? PMID34440103show ga BACKGROUND: COVID-19 clinical features include a hypercoagulable state that resembles the antiphospholipid syndrome (APS), a disease characterized by thrombosis and presence of antiphospholipid antibodies (aPL). The relationship between aPL-presence and the appearance of thrombi as well as the transience or permanence of aPL in COVID-19 patients is not sufficiently clear. METHODS: A group of 360 COVID-19 patients were followed-up for 6 months. Classic aPL, anti-B2GPI IgA, anti-phosphatidylserine/prothrombin IgG/M and anti-SARS-CoV-2 antibodies were determined at acute phase and >12 weeks later. The reference group included 143 healthy volunteers of the same age-range distribution. RESULTS: aPL prevalence was similar in COVID-19 patients and the reference population. aPL presence in both determinations was significantly associated with thrombosis (OR: 2.33 and 3.71), strong agreement being found for classic aPL and anti-B2GPI IgA (Weighted kappa: 0.85-0.91). Thrombosis-associated aPL occurred a median of 17 days after hospital admission (IQR: 6-28) vs. 4 days for the rest (IQR: 3-7). Although anti-SARS-CoV-2 antibodies levels increased during convalescence, aPL hardly changed. CONCLUSIONS: Most COVID-19 patients would carry these aPL before the infection. At least two mechanisms could be behind thrombosis, early immune-dysregulation-mediated thrombosis after infection and belated-aPL-mediated thrombosis, with SARS-CoV-2 behaving as a second hit. ?Anti-Phospholipid Antibodies and COVID-19 Thrombosis: A Co-Star, Not a(epmc).pdf DeepDyve Pubget Overpricing