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10.1111/jth.15671 http://scihub22266oqcxt.onion/10.1111/jth.15671 35150462!9115133!35150462     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35150462&cmd=llinks): Failed to open stream: HTTP request failed! 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Thrombosis pathways in COVID-19 vs influenza-associated ARDS: A targeted proteomics approach |pdf=|usr=}}{{35150462}} gab.com Text Thrombosis pathways in COVID-19 vs influenza-associated ARDS: A targeted proteomics approach JO: J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=35150462 #FOAvip BACKGROUND: Pulmonary embolism (PE) occurs in one-third of critically-ill COVID-19 patients. Although prior studies identified several pathways contributing to thrombogenicity, it is unknown whether this is COVID-19-specific or also occurs in ARDS patients with another infection. OBJECTIVE: To compare pathway activity among patients having COVID-19 with PE (C19PE+), COVID-19 without PE (C19PE-), and influenza-associated ARDS (IAA) using a targeted proteomics approach. METHODS: We exploited an existing biorepository containing daily plasma samples to carefully match C19PE+ cases to C19PE- and IAA controls on mechanical ventilation duration, PEEP, FiO2, and cardiovascular-SOFA (n = 15 per group). Biomarkers representing various thrombosis pathways were measured using proximity extension- and ELISA-assays. Summed z-scores of individual biomarkers were used to represent total pathway activity. RESULTS: We observed no relevant between-group differences among 22 biomarkers associated with activation of endothelium, platelets, complement, coagulation, fibrinolysis or inflammation, except sIL-1RT2 and sST2, which were lower in C19PE- than IAA (log2-Foldchange -0.67, p = .022 and -1.78, p = .022, respectively). However, total pathway analysis indicated increased activation of endothelium (z-score 0.2 [-0.3-1.03] vs. 0.98 [-2.5--0.3], p = .027), platelets (1.0 [-1.3-3.0] vs. -3.3 [-4.1--0.6], p = .023) and coagulation (0.8 [-0.5-2.0] vs. -1.0 [-1.6-1.0], p = .023) in COVID-19 patients (C19PE+/C19PE- groups combined) compared to IAA. CONCLUSION: We observed only minor differences between matched C19PE+, C19PE-, and IAA patients, which suggests individual biomarkers mostly reflect disease severity. However, analysis of total pathway activity suggested upregulation of some distinct processes in COVID-19 could be etiologically related to increased PE-risk. Twit Text FOAVip Thrombosis pathways in COVID-19 vs influenza-associated ARDS: A targeted proteomics approach ????J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=35150462 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35150462 #FOAvip English Wikipedia <ref>{{Cite pmid|35150462}}</ref> Thrombosis pathways in COVID-19 vs influenza-associated ARDS: A targeted proteomics approach #MMPMID35150462 Rademaker E; Doorduijn DJ; Kusadasi N; Maas C; Drylewicz J; Huisman A; Hoefer IE; Bonten MJM; Derde LPG; Rooijakkers SHM; Cremer OL J Thromb Haemost 2022[May]; 20 (5): 1206-1212 PMID35150462show ga BACKGROUND: Pulmonary embolism (PE) occurs in one-third of critically-ill COVID-19 patients. Although prior studies identified several pathways contributing to thrombogenicity, it is unknown whether this is COVID-19-specific or also occurs in ARDS patients with another infection. OBJECTIVE: To compare pathway activity among patients having COVID-19 with PE (C19PE+), COVID-19 without PE (C19PE-), and influenza-associated ARDS (IAA) using a targeted proteomics approach. METHODS: We exploited an existing biorepository containing daily plasma samples to carefully match C19PE+ cases to C19PE- and IAA controls on mechanical ventilation duration, PEEP, FiO2, and cardiovascular-SOFA (n = 15 per group). Biomarkers representing various thrombosis pathways were measured using proximity extension- and ELISA-assays. Summed z-scores of individual biomarkers were used to represent total pathway activity. RESULTS: We observed no relevant between-group differences among 22 biomarkers associated with activation of endothelium, platelets, complement, coagulation, fibrinolysis or inflammation, except sIL-1RT2 and sST2, which were lower in C19PE- than IAA (log2-Foldchange -0.67, p = .022 and -1.78, p = .022, respectively). However, total pathway analysis indicated increased activation of endothelium (z-score 0.2 [-0.3-1.03] vs. 0.98 [-2.5--0.3], p = .027), platelets (1.0 [-1.3-3.0] vs. -3.3 [-4.1--0.6], p = .023) and coagulation (0.8 [-0.5-2.0] vs. -1.0 [-1.6-1.0], p = .023) in COVID-19 patients (C19PE+/C19PE- groups combined) compared to IAA. CONCLUSION: We observed only minor differences between matched C19PE+, C19PE-, and IAA patients, which suggests individual biomarkers mostly reflect disease severity. However, analysis of total pathway activity suggested upregulation of some distinct processes in COVID-19 could be etiologically related to increased PE-risk. |*COVID-19/complications[MESH] |*Influenza, Human/complications/diagnosis[MESH] |*Pulmonary Embolism/diagnosis[MESH] |*Respiratory Distress Syndrome[MESH] |*Thrombosis[MESH] |Biomarkers[MESH] |Humans[MESH] |Proteomics[MESH]Thrombosis pathways in COVID-19 vs influenza-associated ARDS: A targe(epmc).pdf DeepDyve Pubget Overpricing