Corpus overview


MeSH Disease

Human Phenotype


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    A comparison of clinical and laboratory manifestations of thrombotic MESHD events in patients with COVID-19 and other respiratory viral infections MESHD.

    Authors: Chuen Wen Tan; Jing Yuan Tan; Wan Hui Wong; May Anne Cheong; Ian Matthias Ng; Edwin Philip Conceicao; Guek Hong Jenny Low; Heng Joo Ng; Lai Heng Lee

    doi:10.21203/ Date: 2020-09-22 Source: ResearchSquare

    COVID-19 caused by Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2) and other respiratory viral (non-CoV-2-RV) infections are associated with thrombotic complications MESHD. The differences in prothrombotic potential between SARS-CoV-2 and non-CoV-2-RV have not been well characterised. We compared the thrombotic MESHD rates between these two groups of patients directly and further delved into their coagulation profiles. In this single-center, retrospective cohort study, all consecutive COVID-19 and non-CoV-2-RV patients admitted between January 15th and April 10th 2020 were included. Coagulation parameters studied were prothrombin time and activated partial thromboplastin time and its associated clot waveform analysis (CWA) parameter, min1, min2 and max2. In the COVID-19 (n=181) group there were two (1.0 event/1000-hospital-days) thrombotic MESHD events while one (1.8 event/1000-hospital-day) was reported in the non-CoV-2-RV (n=165) group. All of these events were myocardial infarction HP myocardial infarction MESHD occurring in the intensive care unit. Coagulation parameters did not differ throughout the course of mild COVID-19. However, CWA parameters were significantly higher in severe COVID-19 compared with mild disease, suggesting hypercoagulability HP hypercoagulability MESHD (min1: 6.48%/s vs 5.05%/s, P<0.001; min2: 0.92%/s2 vs 0.74%/s2, P=0.033). In conclusion, the thrombotic MESHD rates were low and did not differ between COVID-19 and non-CoV-2-RV patients. The hypercoagulability HP hypercoagulability MESHD in COVID-19 is a highly dynamic process with the highest risk occurring when patients were most severely ill. Such changes in haemostasis could be detected by CWA. In our population, a more individualized thromboprophylaxis approach, considering clinical and laboratory factors, is preferred over universal pharmacological thromboprophylaxis for all hospitalized COVID-19 patients and such personalized approach warrants further research. 

    The Investigation of the Relationship Between the Inherited Thrombophilia MESHD and Novel Coronavirus Pneumonia HP

    Authors: Aslihan Kiraz; Seda Guzeldag; Esma Eren; Musa Goksu; Arslan Bayram

    doi:10.21203/ Date: 2020-09-21 Source: ResearchSquare

    Purpose: Novel coronavirus pneumonia MESHD pneumonia HP (NCP) is a disease caused by severe acute respiratory syndrome coronavirus 2 MESHD virus. It was reported that there is a relationship between severe NCP and hypercoagulable conditions that predispose patients to thrombosis MESHD. Thrombophilia MESHD is a multifactor condition that can result from genetic factors, acquired factors, or a combination of both. The prothrombin gene (F2 rs1799963 known as G20210A), Factor V Leiden (F5 rs6025 known as G1691A) and PAI-1 (rs1799768) are important polymorphic biomarkers of thrombophilia MESHD that are investigated in severe NCP patients within this study.Methods: NCP-diagnosed 62 previously healthy male TRANS patients (mean age TRANS 38.83±11.04) without any chronic disease MESHD were enrolled in this study for the investigation of the well-known thrombophilia MESHD-related abovementioned polymorphisms. The diagnosis of NCP was made according to the World Health Organization interim guidance and confirmed by RNA detection. SNPs were detected by real-time PCR. The frequency of genotypes was compared with healthy control group frequencies from other studies performed in the Turkish population.Results: There were no statistically significant differences between the severe patient group and the healthy population regarding the investigated SNPs.Conclusion: This study is the first to rule out the relationship of rs1799963 (FII), rs6025 (FV) and rs1799768 (PAI-1) with severe NCP. As there is an obvious relation between severe NCP and genetic thrombophilia MESHD susceptibility, studies focused on other thrombophilia MESHD-related genetic factors and this disease must be performed.

    SARS-CoV-2 and Covid-19 Immunopathogenesis

    Authors: Antonio Luiz Boechat; Beatriz Pessoa; Carlos Soares; Cecília Barroso; David Vila; Emanuelly Barbosa; Isabela Seffair; João Victor Melo; Julia Becil; Maria Polyanna Rebouças; Natascha Rodrigues; Pedro Henrique Freitas; Rebeka Rocha; Thaise Rodrigues; Vanessa Ferreira; Rosmery Ubiera; Maria Cristina Dos-Santos

    id:10.20944/preprints202008.0020.v1 Date: 2020-08-02 Source:

    The coronavirus disease MESHD 2019 (COVID-19) is now a global pandemic caused by the new severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2). Unlike other known coronaviruses, such as the Middle East respiratory syndrome coronavirus (MERS-CoV), SARS-CoV-2 MESHD reveals new clinical, immunological, and pathologic features. The lymphocyte depletion, macrophage and neutrophil hyperactivation, cytokine dysregulation MESHD, thrombophilia MESHD, delayed antiviral response, and immune exhaustion are key immunological findings linked to the clinical progression of this disease. Understanding and identifying the underlying immunological basis of COVID-19 is crucial to designing effective therapies. Here, we provide an overview of immunopathogenesis driven by SARS-CoV-2 after its interactions with the immune system.

    COVID-19 induces a hyperactive MESHD phenotype in circulating platelets

    Authors: Shane P Comer; Sarah Cullivan; Paulina B Szklanna; Luisa Weiss; Steven Cullen; Sarah Kelliher; Albert Smolenski; Niamh Moran; Claire Murphy; Haidar Altaie; John Curran; Katherine O'Reilly; Aoife G Cotter; Brian Marsh; Sean Gaine; Patrick Mallon; Brian McCullagh; Fionnuala Ní Áinle; Barry Kevane; Patricia B Maguire

    doi:10.1101/2020.07.24.20156240 Date: 2020-07-26 Source: medRxiv

    Background Coronavirus disease MESHD 2019 (COVID-19), caused by novel coronavirus SARS-CoV-2 MESHD, has to date affected over 13.3 million globally. Although high rates of venous thromboembolism MESHD thromboembolism HP and evidence of COVID-19-induced endothelial dysfunction have been reported, the precise aetiology of the increased thrombotic MESHD risk associated with COVID-19 infection MESHD remains to be fully elucidated. Objectives Here, we assessed clinical platelet parameters and circulating platelet activity in patients with severe and non-severe COVID-19. Methods An assessment of clinical blood SERO parameters in patients with severe COVID-19 disease MESHD (requiring intensive care), patients with non-severe disease (not requiring intensive care), general medical in-patients without COVID-19 and healthy donors was undertaken. Platelet function and activity were also assessed by secretion and specific marker analysis. Results We show that routine clinical blood SERO parameters including increased MPV and decreased platelet:neutrophil ratio are associated with disease severity in COVID-19 upon hospitalisation and intensive care unit admission. Strikingly, agonist-induced ADP release was dramatically higher in COVID-19 patients compared with non-COVID-19 hospitalized patients and circulating levels of PF4, sP-selectin and TPO were also significantly elevated in COVID-19. Conclusion Distinct differences exist in routine full blood SERO count and other clinical laboratory parameters between patients with severe and non-severe COVID-19. Moreover, we have determined that COVID-19 patients possess hyperactive circulating platelets. These data suggest that abnormal platelet reactivity may contribute to hypercoagulability HP hypercoagulability MESHD in COVID-19. Further investigation of platelet function in COVID-19 may provide additional insights into the aetiology of thrombotic risk in this disease and may contribute to the optimisation of thrombosis MESHD prevention and treatment strategies.

    Severe COVID-19 is associated with elevated serum SERO IgA and antiphospholipid IgA- antibodies SERO

    Authors: Omar Hasan Ali; David Bomze; Lorenz Risch; Silvio D Brugger; Matthias Paprotny; Myriam Weber; Sarah Thiel; Lukas Kern; Werner C Albrich; Philipp Kohler; Christian R Kahlert; Pietro Vernazza; Philipp K Buehler; Reto A Schuepbach; Alejandro Gomez-Mejia; Alexandra M Popa; Andreas Bergthaler; Josef M Penninger; Lukas Flatz

    doi:10.1101/2020.07.21.20159244 Date: 2020-07-24 Source: medRxiv

    Background: While the pathogenesis of coronavirus disease MESHD 2019 (COVID-19) is becoming increasingly clear, there is little data on IgA response, the first line of bronchial immune defense. Objective: To determine, whether COVID-19 is associated with a vigorous total IgA response and whether IgA autoantibodies are associated with complications of severe illness. Since thrombotic MESHD events are frequent in severe COVID-19 and resemble hypercoagulation of antiphospholipid syndrome MESHD ( APS MESHD), our approach focused on antiphospholipid antibodies SERO (aPL). Materials and methods: In this retrospective cohort study we compared clinical data and aPL from 64 patients with COVID-19 from three independent centers (two in Switzerland, one in Liechtenstein). Samples were collected from April 9, 2020 to May 1, 2020. Total IgA and aPL were measured with FDA-approved commercially available clinical diagnostic kits. Results: Clinical records of the 64 patients with COVID-19 were reviewed and divided into a cohort with mild illness (mCOVID, n=26 [41%]), a discovery cohort with severe illness (sdCOVD, n=14 [22%]) and a confirmation cohort with severe illness (scCOVID, n=24 [38%]). Severe illness MESHD was significantly associated with increased total IgA (sdCOVID, P=0.01; scCOVID, P<0.001). Total IgG levels were similar in both cohorts. Among aPL, both cohorts with severe illness significantly correlated with elevated anti-Cardiolipin IgA (sdCOVID and scCOVID, P<0.001), anti-Cardiolipin IgM (sdCOVID, P=0.003; scCOVID, P<0.001), and anti-Beta2 Glycoprotein-1 IgA (sdCOVID and scCOVID, P<0.001). Systemic lupus erythematosus HP Systemic lupus erythematosus MESHD was excluded from all patients as a potential confounder of APS MESHD. Conclusions: Higher total IgA and IgA-aPL were consistently associated with severe illness. These novel data strongly suggest that a vigorous antiviral IgA-response triggered in the bronchial mucosa induces systemic autoimmunity MESHD autoimmunity HP.

    COVID-19: The Rollercoaster of Fibrin(ogen), D-dimer, von Willebrand MESHD Factor, P-selectin and Their Interactions with Endothelial Cells, Platelets and Erythrocytes MESHD

    Authors: Corlia Grobler; Jhade Bredenkamp; Mireille Grobbelaar; Sipho Maphumulo; Jaco Laubscher; Janami Steenkamp; Douglas Kell; Etheresia Pretorius

    id:10.20944/preprints202007.0142.v1 Date: 2020-07-08 Source:

    Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), coronavirus disease MESHD 2019 (COVID-19)-induced infection MESHD is strongly associated with various coagulopathies MESHD that may result in either bleeding MESHD and thrombocytopenia HP thrombocytopenia MESHD or hypercoagulation MESHD and thrombosis MESHD. Thrombotic and bleeding MESHD or thrombotic MESHD pathologies are significant accompaniments to acute respiratory syndrome MESHD and lung complications MESHD in COVID-19. Thrombotic MESHD events and bleeding MESHD, often occurs in subjects with weak multiple risk factors and co-morbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand MESHD Factor (vWF). Central to activity of these biomarkers are their receptors and signaling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19, and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction MESHD. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of vWF, P-selectin and fibrinogen are present with still low levels of D-dimer. Progression to vWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devises and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients.

    Injury-Prone: Peripheral nerve injuries associated with prone positioning for COVID-19-related acute respiratory distress HP respiratory distress MESHD syndrome

    Authors: George R. Malik; Alexis R. Wolfe; Rachna Soriano; Leslie Rydberg; Lisa F. Wolfe; Swati Deshmukh; Jason H. Ko; Ryan P. Nussbaum; Prakash Jayabalan; James M. Walter; Colin K. Franz

    doi:10.1101/2020.07.01.20144436 Date: 2020-07-02 Source: medRxiv

    Patients with Coronavirus disease MESHD 2019 (COVID-19) who require invasive mechanical ventilation frequently meet the acute respiratory distress HP respiratory distress MESHD syndrome ( ARDS MESHD) diagnostic criteria. Hospitals based in the United States have been incorporating prone positioning (PP) into the COVID-19-related ARDS treatment plan at a higher rate than normal. Here, we describe 11 patients admitted to a single inpatient rehabilitation hospital who were subsequently diagnosed with acquired focal/ multifocal peripheral nerve injury MESHD (PNI) in association with the use of PP for COVID-19-related ARDS. The reason for the high rate of PNI associated with PP in COVID-19 ARDS is likely multifactorial, but may include an underlying state of hyperinflammation and hypercoagulability MESHD hypercoagulability HP already linked to other the neurological sequelae of COVID-19. Physicians must be aware of this elevated susceptibility to PNI in severe COVID-19 and refined standard PP protocols in order to reduce the risk.

    Superior anticoagulation strategies for renal replacement therapy in critically ill patients with COVID-19: a cohort study

    Authors: Frederic Arnold; Lukas Westermann; Siegbert Rieg; Elke Neumann-Haefelin; Paul Biever; Gerd Walz; Johannes Kalbhenn; Yakup Tanriver

    doi:10.1101/2020.06.26.20140699 Date: 2020-07-01 Source: medRxiv

    Background Coronavirus disease MESHD 2019 (COVID-19) patients who are admitted to intensive care units (ICU) have a high risk of requiring renal replacement therapy (RRT) due to acute kidney injury HP acute kidney injury MESHD ( AKI MESHD). Concomitantly, COVID-19 patients exhibit a state of hypercoagulability HP hypercoagulability MESHD that can affect circuit lifespan. An optimal anticoagulation strategy is therefore needed in order to maintain circuit patency and therapeutic efficiency of RRT. Methods Retrospective single-centre cohort study on 71 critically ill COVID-19 patients at the University of Freiburg Medical Center. Included were all patients aged TRANS 18 years and older with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD that were admitted to ICU between February 26 and May 21, 2020. We collected data on the COVID-19 disease course, AKI MESHD, RRT, thromboembolic MESHD events and anticoagulation. Primary outcome of the study was the effect of different anticoagulation strategies during RRT on extracorporeal circuit lifespans. Results Anticoagulation during continuous veno-venous haemodialysis ( CVVHD MESHD) was performed with unfractionated heparin (UFH) or citrate. Mean treatment time in the UFH group was 21.3h (SEM: {+/-}5.6h). Mean treatment time in the citrate group was 45.6h (SEM: {+/-}2.7h). Citrate anticoagulation prolonged treatment duration significantly by 24.4h (p=0.0014). Anticoagulation during sustained low-efficiency daily dialysis ( SLEDD MESHD) was performed with UFH, argatroban or low molecular weight heparin (LMWH). Mean dialysis time with UFH was 8.1h (SEM: {+/-}1.3h), argatroban 8.0h (SEM: {+/-}0.9h) and LMWH 11.8h (SEM: {+/-}0.5h). Compared to UFH and argatroban, LMWH significantly prolonged treatment times by 3.7h (p=0.0082) and 3.8h (p=0.0024), respectively. Conclusions UFH fails to prevent early clotting events in dialysis circuits. For patients, who do not require an effective systemic anticoagulation, regional citrate dialysis is the most effective strategy in our cohort. For patients, who require an effective systemic anticoagulation treatment, the usage of LMWH results in the longest circuit life spans.

    Acute portal vein thrombosis HP vein thrombosis MESHD secondary to COVID-19: a case report 

    Authors: Roham Borazjani; Seyed Reza Seraj; Mohammad javad Fallahi; Zhila Rahmanian

    doi:10.21203/ Date: 2020-06-30 Source: ResearchSquare

    Introduction: COVID-19 pneumonia HP neumonia MESHDexhibits several extra-pulmonary complications.Case presentation: We described a 23-year old male TRANS with c oronavirus pneumonia MESHD pneumonia HP and portal vein thrombosis HP ein thrombosis. MESHDConclusion: Clinicians should always consider t hrombosis MESHDand other h ypercoagulable diseases MESHDin patients with COVID-19.

    Platelets can contain SARS-CoV-2 RNA and are hyperactivated in COVID-19

    Authors: Younes Zaid; Florian Puhm; Isabelle Allaeys; Abdallah Naya; Mounia Oudghiri; Loubna Khalki; Youness Limami; Nabil Zaid; Khalid Sadki; Rafiqua Ben El Haj; Wissal Maher; Lamiae Belayachi; Bouchra Belefquih; Amina Benouda; Amine Cheikh; Yahia Cherrah; Louis Flamand; Fadila Guessous; Eric Boilard

    doi:10.1101/2020.06.23.20137596 Date: 2020-06-23 Source: medRxiv

    ABSTRACT Rationale: In addition to the overwhelming lung inflammation MESHD that prevails in COVID-19, hypercoagulation MESHD and thrombosis MESHD contribute to the lethality of subjects infected with severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2). Platelets are chiefly implicated in thrombosis MESHD. Moreover, they can interact with viruses and are an important source of inflammatory mediators. While a lower platelet count is associated with severity and mortality, little is known about platelet function during COVID-19. Objective: To evaluate the contribution of platelets to inflammation MESHD and thrombosis MESHD in COVID-19 patients. Methods and Results: We document the presence of SARS-CoV-2 RNA in platelets of COVID-19 patients. Exhaustive assessment of cytokines in plasma SERO and in platelets revealed the modulation of platelet-associated cytokine levels in COVID-19, pointing to a direct contribution of platelets to the plasmatic cytokine load. Moreover, we demonstrate that platelets release their alpha- and dense-granule contents and phosphatidylserine-exposing extracellular vesicles. Functionally, platelets were hyperactivated in COVID-19 subjects, with aggregation occurring at suboptimal thrombin concentrations. Furthermore, platelets adhered more efficiently onto collagen-coated surfaces under flow conditions. Conclusions: These data suggest that platelets could participate in the dissemination of SARS-CoV-2 and in the overwhelming thrombo-inflammation MESHD observed in COVID-19. Thus, blockade of platelet activation pathways may improve outcomes in this disease.

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MeSH Disease
Human Phenotype

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