Corpus overview


MeSH Disease

Human Phenotype


    displaying 1 - 10 records in total 34
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    SARS-CoV-2 and Stroke MESHD Stroke HP Characteristics: A Report from the Multinational COVID-19 Stroke MESHD Stroke HP Study Group

    Authors: Shima Shahjouei; Georgios Tsivgoulis; Rohan Arora; Mohammad Hossein Harirchian; Nasrin Rahimian; Afshin Borhani-Haghighi; Stefania Mondello; Arash Kia; Alireza Vafaei Sadr; Ashkhan Mowla; Venkatesh Avula; Saeed Ansari; Ramin Zand; Vida Abedi; Ghasem Farahmand; Eric Koza; Martin Punter; Annemarei Ranta; Achille Cernigliaro; Alaleh Vaghefi Far; Afshin Borhani-Haghighi; Jiang Li; Oluwaseyi Olulana; Durgesh Chaudhary

    doi:10.1101/2020.08.05.20169169 Date: 2020-08-07 Source: medRxiv

    Background: Stroke MESHD Stroke HP is reported as a consequence of SARS-CoV-2 infection MESHD. However, there is a lack of regarding comprehensive stroke MESHD stroke HP phenotype and characteristics Methods: We conducted a multinational observational study on features of consecutive acute ischemic stroke HP stroke MESHD (AIS), intracranial hemorrhage MESHD intracranial hemorrhage HP (ICH), and cerebral venous or sinus thrombosis MESHD (CVST) among SARS-CoV-2 infected patients. We further investigated the association of demographics, clinical data, geographical regions, and countrie's health expenditure among AIS patients with the risk of large vessel occlusion (LVO), stroke MESHD stroke HP severity as measured by National Institute of Health stroke MESHD stroke HP scale (NIHSS), and stroke MESHD stroke HP subtype as measured by the TOAST criteria. Additionally, we applied unsupervised machine learning algorithms to uncover possible similarities among stroke MESHD stroke HP patients. Results: Among the 136 tertiary centers of 32 countries who participated in this study, 71 centers from 17 countries had at least one eligible stroke MESHD stroke HP patient. Out of 432 patients included, 323(74.8%) had AIS, 91(21.1%) ICH, and 18(4.2%) CVST. Among 23 patients with subarachnoid hemorrhage MESHD subarachnoid hemorrhage HP, 16(69.5%) had no evidence of aneurysm MESHD. A total of 183(42.4%) patients were women, 104(24.1%) patients were younger than 55 years, and 105(24.4%) patients had no identifiable vascular risk factors. Among 380 patients who had known interval onset of the SARS-CoV-2 and stroke MESHD stroke HP, 144(37.8%) presented to the hospital with chief complaints of stroke MESHD stroke HP-related symptoms, with asymptomatic TRANS or undiagnosed SARS-CoV-2 infection MESHD. Among AIS patients 44.5% had LVO; 10% had small artery occlusion according to the TOAST criteria. We observed a lower median NIHSS (8[3-17], versus 11[5-17]; p=0.02) and higher rate of mechanical thrombectomy (12.4% versus 2%; p<0.001) in countries with middle to high-health expenditure when compared to countries with lower health expenditure. The unsupervised machine learning identified 4 subgroups, with a relatively large group with no or limited comorbidities. Conclusions: We observed a relatively high number of young, and asymptomatic TRANS SARS-CoV-2 infections MESHD among stroke MESHD stroke HP patients. Traditional vascular risk factors were absent among a relatively large cohort of patients. Among hospitalized patients, the stroke MESHD stroke HP severity was lower and rate of mechanical thrombectomy was higher among countries with middle to high-health expenditure.

    Suspected Heparin-Induced Thrombocytopenia HP Thrombocytopenia MESHD in a COVID-19 Patient on Extracorporeal Membrane Oxygenation Support: A Case Report.

    Authors: Xuan T. Phan; Tuan Huu Nguyen; Tung T. Tran; Thu-Hien T. Huynh; Thuy-Ha T. Hoang; Vinh-Chau V. Nguyen; Thao N. T. Pham

    doi:10.21203/ Date: 2020-07-29 Source: ResearchSquare

    Background: Extracorporeal membrane oxygenation (ECMO) support can be life-saving in critically ill COVID-19 patients. However, there are many complications associated with this procedure, including Heparin-induced thrombocytopenia HP thrombocytopenia MESHD (HIT.) Despite its rarity in ECMO cases, HIT can lead to devastating consequences and is difficult to manage.Case presentation: In this report, we present a case of a COVID-19 patient on ECMO support who was diagnosed with HIT and required intensive treatment. Initially, the patient showed no remarkable sign of thrombosis MESHD and HIT was only suspected due to newly-developed thrombocytopenia MESHD thrombocytopenia HP and oxygenator dysfunction. Regarding his treatment, since there was no recommended replacement to heparin available to us at the time of diagnosis, we decided to use Rivaroxaban temporarily. No adverse events were recorded during that period. The patient was able to make a full recovery.Conclusion: HIT may jeopardize patient’s care during ECMO. As COVID-19 may bring about a surge in the number of patients requiring ECMO support, we need consented guidance to optimize treatment in this specific situation.

    Massive cerebral venous thrombosis HP venous thrombosis MESHD related to oligosymptomatic COVID-19 infection MESHD: a case report

    Authors: Simone Beretta; Fulvio Da Re; Valentina Francioni; Paolo Remida; Benedetta Storti; Lorenzo Fumagalli; Maria Luisa Piatti; Patrizia Santoro; Diletta Cereda; Claudia Cutellè; Fiammetta Pirro; Danilo Antonio Montisano; Francesca Beretta; Francesco Pasini; Annalisa Cavallero; Ildebrando Appollonio; Carlo Ferrarese

    doi:10.21203/ Date: 2020-07-27 Source: ResearchSquare

    Background: The development of thrombotic coagulopathy is frequent in COVID-19 patients, but the timing after infection MESHD, cerebral venous system involvement, treatment and outcome are uncertain.Case Presentation: We report a case of massive cerebral venous thrombosis HP venous thrombosis MESHD occurring in the late phase of COVID-19 infection MESHD. Mild respiratory symptoms, without fever MESHD fever HP, started three weeks before headache MESHD headache HP and acute neurological deficits. She had no dyspnea MESHD dyspnea HP, although she was hypoxic and with typical COVID-19 associated interstitial pneumonia MESHD pneumonia HP. Brain CT scan showed a left parietal hypodense lesion with associated sulcal subarachnoid haemorrhage. CT angiography showed a massive cerebral vein thrombosis MESHD. An asymptomatic TRANS concomitant right internal iliac vein thrombosis MESHD was found. Both cerebral venous thrombosis HP venous thrombosis MESHD and deep venous thrombosis HP venous thrombosis MESHD were effectively treated with unfractionated heparin started on the day of admission, then shifted to low molecular weight heparin, with a favorable clinical course. Nasopharyngel swab, repeated twice, tested negative for SARS-CoV-2. Serological tests SERO confirmed SARS-CoV-2 infection MESHD. Conclusions: Our case supports active surveillance and prevention of thrombotic complications associated with COVID-19, which may affect both peripheral and cerebral venous system. Early initiation of unfractionated heparin may lead to good neurological outcome.

    Clinical Features and Histopathological Changes of Skeletal Muscle in Patients with COVID-19: Two Case reports

    Authors: Mei-Yan Liao; Ping Duan; Zhen-Yu Pan; Yu-Xiang Cai; Wei Fan; An-Song Ping

    doi:10.21203/ Date: 2020-07-19 Source: ResearchSquare

    BackgroundTo the best of our knowledge, muscle soreness is a common manifestation for the coronavirus disease MESHD-19 (COVID-19) patients, but the mechanism of the severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) injury to skeletal muscle remains unclear, there has been no publication focused on muscle involvement in COVID-19 patients.Case presentationWe present the case of two Chinese men with COVID-19, whose common symptoms were fatigue MESHD fatigue HP and muscle soreness. They went through different treatments, patient 1, 81-year-old, eventually died of multi-organ failure, and patient 2, 53-year-old, underwent amputation of the mid-lower section of left thigh. Laboratory tests in both patients showed abnormal biochemical parameters associated with skeletal muscle injury. We obtained skeletal muscle samples from these two patients, one from postmortem biopsy of gastrocnemius muscle and the other from a resected left lower limb due to thrombosis MESHD. The pathological findings in patient 1 were mainly scattered atrophic muscles, while fiber necrosis HP necrosis MESHD and minor inflammation MESHD were identified in patient 2, and the mild infiltrations were confirmed by CD68 and LCA staining to be predominantly macrophages and lymphocytes.ConclusionsWe report the clinical and laboratory features together with histopathological findings in skeletal muscle tissues from two COVID-19 cases and speculate that the SARS-CoV-2 may cause skeletal muscle injury. Due to the particularity of individual differences in case reports, the background of chronic neuromuscular disease MESHD in patient 1 and a minimal compartment syndrome MESHD caused by thrombosis MESHD in patient 2 need to be excluded prior to the conclusion that the skeletal muscles have been involved in COVID-19.

    Asymptomatic TRANS COVID-19 Patient, Occurrence of Fatal Pulmonary Arterial Thrombosis HP Thrombosis MESHD.

    Authors: Franca Del Nonno; Daniele Colombo; Roberta Nardacci; Laura Falasca

    doi:10.21203/ Date: 2020-07-17 Source: ResearchSquare

    The induction of hypercoagulability HP is one of the pathophysiological mechanism in patients with a severe presentation of the SARS-CoV-2 infection MESHD that can contribute to death MESHD. A considerable number of SARS-Cov-2 infected individuals could be asymptomatic TRANS and they don’t need medical treatment. We reported autoptic evidences of COVID-19 trombotic fatal lesions in a asymptomatic COVID-19 patient after negative conversion.This study provides evidences that an appropriate diagnostic screening for thrombotic complications and the early treatment recommendations of antithrombotic drugs could represent an important topic even in asymptomatic TRANS individuals. 

    Coagulopathy and Thrombosis MESHD as a Result of Severe COVID-19 Infection MESHD: A Microvascular Focus

    Authors: Upendra K. Katneni; Aikaterini Alexaki; Ryan C. Hunt; Tal Schiller; Michael DiCuccio; Paul W. Buehler; Juan C. Ibla; Chava Kimchi-Sarfaty

    id:10.20944/preprints202005.0385.v2 Date: 2020-07-15 Source:

    Coronavirus disease MESHD of 2019 (COVID-19) is the clinical manifestation of the respiratory infection MESHD caused by severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2). While primarily recognized as a respiratory disease MESHD, it is clear that COVID-19 is systemic illness impacting multiple organ systems. One defining clinical feature of COVID-19 has been the high incidence of thrombotic events. The underlying processes and risk factors for the occurrence of thrombotic events in COVID-19 remain inadequately understood. While severe bacterial, viral or fungal infections MESHD are well recognized to activate the coagulation system, COVID-19 associated coagulopathy is likely to have unique mechanistic features. Inflammatory-driven processes are likely primary drivers of coagulopathy in COVID-19, but the exact mechanisms linking inflammation MESHD to dysregulated hemostasis and thrombosis MESHD are yet to be delineated. Cumulative findings of microvascular thrombosis MESHD has raised question if the endothelium and microvasculature should be a point of investigative focus. Von Willebrand Factor (VWF) and its protease, ADAMTS13 play important role in the maintenance of microvascular hemostasis. In inflammatory conditions, imbalanced VWF-ADAMTS13 characterized by elevated VWF levels and inhibited and/or reduced activity of ADAMTS13 has been reported. Also, an imbalance between ADAMTS13 activity and VWF antigen is associated with organ dysfunction and death MESHD in patients with systemic inflammation MESHD. A thorough understanding of VWF-ADAMTS13 interactions during early and advanced phases of COVID-19 could help better define the pathophysiology, guide thromboprophylaxis and treatment and improve clinical prognosis.

    COVID-19: Role of the Inflammasome

    Authors: Claudio G. Gallo; Sirio Fiorino; Giovanni Posabella; Donato Antonacci; Antonio Tropeano; Emanuele Pausini; Carlotta Pausini; Tommaso Guarniero; Marco Zancanaro

    id:202007.0246/v1 Date: 2020-07-12 Source:

    Covid-19 disease MESHD is caused by SARS Cov-2 virus. Despite its high transmissibility TRANS, the CFR (Case Fatality Rate) of COVID-19 seems to be lower than the SARS (9,5%) and MERS (34,4%) ones93 , but higher than the influenza one (0-1%)94,95 . The disease is asymptomatic MESHD asymptomatic TRANS or paucisymptomatic in most of the patients, although in few cases it can be characterized by serious complications. The main causes of hospitalization in intensive care are represented by ALI ( Acute Lung Injury MESHD), ARDS (Acute Respiratory Distress HP Syndrome MESHD), cardiovascular problems and coagulopathies (diffuse thrombosis MESHD, microthrombosis, embolisms MESHD, myocarditis MESHD myocarditis HP, arrhytmias, heart failure MESHD, stroke MESHD stroke HP)96-98, acute nephropathy99,100 and encephalopathies101. The virus presence in the vascular wall can cause endotheliitis, which triggers the process of diffuse coagulation that can lead to a worsening of the systemic inflammation MESHD. The exaggerated inflammatory response seems to be connected with the development of ARDS, MOF ( Multiple Organ Failure MESHD) and coagulopathies102-107.

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

    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 MESHD coronavirus 2 (SARS-Cov-2), coronavirus disease MESHD 2019 (COVID-19)-induced infection MESHD is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia MESHD thrombocytopenia HP or hypercoagulation and thrombosis MESHD. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome MESHD and lung complications in COVID-19. Thrombotic events and bleeding, 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 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. During the progression of the disease MESHD, 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 MESHD, 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.

    COVID-19: Comprehensive Synopsis of Suggested Pathophysiological Mechanisms and Repurposed Drugs

    Authors: Mathijs Binkhorst; Annette K. Offringa; Johannes G. van der Hoeven

    id:10.20944/preprints202007.0108.v1 Date: 2020-07-07 Source:

    During the current COVID-19 pandemic caused by SARS-CoV-2, clinicians and scientists are working assiduously to unravel its pathophysiology and find effective treatments. An impressive number of papers has been published on SARS-CoV-2, exposing the complexity of the disease MESHD, the tendency of scientists to form hypotheses within their area of expertise, and the lack of orchestration of research. Hypotheses and research findings mainly complement each other, though sometimes controversies can be discerned among various theories and study results. Our overview aims to portray the ‘big picture’ of COVID-19, visualising the interwovenness of different pathophysiological pathways, with a focus on cytokine-induced pathology, the sequelae of ACE2 downregulation, and thrombosis MESHD associated with microvascular injury. It aids in overseeing the effects of repurposed drugs on intended targets, but also alerts to the (adverse) effects on interacting pathways. The overview shows how comorbidities probably increase susceptibility to (severe) COVID-19 and provides the possible pathophysiological origin of signs, symptoms MESHD, and biochemical abnormalities.

    The Emerging Role of Neutrophil Extracellular Traps in Severe Acute Respiratory Syndrome MESHD Coronavirus 2 (COVID-19)

    Authors: Angélica Arcanjo; Jorgete Logullo; Camilla Cristie Barreto Menezes; Thais Chrispim de Souza Cravalho Giangiarulo; Shana Priscila Coutinho Barroso; Adriane Todeschini; Leonardo Freire-de-Lima; Debora Ricardo Decoté; Celio Geraldo Freire-de-Lima; Fátima Conceição Silva; Wilson Savino; Alexandre Morrot

    doi:10.21203/ Date: 2020-07-06 Source: ResearchSquare

    The novel coronavirus SARS-CoV2 causes COVID-19, a highly pathogenic viral infection MESHD threatening millions. The majority of those infected are asymptomatic TRANS or mildly symptomatic showing typical clinical signs of common cold MESHD. However approximately 20% of the patients can progress to acute respiratory distress HP syndrome MESHD (ARDS) and eventually death MESHD in about 5% of cases. Recently, angiotensin-converting enzyme 2 (ACE2) has been shown to be a functional receptor for virus entry into host target cells. The upregulation of ACE2 in patients with comorbidities may represent a propensity for increased viral load and spreading of infection MESHD to extrapulmonary tissues. This systemic infection MESHD is associated with higher neutrophil to lymphocyte ratio in infected tissues and high levels of pro-inflammatory cytokines leading to an extensive microthrombus formation with multiorgan failure. Herein we investigated whether SARS-CoV2 can stimulate extracellular neutrophils traps (NETs) in a process called NETosis. We demonstrated for the first time that SARS-CoV2 in fact is able to activate NETosis in human neutrophils. Our findings indicated that this process is associated with increased levels of intracellular Reactive Oxygen Species (ROS) in neutrophils. The ROS-NET pathway plays a role in thrombosis MESHD formation and our study suggest the importance of this target for therapy approaches against disease MESHD.

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MeSH Disease
Human Phenotype

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