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2.
Emerg Microbes Infect ; 9(1): 1514-1522, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-611844

ABSTRACT

We previously made the hypothesis that STING contributes to COVID-19. The present review detail new arguments for over-activation of STING pathways in COVID-19, following the description of hyper-coagulability and Kawasaki-like diseases in children. Indeed, Kawasaki disease is induced by overreaction of innate cells following exposition to various viruses, including herpes viruses which trigger STING. It predisposes to diffuse vasculitis and aneurysms, whereas STING is over-expressed in arterial aneurisms. The redness at the inoculation site of bacillus Calmette-Guérin, a specific feature of Kawasaki disease, is reproduced by activation of the STING pathway, which is inhibited upstream by aspirin, intravenous immunoglobulins, and Vitamin-D. SARS-CoV2 binding to ACE2 can lead to excessive angiotensin II signaling, which activates the STING pathway in mice. Over-activation of the STING-pathway promotes hyper-coagulability through release of interferon-ß and tissue factor by monocytes-macrophages. Aspirin and dipyridamole, besides their anti-platelet activity, also reduce tissue factor procoagulant activity, and aspirin inhibits the STING pathway upstream of STING. Aspirin and dipyridamole may be used, in combination with drugs blocking downstream the activation of the STING pathway, like inhibitors of IL-6R and JAK/STAT pathways. The risk of bleeding should be low as bleeding has not been reported in severe COVID-19 patients.


Subject(s)
Coronavirus Infections/complications , Membrane Proteins/metabolism , Mucocutaneous Lymph Node Syndrome/etiology , Pneumonia, Viral/complications , Angiotensin II/metabolism , Animals , Aspirin/therapeutic use , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/metabolism , Blood Coagulation Disorders/virology , Coronavirus Infections/drug therapy , Coronavirus Infections/metabolism , Dipyridamole/therapeutic use , Humans , Immunoglobulins, Intravenous/therapeutic use , Interferons/metabolism , Mice , Mucocutaneous Lymph Node Syndrome/metabolism , Pandemics , Platelet Aggregation Inhibitors/therapeutic use , Pneumonia, Viral/drug therapy , Pneumonia, Viral/metabolism , Signal Transduction , Thrombosis/drug therapy , Thrombosis/metabolism , Thrombosis/virology
3.
J Exp Med ; 217(8)2020 08 03.
Article in English | MEDLINE | ID: covidwho-607919

ABSTRACT

The renin-angiotensin system (RAS) has long been appreciated as a major regulator of blood pressure, but has more recently been recognized as a mechanism for modulating inflammation as well. While there has been concern in COVID-19 patients over the use of drugs that target this system, the RAS has not been explored fully as a druggable target. The abbreviated description of the RAS suggests that its dysregulation may be at the center of COVID-19.


Subject(s)
Coronavirus Infections/physiopathology , Lung Diseases/physiopathology , Lung/virology , Pneumonia, Viral/physiopathology , Angiotensin I/metabolism , Animals , Blood Coagulation Disorders/virology , Coronavirus Infections/etiology , Coronavirus Infections/metabolism , Cytokines/metabolism , Humans , Hypertension/physiopathology , Lung/metabolism , Lung/physiopathology , Lung Diseases/metabolism , Lung Diseases/virology , Obesity/physiopathology , Pandemics , Peptide Fragments/metabolism , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/etiology , Pneumonia, Viral/metabolism , Receptor, Angiotensin, Type 1/metabolism , Severity of Illness Index
4.
Dig Dis Sci ; 65(8): 2181-2186, 2020 08.
Article in English | MEDLINE | ID: covidwho-598781

ABSTRACT

Coronavirus disease of 2019 (COVID-19) can be associated with high morbidity and mortality; patients with severe clinical manifestations may develop significant coagulopathy as well as unexpected thromboembolic complications. In response, centers are increasingly treating selected patients with intermediate-dose prophylactic or even therapeutic dose anticoagulation in order to prevent potentially catastrophic thrombotic complications. With this changing practice, the authors suspect that inpatient gastrointestinal consult teams across the country will be frequently managing COVID-19 patients with gastrointestinal bleeding (GIB). In order to reduce potentially avoidable hospital readmissions for GIB while improving patient outcomes, it is imperative to appropriately risk-stratify patients prior to initiation of anticoagulation. In this review, we discuss how to appropriately identify high-risk patients for GIB and how to mitigate GIB risk with proton-pump inhibitor co-therapy, medication reconciliation, and Helicobacter pylori testing and treating in this complex and morbid population.


Subject(s)
Anticoagulants/adverse effects , Blood Coagulation Disorders , Coronavirus Infections/blood , Gastrointestinal Hemorrhage , Pneumonia, Viral/blood , Proton Pump Inhibitors/therapeutic use , Risk Adjustment/methods , Anticoagulants/administration & dosage , Betacoronavirus/isolation & purification , Blood Coagulation Disorders/prevention & control , Blood Coagulation Disorders/virology , Chemoprevention/methods , Chemoprevention/standards , Gastrointestinal Hemorrhage/chemically induced , Gastrointestinal Hemorrhage/prevention & control , Humans , Pandemics
5.
Intensive Care Med ; 46(7): 1339-1348, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-597960

ABSTRACT

Acute kidney injury (AKI) has been reported in up to 25% of critically-ill patients with SARS-CoV-2 infection, especially in those with underlying comorbidities. AKI is associated with high mortality rates in this setting, especially when renal replacement therapy is required. Several studies have highlighted changes in urinary sediment, including proteinuria and hematuria, and evidence of urinary SARS-CoV-2 excretion, suggesting the presence of a renal reservoir for the virus. The pathophysiology of COVID-19 associated AKI could be related to unspecific mechanisms but also to COVID-specific mechanisms such as direct cellular injury resulting from viral entry through the receptor (ACE2) which is highly expressed in the kidney, an imbalanced renin-angotensin-aldosteron system, pro-inflammatory cytokines elicited by the viral infection and thrombotic events. Non-specific mechanisms include haemodynamic alterations, right heart failure, high levels of PEEP in patients requiring mechanical ventilation, hypovolemia, administration of nephrotoxic drugs and nosocomial sepsis. To date, there is no specific treatment for COVID-19 induced AKI. A number of investigational agents are being explored for antiviral/immunomodulatory treatment of COVID-19 and their impact on AKI is still unknown. Indications, timing and modalities of renal replacement therapy currently rely on non-specific data focusing on patients with sepsis. Further studies focusing on AKI in COVID-19 patients are urgently warranted in order to predict the risk of AKI, to identify the exact mechanisms of renal injury and to suggest targeted interventions.


Subject(s)
Acute Kidney Injury/virology , Betacoronavirus/isolation & purification , Coronavirus Infections/complications , Pneumonia, Viral/complications , Renin-Angiotensin System/physiology , Acute Kidney Injury/drug therapy , Acute Kidney Injury/physiopathology , Acute Kidney Injury/therapy , Betacoronavirus/physiology , Blood Coagulation Disorders/virology , Coronavirus Infections/metabolism , Coronavirus Infections/urine , Creatinine/blood , Critical Illness , Hematuria/etiology , Humans , Kidney/physiopathology , Kidney/virology , Pandemics , Pneumonia, Viral/metabolism , Pneumonia, Viral/urine , Proteinuria/etiology , Urinalysis , Urine/chemistry , Urine/virology
6.
Am J Physiol Lung Cell Mol Physiol ; 319(2): L211-L217, 2020 08 01.
Article in English | MEDLINE | ID: covidwho-595634

ABSTRACT

Coronavirus disease 2019 (COVID-19), the clinical syndrome associated with infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has impacted nearly every country in the world. Despite an unprecedented focus of scientific investigation, there is a paucity of evidence-based pharmacotherapies against this disease. Because of this lack of data-driven treatment strategies, broad variations in practice patterns have emerged. Observed hypercoagulability in patients with COVID-19 has created debate within the critical care community on the therapeutic utility of heparin. We seek to provide an overview of the data supporting the therapeutic use of heparin, both unfractionated and low molecular weight, as an anticoagulant for the treatment of SARS-CoV-2 infection. Additionally, we review preclinical evidence establishing biological plausibility for heparin and synthetic heparin-like drugs as therapies for COVID-19 through antiviral and anti-inflammatory effects. Finally, we discuss known adverse effects and theoretical off-target effects that may temper enthusiasm for the adoption of heparin as a therapy in COVID-19 without confirmatory prospective randomized controlled trials. Despite previous failures of anticoagulants in critical illness, plausibility of heparin for COVID-19 is sufficiently robust to justify urgent randomized controlled trials to determine the safety and effectiveness of this therapy.


Subject(s)
Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , Blood Coagulation Disorders/drug therapy , Coronavirus Infections/drug therapy , Heparin/therapeutic use , Pneumonia, Viral/drug therapy , Blood Coagulation Disorders/epidemiology , Blood Coagulation Disorders/virology , Coronavirus Infections/complications , Coronavirus Infections/transmission , Coronavirus Infections/virology , Humans , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/transmission , Pneumonia, Viral/virology
7.
Curr Cardiol Rep ; 22(7): 52, 2020 06 11.
Article in English | MEDLINE | ID: covidwho-593517

ABSTRACT

PURPOSE OF REVIEW: Novel coronavirus disease 2019 (COVID-19) has been associated with an increased risk of arterial and venous thromboembolic (VTE) diseases. However, there is a limited amount of data regarding the prevention and management of VTE in severe hospitalized COVID-19 patients. RECENT FINDINGS: In this article, we review currently available clinical data, and mechanisms for COVID-associated coagulopathy, and propose algorithms for screening, prevention (including extended-duration prophylaxis), and treatment of these patients. Although these recommendations are subject to change given rapidly evolving data, we provide a framework that can guide clinicians in managing thrombotic complications in this challenging condition.


Subject(s)
Anticoagulants , Blood Coagulation Disorders/virology , Coronavirus Infections , Coronavirus , Pandemics , Pneumonia, Viral , Venous Thromboembolism , Anticoagulants/therapeutic use , Betacoronavirus , Coronavirus Infections/complications , Heparin , Heparin, Low-Molecular-Weight , Humans , Male , Pneumonia, Viral/complications , Prospective Studies , Retrospective Studies , Risk Factors , Venous Thromboembolism/prevention & control , Venous Thromboembolism/virology
8.
J Thromb Thrombolysis ; 50(2): 298-301, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-437398

ABSTRACT

This study investigates the association between the treatment with heparin and mortality in patients admitted with Covid-19. Routinely recorded, clinical data, up to the 24th of April 2020, from the 2075 patients with Covid-19, admitted in 17 hospitals in Spain between the 1st of March and the 20th of April 2020 were used. The following variables were extracted for this study: age, gender, temperature, and saturation of oxygen on admission, treatment with heparin, hydroxychloroquine, azithromycin, steroids, tocilizumab, a combination of lopinavir with ritonavir, and oseltamivir, together with data on mortality. Multivariable logistic regression models were used to investigate the associations. At the time of collecting the data, 301 patients had died, 1447 had been discharged home from the hospitals, 201 were still admitted, and 126 had been transferred to hospitals not included in the study. Median follow up time was 8 (IQR 5-12) days. Heparin had been used in 1734 patients. Heparin was associated with lower mortality when the model was adjusted for age and gender, with OR (95% CI) 0.55 (0.37-0.82) p = 0.003. This association remained significant when saturation of oxygen < 90%, and temperature > 37 °C were added to de model with OR 0.54 (0.36-0.82) p = 0.003, and also when all the other drugs were included as covariates OR 0.42 (0.26-0.66) p < 0.001. The association between heparin and lower mortality observed in this study can be acknowledged by clinicians in hospitals and in the community. Randomized controlled trials to assess the causal effects of heparin in different therapeutic regimes are required.


Subject(s)
Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , Blood Coagulation Disorders/drug therapy , Blood Coagulation/drug effects , Coronavirus Infections/drug therapy , Heparin/therapeutic use , Pneumonia, Viral/drug therapy , Aged , Anticoagulants/adverse effects , Antiviral Agents/adverse effects , Betacoronavirus/pathogenicity , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/virology , Coronavirus Infections/blood , Coronavirus Infections/mortality , Coronavirus Infections/virology , Female , Heparin/adverse effects , Hospital Mortality , Host-Pathogen Interactions , Humans , Male , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Risk Assessment , Risk Factors , Spain , Time Factors , Treatment Outcome
9.
Monaldi Arch Chest Dis ; 90(2)2020 May 19.
Article in English | MEDLINE | ID: covidwho-306290

ABSTRACT

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging cross- talk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improvethe clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecular-weight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach.


Subject(s)
Blood Coagulation Disorders/virology , Coronavirus Infections/blood , Pneumonia, Viral/blood , Betacoronavirus/isolation & purification , Blood Coagulation/physiology , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/epidemiology , Coronavirus Infections/epidemiology , Humans , Pandemics , Pneumonia, Viral/epidemiology
11.
J Thromb Thrombolysis ; 50(2): 281-286, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-232649

ABSTRACT

Critically ill patients with COVID-19 pneumonia suffered both high thrombotic and bleeding risk. The effect of SARS-CoV-2 on coagulation and fibrinolysis is not well known. We conducted a retrospective study of critically ill patients admitted to an intensive care unit (ICU) a cause of severe COVID-19 pneumonia and we evaluated coagulation function using rotational thromboelastometry (ROTEM) on day of admission (T0) and 5 (T5) and 10 (T10) days after admission to ICU. Coagulation standard parameters were also evaluated. Forty patients were enrolled into the study. The ICU and the hospital mortality were 10% and 12.5%, respectively. On ICU admission, prothrombin time was slightly reduced and it increased significantly at T10 (T0 = 65.1 ± 9.8 vs T10 = 85.7 ± 1.5, p = 0.002), while activated partial thromboplastin time and fibrinogen values were higher at T0 than T10 (32.2 ± 2.9 vs 27.2 ± 2.1, p = 0.017 and 895.1 ± 110 vs 332.5 ± 50, p = 0.002, respectively); moreover, whole blood thromboelastometry profiles were consistent with hypercoagulability characterized by an acceleration of the propagation phase of blood clot formation [i.e., CFT below the lower limit in INTEM 16/40 patients (40%) and EXTEM 20/40 patients (50%)] and significant higher clot strength [MCF above the upper limit in INTEM 20/40 patients (50%), in EXTEM 28/40 patients (70%) and in FIBTEM 29/40 patients (72.5%)]; however, this hypercoagulable state persists in the first five days, but it decreases ten day after, without returning to normal values. No sign of secondary hyperfibrinolysis or sepsis induced coagulopathy (SIC) were found during the study period. In six patients (15%) a deep vein thrombosis and in 2 patients (5%) a thromboembolic event, were found; 12 patients (30%) had a catheter-related thrombosis. ROTEM analysis confirms that patients with severe COVID-19 pneumonia had a hypercoagulation state that persisted over time.


Subject(s)
Betacoronavirus/pathogenicity , Blood Coagulation Disorders/diagnosis , Blood Coagulation , Coronavirus Infections/diagnosis , Pneumonia, Viral/diagnosis , Thrombelastography , Thromboembolism/diagnosis , Thrombophilia/diagnosis , Aged , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/mortality , Blood Coagulation Disorders/virology , Coronavirus Infections/blood , Coronavirus Infections/mortality , Coronavirus Infections/virology , Critical Illness , Female , Hospital Mortality , Host-Pathogen Interactions , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Predictive Value of Tests , Prognosis , Reproducibility of Results , Retrospective Studies , Risk Factors , Severity of Illness Index , Thromboembolism/blood , Thromboembolism/mortality , Thromboembolism/virology , Thrombophilia/blood , Thrombophilia/mortality , Thrombophilia/virology , Time Factors
13.
Anaesthesia ; 75(8): 1105-1113, 2020 08.
Article in English | MEDLINE | ID: covidwho-134623

ABSTRACT

As COVID-19 disease escalates globally, optimising patient outcome during this catastrophic healthcare crisis is the number one priority. The principles of patient blood management are fundamental strategies to improve patient outcomes and should be given high priority in this crisis situation. The aim of this expert review is to provide clinicians and healthcare authorities with information regarding how to apply established principles of patient blood management during the COVID-19 pandemic. In particular, this review considers the impact of the COVID-19 pandemic on blood supply and specifies important aspects of donor management. We discuss how preventative and control measures implemented during the COVID-19 crisis could affect the prevalence of anaemia, and highlight issues regarding the diagnosis and treatment of anaemia in patients requiring elective or emergency surgery. In addition, we review aspects related to patient blood management of critically ill patients with known or suspected COVID-19, and discuss important alterations of the coagulation system in patients hospitalised due to COVID-19. Finally, we address special considerations pertaining to supply-demand and cost-benefit issues of patient blood management during the COVID-19 pandemic.


Subject(s)
Betacoronavirus , Blood Donors/supply & distribution , Coronavirus Infections/prevention & control , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Anemia/complications , Anemia/diagnosis , Anemia/therapy , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/virology , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Elective Surgical Procedures , Emergencies , Humans , Operative Blood Salvage , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , Preoperative Care/methods
14.
J Thromb Haemost ; 18(7): 1747-1751, 2020 07.
Article in English | MEDLINE | ID: covidwho-72064

ABSTRACT

BACKGROUND: Few observations exist with respect to the pro-coagulant profile of patients with COVID-19 acute respiratory distress syndrome (ARDS). Reports of thromboembolic complications are scarce but suggestive for a clinical relevance of the problem. OBJECTIVES: Prospective observational study aimed to characterize the coagulation profile of COVID-19 ARDS patients with standard and viscoelastic coagulation tests and to evaluate their changes after establishment of an aggressive thromboprophylaxis. METHODS: Sixteen patients with COVID-19 ARDS received a complete coagulation profile at the admission in the intensive care unit. Ten patients were followed in the subsequent 7 days, after increasing the dose of low molecular weight heparin, antithrombin levels correction, and clopidogrel in selected cases. RESULTS: At baseline, the patients showed a pro-coagulant profile characterized by an increased clot strength (CS, median 55 hPa, 95% interquartile range 35-63), platelet contribution to CS (PCS, 43 hPa; interquartile range 24-45), fibrinogen contribution to CS (FCS, 12 hPa; interquartile range 6-13.5) elevated D-dimer levels (5.5 µg/mL, interquartile range 2.5-6.5), and hyperfibrinogenemia (794 mg/dL, interquartile range 583-933). Fibrinogen levels were associated (R2  = .506, P = .003) with interleukin-6 values. After increasing the thromboprophylaxis, there was a significant (P = .001) time-related decrease of fibrinogen levels, D-dimers (P = .017), CS (P = .013), PCS (P = .035), and FCS (P = .038). CONCLUSION: The pro-coagulant pattern of these patients may justify the clinical reports of thromboembolic complications (pulmonary embolism) during the course of the disease. Further studies are needed to assess the best prophylaxis and treatment of this condition.


Subject(s)
Betacoronavirus/pathogenicity , Blood Coagulation Disorders/blood , Blood Coagulation , Coronavirus Infections/blood , Pneumonia, Viral/blood , Aged , Anticoagulants/administration & dosage , Biomarkers/blood , Blood Coagulation/drug effects , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/virology , Blood Coagulation Tests , Coronavirus Infections/diagnosis , Coronavirus Infections/drug therapy , Coronavirus Infections/virology , Female , Fibrinolytic Agents/administration & dosage , Host-Pathogen Interactions , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/drug therapy , Pneumonia, Viral/virology , Prospective Studies , Treatment Outcome
15.
Lancet ; 395(10235): 1517-1520, 2020 05 09.
Article in English | MEDLINE | ID: covidwho-72046

ABSTRACT

Since the outbreak of coronavirus disease 2019 (COVID-19), clinicians have tried every effort to understand the disease, and a brief portrait of its clinical features have been identified. In clinical practice, we noticed that many severe or critically ill COVID-19 patients developed typical clinical manifestations of shock, including cold extremities and weak peripheral pulses, even in the absence of overt hypotension. Understanding the mechanism of viral sepsis in COVID-19 is warranted for exploring better clinical care for these patients. With evidence collected from autopsy studies on COVID-19 and basic science research on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV, we have put forward several hypotheses about SARS-CoV-2 pathogenesis after multiple rounds of discussion among basic science researchers, pathologists, and clinicians working on COVID-19. We hypothesise that a process called viral sepsis is crucial to the disease mechanism of COVID-19. Although these ideas might be proven imperfect or even wrong later, we believe they can provide inputs and guide directions for basic research at this moment.


Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections , Cytokines/metabolism , Lung , Pandemics , Pneumonia, Viral , Sepsis/virology , Autopsy , Blood Coagulation Disorders/virology , Coronavirus Infections/complications , Critical Illness , Endothelium , Epithelium , Humans , Inflammation , Lung/immunology , Lung/pathology , Macrophages , Pneumonia, Viral/complications , Severity of Illness Index , Shock/etiology
16.
J Clin Virol ; 127: 104362, 2020 06.
Article in English | MEDLINE | ID: covidwho-47313

ABSTRACT

Coronavirus disease 2019 (COVID-19) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus strain disease, has recently emerged in China and rapidly spread worldwide. This novel strain is highly transmittable and severe disease has been reported in up to 16% of hospitalized cases. More than 600,000 cases have been confirmed and the number of deaths is constantly increasing. COVID-19 hospitalized patients, especially those suffering from severe respiratory or systemic manifestations, fall under the spectrum of the acutely ill medical population, which is at increased venous thromboembolism risk. Thrombotic complications seem to emerge as an important issue in patients infected with COVID-19. Preliminary reports on COVID-19 patients' clinical and laboratory findings include thrombocytopenia, elevated D-dimer, prolonged prothrombin time, and disseminated intravascular coagulation. As the pandemic is spreading and the whole picture is yet unknown, we highlight the importance of coagulation disorders in COVID-19 infected patients and review relevant data of previous coronavirus epidemics caused by the severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1) and the Middle East Respiratory Syndrome coronavirus (MERS-CoV).


Subject(s)
Blood Coagulation Disorders/virology , Coronavirus Infections/complications , Pneumonia, Viral/complications , Severe Acute Respiratory Syndrome/complications , Animals , China , Coronavirus Infections/blood , Disseminated Intravascular Coagulation/virology , Fibrin Fibrinogen Degradation Products/analysis , Humans , Mice , Middle East Respiratory Syndrome Coronavirus , Pandemics , Pneumonia, Viral/blood , Severe Acute Respiratory Syndrome/blood , Thrombocytopenia/virology
17.
J Thromb Haemost ; 18(7): 1752-1755, 2020 07.
Article in English | MEDLINE | ID: covidwho-42076

ABSTRACT

A prothrombotic coagulopathy is commonly found in critically ill COVID-19 patients with acute respiratory distress syndrome (ARDS). A unique feature of COVID-19 respiratory failure is a relatively preserved lung compliance and high Alveolar-arterial oxygen gradient, with pathology reports consistently demonstrating diffuse pulmonary microthrombi on autopsy, all consistent with a vascular occlusive etiology of respiratory failure rather than the more classic findings of low-compliance in ARDS. The COVID-19 pandemic is overwhelming the world's medical care capacity with unprecedented needs for mechanical ventilators and high rates of mortality once patients progress to needing mechanical ventilation, and in many environments including in parts of the United States the medical capacity is being exhausted. Fibrinolytic therapy has previously been used in a Phase 1 clinical trial that led to reduced mortality and marked improvements in oxygenation. Here we report a series of three patients with severe COVID-19 respiratory failure who were treated with tissue plasminogen activator. All three patients had a temporally related improvement in their respiratory status, with one of them being a durable response.


Subject(s)
Betacoronavirus/pathogenicity , Blood Coagulation Disorders/drug therapy , Coronavirus Infections/drug therapy , Fibrinolysis/drug effects , Fibrinolytic Agents/administration & dosage , Pneumonia, Viral/drug therapy , Thrombolytic Therapy , Tissue Plasminogen Activator/administration & dosage , Aged , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/virology , Coronavirus Infections/blood , Coronavirus Infections/diagnosis , Coronavirus Infections/virology , Fatal Outcome , Female , Fibrinolytic Agents/adverse effects , Host-Pathogen Interactions , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/diagnosis , Pneumonia, Viral/virology , Recovery of Function , Thrombolytic Therapy/adverse effects , Tissue Plasminogen Activator/adverse effects , Treatment Outcome
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