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1.
J Hematol Oncol ; 14(1): 87, 2021 06 04.
Article in English | MEDLINE | ID: covidwho-1259207

ABSTRACT

Cases of thrombotic thrombocytopenia induced by coronavirus disease 2019 (COVID-19) vaccines have been reported recently. Herein, we describe the first case of another critical disorder, hemophagocytic lymphohistiocytosis (HLH), in a healthy individual after COVID-19 vaccination. A 43-year-old Chinese farmer developed malaise, vomiting, and persistent high fever (up to 39.7 °C) shortly after receiving the first dose of the inactivated SARS-CoV-2 vaccine. The initial evaluation showed pancytopenia (neutrophil count, 0.70 × 109/L; hemoglobin, 113 g/L; platelet, 27 × 109/L), elevated triglyceride (2.43 mmol/L), and decreased fibrinogen (1.41 g/L). Further tests showed high serum ferritin levels (8140.4 µg/L), low NK cell cytotoxicity (50.13%-60.83%), and positive tests for Epstein-Barr virus (EBV) DNA. Hemophagocytosis was observed in the bone marrow. Therefore, HLH was confirmed, and dexamethasone acetate (10 mg/day) was immediately prescribed without etoposide. Signs and abnormal laboratory results resolved gradually, and the patient was discharged. HLH is a life-threatening hyperinflammatory syndrome caused by aberrantly activated macrophages and cytotoxic T cells, which may rapidly progress to terminal multiple organ failure. In this case, HLH was induced by the COVID-19 vaccination immuno-stimulation on a chronic EBV infection background. This report indicates that it is crucial to exclude the presence of active EBV infection or other common viruses before COVID-19 vaccination.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , Lymphohistiocytosis, Hemophagocytic/etiology , Adult , Anti-Inflammatory Agents/therapeutic use , Bone Marrow/pathology , Dexamethasone/analogs & derivatives , Dexamethasone/therapeutic use , Humans , Lymphohistiocytosis, Hemophagocytic/blood , Lymphohistiocytosis, Hemophagocytic/diagnosis , Lymphohistiocytosis, Hemophagocytic/drug therapy , Male , SARS-CoV-2/isolation & purification
2.
Eur J Prev Cardiol ; 28(14): 1599-1609, 2021 12 20.
Article in English | MEDLINE | ID: covidwho-1091243

ABSTRACT

AIMS: Cardiovascular diseases (CVDs) increase mortality risk from coronavirus infection (COVID-19). There are also concerns that the pandemic has affected supply and demand of acute cardiovascular care. We estimated excess mortality in specific CVDs, both 'direct', through infection, and 'indirect', through changes in healthcare. METHODS AND RESULTS: We used (i) national mortality data for England and Wales to investigate trends in non-COVID-19 and CVD excess deaths; (ii) routine data from hospitals in England (n = 2), Italy (n = 1), and China (n = 5) to assess indirect pandemic effects on referral, diagnosis, and treatment services for CVD; and (iii) population-based electronic health records from 3 862 012 individuals in England to investigate pre- and post-COVID-19 mortality for people with incident and prevalent CVD. We incorporated pre-COVID-19 risk (by age, sex, and comorbidities), estimated population COVID-19 prevalence, and estimated relative risk (RR) of mortality in those with CVD and COVID-19 compared with CVD and non-infected (RR: 1.2, 1.5, 2.0, and 3.0).Mortality data suggest indirect effects on CVD will be delayed rather than contemporaneous (peak RR 1.14). CVD service activity decreased by 60-100% compared with pre-pandemic levels in eight hospitals across China, Italy, and England. In China, activity remained below pre-COVID-19 levels for 2-3 months even after easing lockdown and is still reduced in Italy and England. For total CVD (incident and prevalent), at 10% COVID-19 prevalence, we estimated direct impact of 31 205 and 62 410 excess deaths in England (RR 1.5 and 2.0, respectively), and indirect effect of 49 932 to 99 865 deaths. CONCLUSION: Supply and demand for CVD services have dramatically reduced across countries with potential for substantial, but avoidable, excess mortality during and after the pandemic.


Subject(s)
COVID-19 , Cardiovascular Diseases , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/epidemiology , Communicable Disease Control , Humans , Pandemics , SARS-CoV-2
3.
J Thromb Haemost ; 19(4): 1038-1048, 2021 04.
Article in English | MEDLINE | ID: covidwho-1061045

ABSTRACT

BACKGROUND: High incidence of asymptomatic venous thromboembolism (VTE) has been observed in severe COVID-19 patients, but the characteristics of symptomatic VTE in general COVID-19 patients have not been described. OBJECTIVES: To comprehensively explore the prevalence and reliable risk prediction for VTE in COVID-19 patients. METHODS/RESULTS: This retrospective study enrolled all COVID-19 patients with a subsequent VTE in 16 centers in China from January 1 to March 31, 2020. A total of 2779 patients were confirmed with COVID-19. In comparison to 23,434 non-COVID-19 medical inpatients, the odds ratios (ORs) for developing symptomatic VTE in severe and non-severe hospitalized COVID-19 patients were 5.94 (95% confidence interval [CI] 3.91-10.09) and 2.79 (95% CI 1.43-5.60), respectively. When 104 VTE cases and 208 non-VTE cases were compared, pulmonary embolism cases had a higher rate for in-hospital death (OR 6.74, 95% CI 2.18-20.81). VTE developed at a median of 21 days (interquartile range 13.25-31) since onset. Independent factors for VTE were advancing age, cancer, longer interval from symptom onset to admission, lower fibrinogen and higher D-dimer on admission, and D-dimer increment (DI) ≥1.5-fold; of these, DI ≥1.5-fold had the most significant association (OR 14.18, 95% CI 6.25-32.18, p = 2.23 × 10-10 ). A novel model consisting of three simple coagulation variables (fibrinogen and D-dimer levels on admission, and DI ≥1.5-fold) showed good prediction for symptomatic VTE (area under the curve 0.865, 95% CI 0.822-0.907, sensitivity 0.930, specificity 0.710). CONCLUSIONS: There is an excess risk of VTE in hospitalized COVID-19 patients. This novel model can aid early identification of patients who are at high risk for VTE.


Subject(s)
Biomarkers/blood , COVID-19/complications , Fibrin Fibrinogen Degradation Products/analysis , Venous Thromboembolism/diagnosis , Venous Thrombosis/epidemiology , Aged , COVID-19/blood , COVID-19/diagnosis , COVID-19/therapy , China/epidemiology , Female , Hospital Mortality , Humans , Immunization, Passive , Male , Middle Aged , Retrospective Studies , Risk Factors , SARS-CoV-2 , Venous Thromboembolism/blood , Venous Thromboembolism/epidemiology , Venous Thromboembolism/etiology , Venous Thrombosis/blood , Venous Thrombosis/etiology
4.
J Proteome Res ; 20(1): 49-59, 2021 01 01.
Article in English | MEDLINE | ID: covidwho-989659

ABSTRACT

Since the novel coronavirus pandemic, people around the world have been touched in varying degrees, and this pandemic has raised a major global health concern. As there is no effective drug or vaccine, it is urgent to find therapeutic drugs that can serve to deal with the current epidemic situation in all countries and regions. We searched drugs and response measures for SARS-CoV-2 in the PubMed database, and then updated the potential targets and therapeutic drugs from the perspective of the viral replication cycle. The drug research studies of the viral replication cycle are predominantly focused on the process of the virus entering cells, proteases, and RdRp. The inhibitors of the virus entry to cells and RdRp, such as Arbidol, remdesivir, favipiravir, EIDD-2081, and ribavirin, are in clinical trials, while most of the protease inhibitors are mainly calculated by molecular docking technology, which needs in vivo and in vitro experiments to prove the effect for SARS-CoV-2. This review summarizes the drugs targeting the viral replication process and provides a basis and directions for future drug development and reuse on the protein level of COVID-19.


Subject(s)
Antiviral Agents/pharmacology , SARS-CoV-2/drug effects , Virus Replication/drug effects , Angiotensin-Converting Enzyme 2/metabolism , Animals , Antiviral Agents/chemistry , Basigin/metabolism , Coronavirus 3C Proteases/antagonists & inhibitors , Coronavirus 3C Proteases/metabolism , Coronavirus Nucleocapsid Proteins/chemistry , Coronavirus Nucleocapsid Proteins/metabolism , Coronavirus RNA-Dependent RNA Polymerase/metabolism , Dipeptidyl Peptidase 4/metabolism , Furin/antagonists & inhibitors , Furin/metabolism , Host-Pathogen Interactions/drug effects , Humans , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology , Serine Endopeptidases/metabolism , Small Molecule Libraries/pharmacology , Spike Glycoprotein, Coronavirus/chemistry , Spike Glycoprotein, Coronavirus/metabolism
6.
J Am Coll Cardiol ; 75(23): 2950-2973, 2020 06 16.
Article in English | MEDLINE | ID: covidwho-547082

ABSTRACT

Coronavirus disease-2019 (COVID-19), a viral respiratory illness caused by the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), may predispose patients to thrombotic disease, both in the venous and arterial circulations, because of excessive inflammation, platelet activation, endothelial dysfunction, and stasis. In addition, many patients receiving antithrombotic therapy for thrombotic disease may develop COVID-19, which can have implications for choice, dosing, and laboratory monitoring of antithrombotic therapy. Moreover, during a time with much focus on COVID-19, it is critical to consider how to optimize the available technology to care for patients without COVID-19 who have thrombotic disease. Herein, the authors review the current understanding of the pathogenesis, epidemiology, management, and outcomes of patients with COVID-19 who develop venous or arterial thrombosis, of those with pre-existing thrombotic disease who develop COVID-19, or those who need prevention or care for their thrombotic disease during the COVID-19 pandemic.


Subject(s)
Anticoagulants/pharmacology , Betacoronavirus/isolation & purification , Coronavirus Infections , Fibrinolytic Agents/pharmacology , Pandemics , Platelet Aggregation Inhibitors/pharmacology , Pneumonia, Viral , Thromboembolism , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Humans , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , SARS-CoV-2 , Thromboembolism/drug therapy , Thromboembolism/epidemiology , Thromboembolism/etiology , Thromboembolism/physiopathology , Treatment Outcome
8.
Thromb Haemost ; 120(7): 1004-1024, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-418767

ABSTRACT

Coronavirus disease 2019 (COVID-19), currently a worldwide pandemic, is a viral illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The suspected contribution of thrombotic events to morbidity and mortality in COVID-19 patients has prompted a search for novel potential options for preventing COVID-19-associated thrombotic disease. In this article by the Global COVID-19 Thrombosis Collaborative Group, we describe novel dosing approaches for commonly used antithrombotic agents (especially heparin-based regimens) and the potential use of less widely used antithrombotic drugs in the absence of confirmed thrombosis. Although these therapies may have direct antithrombotic effects, other mechanisms of action, including anti-inflammatory or antiviral effects, have been postulated. Based on survey results from this group of authors, we suggest research priorities for specific agents and subgroups of patients with COVID-19. Further, we review other agents, including immunomodulators, that may have antithrombotic properties. It is our hope that the present document will encourage and stimulate future prospective studies and randomized trials to study the safety, efficacy, and optimal use of these agents for prevention or management of thrombosis in COVID-19.


Subject(s)
Coronavirus Infections/immunology , Fibrinolytic Agents/therapeutic use , Inflammation/drug therapy , Pneumonia, Viral/immunology , Thrombosis/drug therapy , Animals , Anti-Inflammatory Agents/therapeutic use , Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Glycosaminoglycans/therapeutic use , Hemostasis , Humans , Inflammation/complications , Inflammation/immunology , Pandemics , Platelet Aggregation Inhibitors/therapeutic use , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , SARS-CoV-2 , Thrombosis/complications , Thrombosis/immunology
10.
J Clin Virol ; 127: 104392, 2020 06.
Article in English | MEDLINE | ID: covidwho-133664

ABSTRACT

BACKGROUND: A few studies have revealed the clinical characteristics of hospitalized patients with COVID-19. However, predictive factors for the outcomes remain unclear. OBJECTIVE: Attempted to determine the predictive factors for the poor outcomes of patients with COVID-19. STUDY DESIGN: This is a single-center, retrospective study. Clinical, laboratory, and treatment data were collected and analyzed from 111 hospitalized patients with laboratory-confirmed COVID-19 in Union Hospital. The gathered data of discharged and deteriorated patients were compared. RESULTS: Among these 111 patients, 93 patients were discharged and 18 patients were deteriorated. The lymphocyte count (0.56 G/L [0.47-0.63] vs 1.30 G/L [0.95-1.65]) was lower in the deteriorated group than those in the discharged group. The numbers of pulmonary lobe involved (5.00 [5.00-5.00] vs 4.00 [2.00-5.00]), serum C-reactive protein (CRP, 79.52 mg/L [61.25-102.98] vs 7.93 mg/L [3.14-22.50]), IL-6 (35.72 pg/mL [9.24-85.19] vs 5.09 pg/mL [3.16-9.72]), and IL-10 (5.35 pg/mL [4.48-7.84] vs 3.97 pg/mL [3.34-4.79]) concentrations in deteriorated patients were elevated compared with discharged patients. Multivariate logistic regression analysis showed that male gender (OR, 24.8 [1.8-342.1]), comorbidity (OR, 52.6 [3.6-776.4]), lymphopenia (OR, 17.3 [1.1-261.8]), and elevated CRP (OR, 96.5 [4.6-2017.6]) were the independent risk factors for the poor prognosis in COVID-19 patients. CONCLUSIONS: This finding would facilitate the early identification of high-risk COVID-19 patients.


Subject(s)
Coronavirus Infections/diagnosis , Disease Progression , Hospitalization/statistics & numerical data , Pneumonia, Viral/diagnosis , Adult , Aged , Aged, 80 and over , Betacoronavirus , C-Reactive Protein/analysis , COVID-19 , Comorbidity , Coronavirus Infections/blood , Cytokines/blood , Female , Humans , Lymphocyte Count , Male , Middle Aged , Multivariate Analysis , Pandemics , Pneumonia, Viral/blood , Predictive Value of Tests , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Sex Factors
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