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1.
Eur J Med Res ; 26(1): 45, 2021 May 14.
Article in English | MEDLINE | ID: covidwho-1229005

ABSTRACT

BACKGROUND: Hematological comparison of coronavirus disease (COVID-19) and other viral pneumonias can provide insights into COVID-19 treatment. METHODS: In this retrospective case-control single-center study, we compared the data of 126 patients with viral pneumonia during different outbreaks [severe acute respiratory syndrome (SARS) in 2003, influenza A (H1N1) in 2009, human adenovirus type 7 in 2018, and COVID-19 in 2020]. RESULTS: One of the COVID-19 characteristics was a continuous decline in the hemoglobin level. The neutrophil count was related to the aggravation of COVID-19 and SARS. Thrombocytopenia occurred in patients with SARS and severe COVID-19 even at the recovery stage. Lymphocytes were related to the entire course of adenovirus infection, recovery of COVID-19, and disease development of SARS. CONCLUSIONS: Dynamic changes in hematological counts could provide a reference for the pathogenesis and prognosis of pneumonia caused by respiratory viruses in clinics.


Subject(s)
Adenovirus Infections, Human/blood , COVID-19/blood , Influenza, Human/blood , Pneumonia, Viral/blood , Severe Acute Respiratory Syndrome/blood , Adenovirus Infections, Human/pathology , Adolescent , Adult , Aged , Aged, 80 and over , COVID-19/pathology , Case-Control Studies , Female , Hemoglobins/analysis , Humans , Influenza, Human/pathology , Lymphocyte Count , Male , Middle Aged , Neutrophils/cytology , Pneumonia, Viral/pathology , Retrospective Studies , SARS-CoV-2/immunology , Severe Acute Respiratory Syndrome/pathology , Thrombocytopenia/pathology , Young Adult
2.
Int J Mol Sci ; 22(9)2021 May 07.
Article in English | MEDLINE | ID: covidwho-1224028

ABSTRACT

Numbers of patients with coronavirus disease 2019 (COVID-19) have increased rapidly worldwide. Plasma levels of full-length galectin-9 (FL-Gal9) and osteopontin (FL-OPN) as well as their truncated forms (Tr-Gal9, Ud-OPN, respectively), are representative inflammatory biomarkers. Here, we measured FL-Gal9, FL-OPN, Tr-Gal9, and Ud-OPN in 94 plasma samples obtained from 23 COVID-19-infected patients with mild clinical symptoms (CV), 25 COVID-19 patients associated with pneumonia (CP), and 14 patients with bacterial infection (ID). The four proteins were significantly elevated in the CP group when compared with healthy individuals. ROC analysis between the CV and CP groups showed that C-reactive protein had the highest ability to differentiate, followed by Tr-Gal9 and ferritin. Spearman's correlation analysis showed that Tr-Gal9 and Ud-OPN but not FL-Gal9 and FL-OPN, had a significant association with laboratory markers for lung function, inflammation, coagulopathy, and kidney function in CP patients. CP patients treated with tocilizumab had reduced levels of FL-Gal9, Tr-Gal9, and Ud-OPN. It was suggested that OPN is cleaved by interleukin-6-dependent proteases. These findings suggest that the cleaved forms of OPN and galectin-9 can be used to monitor the severity of pathological inflammation and the therapeutic effects of tocilizumab in CP patients.


Subject(s)
COVID-19/blood , Galectins/blood , Osteopontin/blood , Pneumonia/blood , Severe Acute Respiratory Syndrome/blood , Adult , Aged , Aged, 80 and over , Antibodies, Monoclonal, Humanized/therapeutic use , Biomarkers/metabolism , COVID-19/drug therapy , COVID-19/physiopathology , Female , Humans , Inflammation/metabolism , Kidney/metabolism , Kidney/pathology , Kidney/virology , Male , Middle Aged , Pneumonia/complications , Pneumonia/drug therapy , Pneumonia/virology , ROC Curve , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/drug therapy , Severe Acute Respiratory Syndrome/virology , Severity of Illness Index , Young Adult
3.
Cell Transplant ; 30: 963689721996217, 2021.
Article in English | MEDLINE | ID: covidwho-1181030

ABSTRACT

COVID-19 has spread worldwide, including the United States, United Kingdom, and Italy, along with its site of origin in China, since 2020. The virus was first found in the Wuhan seafood market at the end of 2019, with a controversial source. The clinical symptoms of COVID-19 include fever, cough, and respiratory tract inflammation, with some severe patients developing an acute and chronic lung injury, such as acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF). It has already claimed approximately 300 thousand human lives and the number is still on the rise; the only way to prevent the infection is to be safe till vaccines and reliable treatments develop. In previous studies, the use of mesenchymal stem cells (MSCs) in clinical trials had been proven to be effective in immune modulation and tissue repair promotion; however, their efficacy in treating COVID-19 remains underestimated. Here, we report the findings from past experiences of SARS and MSCs, and how SARS could also induce PF. Such studies may help to understand the rationale for the recent cell-based therapies for COVID-19.


Subject(s)
COVID-19/complications , Mesenchymal Stem Cell Transplantation , Pulmonary Fibrosis/etiology , Animals , COVID-19/blood , COVID-19/pathology , COVID-19/therapy , Coronavirus/isolation & purification , Humans , Mesenchymal Stem Cell Transplantation/methods , Pulmonary Fibrosis/blood , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , Renin-Angiotensin System , SARS-CoV-2/isolation & purification , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/pathology , Severe Acute Respiratory Syndrome/therapy , Transforming Growth Factor beta/blood
4.
Front Immunol ; 12: 629193, 2021.
Article in English | MEDLINE | ID: covidwho-1140644

ABSTRACT

Hyper-induction of pro-inflammatory cytokines, also known as a cytokine storm or cytokine release syndrome (CRS), is one of the key aspects of the currently ongoing SARS-CoV-2 pandemic. This process occurs when a large number of innate and adaptive immune cells activate and start producing pro-inflammatory cytokines, establishing an exacerbated feedback loop of inflammation. It is one of the factors contributing to the mortality observed with coronavirus 2019 (COVID-19) for a subgroup of patients. CRS is not unique to the SARS-CoV-2 infection; it was prevalent in most of the major human coronavirus and influenza A subtype outbreaks of the past two decades (H5N1, SARS-CoV, MERS-CoV, and H7N9). With a comprehensive literature search, we collected changing the cytokine levels from patients upon infection with the viral pathogens mentioned above. We analyzed published patient data to highlight the conserved and unique cytokine responses caused by these viruses. Our curation indicates that the cytokine response induced by SARS-CoV-2 is different compared to other CRS-causing respiratory viruses, as SARS-CoV-2 does not always induce specific cytokines like other coronaviruses or influenza do, such as IL-2, IL-10, IL-4, or IL-5. Comparing the collated cytokine responses caused by the analyzed viruses highlights a SARS-CoV-2-specific dysregulation of the type-I interferon (IFN) response and its downstream cytokine signatures. The map of responses gathered in this study could help specialists identify interventions that alleviate CRS in different diseases and evaluate whether they could be used in the COVID-19 cases.


Subject(s)
COVID-19/immunology , Cytokine Release Syndrome/immunology , Influenza A virus/immunology , Influenza, Human/immunology , Middle East Respiratory Syndrome Coronavirus/immunology , SARS Virus/immunology , SARS-CoV-2/immunology , Severe Acute Respiratory Syndrome/immunology , Severity of Illness Index , COVID-19/blood , COVID-19/pathology , COVID-19/virology , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/virology , Cytokines/blood , Humans , Inflammation/immunology , Influenza, Human/blood , Influenza, Human/virology , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/virology
5.
Eur Rev Med Pharmacol Sci ; 25(3): 1743-1751, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1102761

ABSTRACT

OBJECTIVE: This study evaluated the ability of mid-regional proadrenomedullin (MR-proADM) to identify disease severity in Coronavirus disease 2019 (COVID-19) patients in comparison to conventional inflammatory biomarkers and clinical scores. PATIENTS AND METHODS: In an observational trial, COVID-19 acute respiratory distress syndrome (ARDS) patients were enrolled. MR-proADM, C-reactive protein (CRP), procalcitonin (PCT) and lactic acid (LA) were measured in all patients at admission (T0), at 24 hours (T1) and in the third (T3) and fifth day (T5) of hospitalization. The aims of this study were to determine the role of MR-proADM to detect patients with high risk of mortality and compare the prognostic value of MR-proADM with commonly used clinical scores (Sequential Organ Failure Assessment score - SOFA score, Acute Physiologic Assessment and Chronic Health Evaluation II score - APACHE II score, and Simplified Acute Physiological score II - SAPS II score). RESULTS: Twenty-one COVID-19 ARDS patients admitted to the Intermediate Care Unit (IMCU) were enrolled. The median MR-proADM values were 2.28, 2.41, 1.96 and 1.89 nmol/L at T0, T1, T3 and T5, respectively. The 30-day all-cause mortality rate was 52.4%. Mean MR-proADM T0 value was significantly higher in non-survivors compared with survivors (3.5 vs. 1.1 nmol/L, p < 0.05). No significant differences were found for the other inflammatory biomarkers. In terms of the area under the receiver-operating characteristic curve (AUC), MR-proADM showed a similar discriminatory power compared with APACHE II, SOFA and SAPS II score (0.81, 0.91, 0.70 and 0.78, respectively). The optimal MR-proADM cut-point cut-off point was 1.07 nmol/L, which corresponds to a sensitivity of 91% and a specificity of 71%. CONCLUSIONS: MR-proADM, in addition to the clinical scores, could be useful to predict outcome in COVID-19 ARDS patients.


Subject(s)
Adrenomedullin/blood , COVID-19/blood , Protein Precursors/blood , SARS-CoV-2 , Severe Acute Respiratory Syndrome/blood , APACHE , Biomarkers/blood , C-Reactive Protein/analysis , COVID-19/mortality , Humans , Italy , Organ Dysfunction Scores , Prognosis , ROC Curve , Severe Acute Respiratory Syndrome/mortality , Severe Acute Respiratory Syndrome/virology
6.
Expert Rev Hematol ; 14(2): 155-173, 2021 02.
Article in English | MEDLINE | ID: covidwho-1044433

ABSTRACT

INTRODUCTION: COVID-19 has similarities to the Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) outbreaks, as severe patients and non-survivors have frequently shown abnormal coagulation profiles. Immune-mediated pathology is a key player in this disease; hence, the role of the complement system needs assessment. The complement system and the coagulation cascade share an intricate network, where multiple mediators maintain a balance between both pathways. Coagulopathy in COVID-19, showing mixed features of complement-mediated and consumption coagulopathy, creates a dilemma in diagnosis and management. AREAS COVERED: Pathophysiology of coagulopathy in COVID-19 patients, with a particular focus on D-dimer and its role in predicting the severity of COVID-19 has been discussed. A comprehensive search of the medical literature on PubMed was done till May 30th, 2020 with the keywords 'COVID-19', 'SARS-CoV-2', 'Coronavirus', 'Coagulopathy', and 'D-dimer'. Twenty-two studies were taken for weighted pooled analysis of D-dimer. EXPERT OPINION: A tailored anticoagulant regimen, including intensification of standard prophylactic regimens with low-molecular-weight heparin is advisable for COVID-19 patients. Atypical manifestations and varying D-dimer levels seen in different populations bring forth the futility of uniform recommendations for anticoagulant therapy. Further, direct thrombin inhibitors and platelet inhibitors in a patient-specific manner should also be considered.


Subject(s)
Blood Coagulation Disorders/etiology , COVID-19/complications , Complement Activation , SARS-CoV-2 , Animals , Anticoagulants/therapeutic use , Biomarkers , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/immunology , Blood Coagulation Disorders/physiopathology , Blood Coagulation Tests , COVID-19/blood , COVID-19/immunology , COVID-19/therapy , China/epidemiology , Comorbidity , Coronavirus Infections/blood , Disseminated Intravascular Coagulation/blood , Disseminated Intravascular Coagulation/epidemiology , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/physiopathology , Ferritins/blood , Fibrin Fibrinogen Degradation Products/analysis , Forecasting , Humans , Immunization, Passive , Inflammation/etiology , Inflammation/physiopathology , Iron Chelating Agents/therapeutic use , Ischemia/blood , Ischemia/etiology , Ischemia/physiopathology , Mice , Prevalence , Severe Acute Respiratory Syndrome/blood , Severity of Illness Index , Thrombophilia/drug therapy , Thrombophilia/etiology , Thrombophilia/physiopathology , Venous Thromboembolism/blood , Venous Thromboembolism/etiology , Venous Thromboembolism/physiopathology
7.
J Glob Antimicrob Resist ; 24: 90-92, 2021 03.
Article in English | MEDLINE | ID: covidwho-1012433

ABSTRACT

Here we present a case series of three patients with COVID-19 (coronavirus disease 2019) who had a cytokine panel that revealed elevation of interleukin-6 (IL-6) but normal levels of interleukin-10 (IL-10), interferon-gamma (INF-γ) and interleukin-8 (IL-8), in contrast to the cytokine signature described in severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). We also documented evidence of a compromised T-cell IFN-γ response in two of these patients.


Subject(s)
COVID-19/immunology , Coronavirus Infections/immunology , Cytokine Release Syndrome , Cytokines/immunology , Severe Acute Respiratory Syndrome/immunology , COVID-19/blood , COVID-19/epidemiology , Coronavirus Infections/blood , Coronavirus Infections/epidemiology , Cytokines/blood , Epidemics , Humans , Male , Middle Aged , New York/epidemiology , SARS-CoV-2/isolation & purification , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/epidemiology , T-Lymphocytes/immunology
8.
Biofactors ; 46(6): 927-933, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-966303

ABSTRACT

Recent articles report elevated markers of coagulation, endothelial injury, and microthromboses in lungs from deceased COVID-19 patients. However, there has been no discussion of what may induce intravascular coagulation. Platelets are critical in the formation of thrombi and their most potent trigger is platelet activating factor (PAF), first characterized by Demopoulos and colleagues in 1979. PAF is produced by cells involved in host defense and its biological actions bear similarities with COVID-19 disease manifestations. PAF can also stimulate perivascular mast cell activation, leading to inflammation implicated in severe acute respiratory syndrome (SARS). Mast cells are plentiful in the lungs and are a rich source of PAF and of inflammatory cytokines, such as IL-1ß and IL-6, which may contribute to COVID-19 and especially SARS. The histamine-1 receptor antagonist rupatadine was developed to have anti-PAF activity, and also inhibits activation of human mast cells in response to PAF. Rupatadine could be repurposed for COVID-19 prophylaxis alone or together with other PAF-inhibitors of natural origin such as the flavonoids quercetin and luteolin, which have antiviral, anti-inflammatory, and anti-PAF actions.


Subject(s)
COVID-19/prevention & control , Cyproheptadine/analogs & derivatives , Disseminated Intravascular Coagulation/prevention & control , Platelet Activating Factor/antagonists & inhibitors , Pulmonary Embolism/prevention & control , SARS-CoV-2/pathogenicity , Severe Acute Respiratory Syndrome/prevention & control , Antiviral Agents/therapeutic use , Blood Platelets/drug effects , Blood Platelets/pathology , Blood Platelets/virology , COVID-19/blood , COVID-19/pathology , COVID-19/virology , Cyproheptadine/therapeutic use , Disseminated Intravascular Coagulation/blood , Disseminated Intravascular Coagulation/pathology , Disseminated Intravascular Coagulation/virology , Gene Expression Regulation , Humans , Inflammation , Interleukin-1beta/genetics , Interleukin-1beta/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Lung/drug effects , Lung/pathology , Lung/virology , Luteolin/therapeutic use , Mast Cells/drug effects , Mast Cells/pathology , Mast Cells/virology , Platelet Activating Factor/genetics , Platelet Activating Factor/metabolism , Pulmonary Embolism/blood , Pulmonary Embolism/pathology , Pulmonary Embolism/virology , Quercetin/therapeutic use , SARS-CoV-2/drug effects , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/pathology , Severe Acute Respiratory Syndrome/virology
9.
Sci Adv ; 6(45)2020 11.
Article in English | MEDLINE | ID: covidwho-842149

ABSTRACT

The current coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus genetically close to SARS-CoV. To investigate the effects of previous SARS-CoV infection on the ability to recognize and neutralize SARS-CoV-2, we analyzed 20 convalescent serum samples collected from individuals infected with SARS-CoV during the 2003 SARS outbreak. All patient sera reacted strongly with the S1 subunit and receptor binding domain (RBD) of SARS-CoV; cross-reacted with the S ectodomain, S1, RBD, and S2 proteins of SARS-CoV-2; and neutralized both SARS-CoV and SARS-CoV-2 S protein-driven infections. Analysis of antisera from mice and rabbits immunized with a full-length S and RBD immunogens of SARS-CoV verified cross-reactive neutralization against SARS-CoV-2. A SARS-CoV-derived RBD from palm civets elicited more potent cross-neutralizing responses in immunized animals than the RBD from a human SARS-CoV strain, informing strategies for development of universal vaccines against emerging coronaviruses.


Subject(s)
Antibodies, Neutralizing/immunology , Antibodies, Viral/immunology , COVID-19/immunology , Immunization/methods , SARS Virus/immunology , SARS-CoV-2/immunology , Severe Acute Respiratory Syndrome/immunology , Spike Glycoprotein, Coronavirus/immunology , Animals , Antibodies, Neutralizing/blood , Antibodies, Viral/blood , COVID-19/virology , COVID-19 Vaccines/immunology , Cross Reactions , Follow-Up Studies , HEK293 Cells , Humans , Mice , Mice, Inbred BALB C , Neutralization Tests , Rabbits , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/virology
11.
Arterioscler Thromb Vasc Biol ; 40(10): 2539-2547, 2020 10.
Article in English | MEDLINE | ID: covidwho-729442

ABSTRACT

OBJECTIVE: To determine the prevalence of D-dimer elevation in coronavirus disease 2019 (COVID-19) hospitalization, trajectory of D-dimer levels during hospitalization, and its association with clinical outcomes. Approach and Results: Consecutive adults admitted to a large New York City hospital system with a positive polymerase chain reaction test for SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) between March 1, 2020 and April 8, 2020 were identified. Elevated D-dimer was defined by the laboratory-specific upper limit of normal (>230 ng/mL). Outcomes included critical illness (intensive care, mechanical ventilation, discharge to hospice, or death), thrombotic events, acute kidney injury, and death during admission. Among 2377 adults hospitalized with COVID-19 and ≥1 D-dimer measurement, 1823 (76%) had elevated D-dimer at presentation. Patients with elevated presenting baseline D-dimer were more likely than those with normal D-dimer to have critical illness (43.9% versus 18.5%; adjusted odds ratio, 2.4 [95% CI, 1.9-3.1]; P<0.001), any thrombotic event (19.4% versus 10.2%; adjusted odds ratio, 1.9 [95% CI, 1.4-2.6]; P<0.001), acute kidney injury (42.4% versus 19.0%; adjusted odds ratio, 2.4 [95% CI, 1.9-3.1]; P<0.001), and death (29.9% versus 10.8%; adjusted odds ratio, 2.1 [95% CI, 1.6-2.9]; P<0.001). Rates of adverse events increased with the magnitude of D-dimer elevation; individuals with presenting D-dimer >2000 ng/mL had the highest risk of critical illness (66%), thrombotic event (37.8%), acute kidney injury (58.3%), and death (47%). CONCLUSIONS: Abnormal D-dimer was frequently observed at admission with COVID-19 and was associated with higher incidence of critical illness, thrombotic events, acute kidney injury, and death. The optimal management of patients with elevated D-dimer in COVID-19 requires further study.


Subject(s)
Coronavirus Infections/blood , Coronavirus Infections/mortality , Critical Illness/epidemiology , Disease Progression , Fibrin Fibrinogen Degradation Products/metabolism , Hospital Mortality/trends , Pneumonia, Viral/blood , Pneumonia, Viral/mortality , Adult , Aged , Biomarkers/blood , COVID-19 , Cause of Death , Cohort Studies , Coronavirus Infections/physiopathology , Databases, Factual , Female , Hospitals, Urban , Humans , Male , Middle Aged , New York City/epidemiology , Pandemics , Pneumonia, Viral/physiopathology , Prevalence , Retrospective Studies , Risk Assessment , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/mortality , Severe Acute Respiratory Syndrome/physiopathology , Severity of Illness Index
12.
Clin Med (Lond) ; 20(5): e178-e182, 2020 09.
Article in English | MEDLINE | ID: covidwho-659698

ABSTRACT

BACKGROUND: COVID-19 infection is characterised, among other features, by a prothrombotic state with high rate of venous thromboembolism (VTE), D-dimer, and fibrinogen levels. Clinical observations have also highlighted that these patients have elevated von Willebrand factor (vWF) and factor VIIIc. METHODS: 24 consecutive COVID-19 positive patients were selected from the intensive care unit (ICU) or the high acuity ward of Brighton and Sussex University Hospitals NHS Trust. RESULTS: The rate of VTE was 25% and mortality rate was 16.7%. Fibrinogen and D-Dimers were elevated, 7.9 (1.6) g/L and 2.4 (2.02) ug/ml respectively. Factor VIIIc and von vWF antigen levels were both extremely elevated at 279 (148) u/dL and 350 (131) % respectively, which are comparable to levels seen in ICU patients with severe sepsis. vWF levels were significantly higher in patients that died (p=0.017) and showed a positive correlation with age. There was a statistically significant association between COVID-19 disease and non-O blood group (p=0.02); 80% (4/5) of COVID-19 patients with VTE were blood group A. CONCLUSION: Very high levels of vWF and factor VIIIc are common in COVID-19 patients, comparable to levels in severely septic non-COVID ICU patients. This could contribute to the hypercoagulable state and increased VTE rate in COVID-19. Further studies are needed to evaluate the use of vWF for stratifying thrombotic risk in COVID-19 and to determine if elevated vWF is contributing to disease pathogenesis.


Subject(s)
Coronavirus Infections/complications , Endothelium, Vascular/pathology , Hospital Mortality/trends , Pneumonia, Viral/complications , Severe Acute Respiratory Syndrome/blood , Venous Thromboembolism/etiology , von Willebrand Factor/metabolism , Biomarkers/blood , COVID-19 , Cohort Studies , Coronavirus Infections/diagnosis , Coronavirus Infections/mortality , Female , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Hospitals, University , Humans , Intensive Care Units , Male , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/mortality , Risk Assessment , Sampling Studies , Severe Acute Respiratory Syndrome/diagnosis , Survival Rate , United Kingdom , Venous Thromboembolism/blood , Venous Thromboembolism/mortality
13.
Clin Appl Thromb Hemost ; 26: 1076029620938149, 2020.
Article in English | MEDLINE | ID: covidwho-651515

ABSTRACT

The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.


Subject(s)
Anticoagulants/therapeutic use , Betacoronavirus , Coronavirus Infections/complications , Pandemics , Pneumonia, Viral/complications , Thrombophilia/etiology , Thrombosis/prevention & control , Angiotensin II/metabolism , Arterial Occlusive Diseases/blood , Arterial Occlusive Diseases/epidemiology , Arterial Occlusive Diseases/etiology , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/epidemiology , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/etiology , Disease Outbreaks , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/prevention & control , Fibrin Fibrinogen Degradation Products/analysis , Fibrinolytic Agents/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Humans , Incidence , Inflammation , Pneumonia, Viral/blood , Pneumonia, Viral/epidemiology , Prognosis , Pulmonary Embolism/etiology , Pulmonary Embolism/prevention & control , Risk , SARS-CoV-2 , Sepsis/blood , Sepsis/complications , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/epidemiology , Thrombophilia/blood , Thrombophilia/drug therapy , Thrombosis/blood , Thrombosis/epidemiology , Thrombosis/etiology , Thrombotic Microangiopathies/etiology , Thrombotic Microangiopathies/prevention & control , Tissue Plasminogen Activator/therapeutic use
14.
Platelets ; 31(5): 627-632, 2020 Jul 03.
Article in English | MEDLINE | ID: covidwho-245402

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a new infectious disease that currently lacks standardized and established laboratory markers to evaluate its severity. In COVID-19 patients, the number of platelets (PLTs) and dynamic changes of PLT-related parameters are currently a concern. The present paper discusses the potential link between PLT parameters and COVID-19. Several studies have identified a link between severe COVID-19 patients and specific coagulation index, in particular, high D-dimer level, prolonged prothrombin time, and low PLT count. These alterations reflect the hypercoagulable state present in severe COVID-19 patients, which could promote microthrombosis in the lungs, as well as in other organs. Further information and more advanced hematological parameters related to PLTs are needed to better estimate this link, also considering COVID-19 patients at different disease stages and stratified in different cohorts based on preexisting co-morbidity, age, and gender. Increasing the understanding of PLT functions in COVID-19 will undoubtedly improve our knowledge on disease pathogenesis, clinical management, and therapeutic options, but could also lead to the development of more precise therapeutic strategies for COVID-19 patients.


Subject(s)
Betacoronavirus , Blood Platelets/physiology , Coronavirus Infections/blood , Pandemics , Pneumonia, Viral/blood , Thrombophilia/etiology , Angiotensin-Converting Enzyme 2 , Anticoagulants/administration & dosage , Anticoagulants/therapeutic use , Biomarkers/blood , Blood Platelets/ultrastructure , COVID-19 , Cell Adhesion Molecules/metabolism , Coronavirus Infections/complications , Coronavirus Infections/pathology , Cytokines/metabolism , Disseminated Intravascular Coagulation/etiology , Drug Interactions , Endothelial Cells/pathology , Endothelium, Vascular/pathology , Fibrin Fibrinogen Degradation Products/analysis , Humans , Inflammation , Lung/pathology , Peptidyl-Dipeptidase A/physiology , Platelet Count , Platelet Function Tests , Pneumonia, Viral/complications , Pneumonia, Viral/pathology , Prothrombin Time , Receptors, Virus/physiology , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/prevention & control , SARS-CoV-2 , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/pathology , Thrombophilia/blood , Thrombophilia/drug therapy , Venous Thrombosis/epidemiology , Venous Thrombosis/etiology , Venous Thrombosis/pathology , Venous Thrombosis/prevention & control
15.
Crit Care ; 24(1): 205, 2020 05 08.
Article in English | MEDLINE | ID: covidwho-209589

ABSTRACT

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has presently become a rapidly spreading and devastating global pandemic. Veno-venous extracorporeal membrane oxygenation (V-V ECMO) may serve as life-saving rescue therapy for refractory respiratory failure in the setting of acute respiratory compromise such as that induced by SARS-CoV-2. While still little is known on the true efficacy of ECMO in this setting, the natural resemblance of seasonal influenza's characteristics with respect to acute onset, initial symptoms, and some complications prompt to ECMO implantation in most severe, pulmonary decompensated patients. The present review summarizes the evidence on ECMO management of severe ARDS in light of recent COVID-19 pandemic, at the same time focusing on differences and similarities between SARS-CoV-2 and ECMO in terms of hematological and inflammatory interplay when these two settings merge.


Subject(s)
Betacoronavirus , Coronavirus Infections/therapy , Extracorporeal Membrane Oxygenation , Pneumonia, Viral/therapy , Blood Coagulation , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/physiopathology , Cytokine Release Syndrome , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/physiopathology , Severe Acute Respiratory Syndrome/therapy , Thrombocytopenia
16.
Int J Mol Sci ; 21(9)2020 May 05.
Article in English | MEDLINE | ID: covidwho-175942

ABSTRACT

Coronaviruses (CoVs), including Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and the novel coronavirus disease-2 (SARS-CoV-2) are a group of enveloped RNA viruses that cause a severe respiratory infection which is associated with a high mortality [...].


Subject(s)
Acute Kidney Injury/mortality , Acute Kidney Injury/virology , Betacoronavirus/pathogenicity , Coronavirus Infections/virology , Kidney Tubules, Proximal/metabolism , Kidney Tubules, Proximal/virology , Pneumonia, Viral/virology , Acute Kidney Injury/physiopathology , Acute Kidney Injury/prevention & control , Angiotensin II/pharmacology , Angiotensin-Converting Enzyme 2 , COVID-19 , Cathepsins/metabolism , Cell Death/drug effects , Coronavirus Infections/mortality , Coronavirus Infections/pathology , Coronavirus Infections/physiopathology , Creatinine/blood , Critical Illness/mortality , Endosomes/drug effects , Endosomes/enzymology , Endosomes/metabolism , Humans , Hydrogen-Ion Concentration , Incidence , Kidney Tubules, Proximal/physiopathology , Lysosomes/drug effects , Lysosomes/enzymology , Lysosomes/metabolism , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/mortality , Pneumonia, Viral/pathology , Pneumonia, Viral/physiopathology , Receptors, Virus/metabolism , SARS-CoV-2 , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/mortality , Severe Acute Respiratory Syndrome/physiopathology , Virus Internalization , Virus Replication
17.
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 , COVID-19 , 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
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