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1.
J Clin Invest ; 131(8)2021 04 15.
Article in English | MEDLINE | ID: covidwho-1186425

ABSTRACT

Several coronavirus disease 2019 (COVID-19) studies have focused on neuropathology. In this issue of the JCI, Qin, Wu, and Chen et al. focused specifically on people whose acute infection lacked obvious neurological involvement. Severely infected patients showed abnormal gray matter volumes, white matter diffusion, and cerebral blood flow compared with healthy controls and those with mild infection. The data remain associative rather than mechanistic, but correlations with systemic immune markers suggest effects of inflammation, hypercoagulation, or other aspects of disease severity. Mechanistic research is warranted. Given the lack of obvious neurological symptoms, neurocognitive assessments were not performed, but the findings suggest that such assessments may be warranted in severely affected patients, even without obvious symptoms. Further, studying CNS involvement of other disorders with overlapping pathophysiologies such as inflammation, coagulation, hypoxia, or direct viral infection may reveal the causes for COVID-19-related neuropathology.


Subject(s)
COVID-19 , Nervous System Diseases , Brain/diagnostic imaging , Cerebrovascular Circulation , Humans , SARS-CoV-2
2.
Clin Appl Thromb Hemost ; 27: 1076029621996445, 2021.
Article in English | MEDLINE | ID: covidwho-1148196

ABSTRACT

BACKGROUND: To investigate the factors associated with elevated fibrinogen (Fbg) levels in COVID-19 patients with and without diabetes (DM) and impaired fasting glucose (IFG). METHODS: According to whether or not their glucose metabolism was impaired, COVID-19 patients were subdivided into 2 groups: 1) with DM and IFG, 2) control group. Their demographic data, medical history, signs and symptoms, laboratory results, and final clinical results were analyzed retrospectively. RESULTS: 28 patients (16.3%) died during hospitalization, including 21 (29.2%) in group 1 and 7 (7.0%) in group 2 (P < 0.001). Fbg levels in groups 1 and 2 were higher than the normal range, at 5.6 g/L (IQR 4.5-7.2 g/L) and 5.0 g/L (IQR 4.0-6.1 g/L), respectively (P = 0.009). Serum ferritin levels, C-reactive protein (CRP), interleukin-6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α), triglycerides (TG) were significantly increased in group 1 compared to those in the control. TG levels were 1.3 mmol/L in the control, while that in group 1 was 1.8 mmol/L. Multiple linear regression showed that the predicting factors of Fbg in the control group were serum ferritin and CRP, R2 = 0.295; in group 1, serum ferritin, CRP, and TG, R2 = 0.473. CONCLUSIONS: Fbg in all COVID-19 patients is related to serum ferritin and CRP involved in inflammation. Furthermore, in COVID-19 patients with insulin resistance, Fbg is linearly positively correlated with TG. This suggests that regulation of TG, insulin resistance, and inflammation may reduce hypercoagulability in COVID-19 patients, especially those with insulin resistance.


Subject(s)
Blood Glucose/analysis , COVID-19/blood , Diabetes Mellitus/blood , Fasting/blood , Fibrinogen/analysis , Insulin Resistance , Thrombophilia/blood , Adult , Aged , Aged, 80 and over , Biomarkers/blood , Blood Coagulation , C-Reactive Protein/analysis , COVID-19/diagnosis , COVID-19/virology , Diabetes Mellitus/diagnosis , Female , Ferritins/blood , Humans , Inflammation Mediators/blood , Male , Middle Aged , Retrospective Studies , Thrombophilia/diagnosis , Thrombophilia/virology , Triglycerides/blood , Up-Regulation , Young Adult
3.
Eur Heart J Case Rep ; 4(5): 1-5, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-1093498

ABSTRACT

BACKGROUND: SARS-CoV-2 is a novel viral illness originating out of Wuhan China in late 2019. This global pandemic has infected nearly 3 million people and accounted for 200 000 deaths worldwide, with those numbers still climbing. CASE SUMMARY: We present a 54-year-old patient who developed respiratory failure requiring endotracheal intubation from her infection with SARS-CoV-2. This patient was subsequently found to have a right ventricular thrombus and bilateral pulmonary emboli, likely contributing to her respiratory status. On the 14th day of hospitalization, the patient was successfully extubated, and 5 days later was discharged to the rehabilitation unit. DISCUSSION: SARS-CoV-2 presents primarily with pulmonary symptoms; however, many patients, particularly those who are severely ill, exhibit adverse events related to hypercoagulability. The exact mechanism explaining this hypercoagulable state has yet to be elucidated, but these thrombotic events have been linked to the increased inflammation caused by SARS-CoV-2. This novel viral illness is still largely misunderstood, but the hypercoagulable state, seen in severely ill patients, appears to play a major role in disease progression and prognosis.

4.
Curr Diabetes Rev ; 17(6): e123120189797, 2021.
Article in English | MEDLINE | ID: covidwho-1004557

ABSTRACT

INTRODUCTION: Currently, diabetes mellitus (DM), as well as coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are major public health issues worldwide. BACKGROUND: It has been suggested that patients with DM are more vulnerable to SARS-CoV-2 infection and suffer from more severe forms of the disease. METHODS: A literature search was performed using PubMed, Scopus, and Google search engines. RESULTS: Angiotensin-converting enzyme-2 (ACE2) is the major receptor of SARS-CoV-2 in the human host. The differential expression of ACE2 in the lungs of patients with DM makes them more susceptible to COVID-19. Additionally, acute or chronic hyperglycemia renders individuals in an immune-suppressive state, with impaired innate and adaptive immunity function, also contributing to the severity of COVID-19 infection among patients with DM. Other factors contributing to a more severe course of COVID-19 include the coexistence of obesity in T2DM, the endothelial inflammation induced by the SARS-CoV-2 infection, which aggravates the endothelial dysfunction observed in both T1DM and T2DM, and the hypercoagulability presented in COVID-19 infection that increases the thrombotic tendency in DM. CONCLUSION: This review summarizes the pathophysiologic mechanisms underlying the coexistence of both pandemics as well as the current recommendations and future perspectives regarding the optimal treatment of inpatients and outpatients with DM in the era of SARS-CoV-2 infection. Notably, the currently recommended drugs for the treatment of severe COVID-19, dexamethasone and remdesivir, may cause hyperglycemia, an adverse effect that physicians should bear in mind when caring for patients with DM and COVID-19.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/epidemiology , Humans , Obesity , Pandemics , SARS-CoV-2
5.
Circ Res ; 2020 Sep 17.
Article in English | MEDLINE | ID: covidwho-992133

ABSTRACT

Rationale: In addition to the overwhelming lung inflammation that prevails in COVID-19, hypercoagulation and thrombosis contribute to the lethality of subjects infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Platelets are chiefly implicated in thrombosis. Moreover, they can interact with viruses and are an important source of inflammatory mediators. While a lower platelet count is associated with severity and mortality, little is known about platelet function during COVID-19. Objective: To evaluate the contribution of platelets to inflammation and thrombosis in COVID-19 patients. Methods and Results: Blood was collected from 115 consecutive COVID-19 patients presenting non-severe (n=71) and severe (n=44) respiratory symptoms. We document the presence of SARS-CoV-2 RNA associated with platelets of COVID-19 patients. Exhaustive assessment of cytokines in plasma and in platelets revealed the modulation of platelet-associated cytokine levels in both non-severe and severe COVID-19 patients, pointing to a direct contribution of platelets to the plasmatic cytokine load. Moreover, we demonstrate that platelets release their alpha- and dense-granule contents in both non-severe and severe forms of COVID-19. In comparison to concentrations measured in healthy volunteers, phosphatidylserine-exposing platelet extracellular vesicles were increased in non-severe, but not in severe cases of COVID-19. Levels of D-dimers, a marker of thrombosis, failed to correlate with any measured indicators of platelet activation. Functionally, platelets were hyperactivated in COVID-19 subjects presenting non-severe and severe symptoms, with aggregation occurring at suboptimal thrombin concentrations. Furthermore, platelets adhered more efficiently onto collagen-coated surfaces under flow conditions. Conclusions: Taken together, the data suggest that platelets are at the frontline of COVID-19 pathogenesis, as they release various sets of molecules through the different stages of the disease. Platelets may thus have the potential to contribute to the overwhelming thrombo-inflammation in COVID-19, and the inhibition of pathways related to platelet activation may improve the outcomes during COVID-19.

6.
Pharmacol Ther ; 219: 107703, 2021 03.
Article in English | MEDLINE | ID: covidwho-813821

ABSTRACT

Coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has currently led to a global pandemic with millions of confirmed and increasing cases around the world. The novel SARS-CoV-2 not only affects the lungs causing severe acute respiratory dysfunction but also leads to significant dysfunction in multiple organs and physiological systems including the cardiovascular system. A plethora of studies have shown the viral infection triggers an exaggerated immune response, hypercoagulation and oxidative stress, which contribute significantly to poor cardiovascular outcomes observed in COVID-19 patients. To date, there are no approved vaccines or therapies for COVID-19. Accordingly, cardiovascular protective and supportive therapies are urgent and necessary to the overall prognosis of COVID-19 patients. Accumulating literature has demonstrated the beneficial effects of n-3 polyunsaturated fatty acids (n-3 PUFA) toward the cardiovascular system, which include ameliorating uncontrolled inflammatory reactions, reduced oxidative stress and mitigating coagulopathy. Moreover, it has been demonstrated the n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are precursors to a group of potent bioactive lipid mediators, generated endogenously, which mediate many of the beneficial effects attributed to their parent compounds. Considering the favorable safety profile for n-3 PUFAs and their metabolites, it is reasonable to consider n-3 PUFAs as potential adjuvant therapies for the clinical management of COVID-19 patients. In this article, we provide an overview of the pathogenesis of cardiovascular complications secondary to COVID-19 and focus on the mechanisms that may contribute to the likely benefits of n-3 PUFAs and their metabolites.


Subject(s)
COVID-19/complications , COVID-19/drug therapy , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/etiology , Fatty Acids, Omega-3/administration & dosage , Animals , COVID-19/diagnosis , Cardiovascular Diseases/diagnosis , Chemotherapy, Adjuvant/methods , Cytokine Release Syndrome/diagnosis , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Humans , Oxidative Stress/drug effects , Oxidative Stress/physiology , Randomized Controlled Trials as Topic/methods
7.
EBioMedicine ; 58: 102887, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-684307

ABSTRACT

The pathogenesis of coronavirus disease 2019 (COVID-19) may be envisaged as the dynamic interaction between four vicious feedback loops chained or happening at once. These are the viral loop, the hyperinflammatory loop, the non-canonical renin-angiotensin system (RAS) axis loop, and the hypercoagulation loop. Severe acute respiratory syndrome (SARS)-coronavirus (CoV)-2 lights the wick by infecting alveolar epithelial cells (AECs) and downregulating the angiotensin converting enzyme-2 (ACE2)/angiotensin (Ang-1-7)/Mas1R axis. The viral feedback loop includes evading the host's innate response, uncontrolled viral replication, and turning on a hyperactive adaptative immune response. The inflammatory loop is composed of the exuberant inflammatory response feeding back until exploding in an actual cytokine storm. Downregulation of the ACE2/Ang-(1-7)/Mas1R axis leaves the lung without a critical defense mechanism and turns the scale to the inflammatory side of the RAS. The coagulation loop is a hypercoagulable state caused by the interplay between inflammation and coagulation in an endless feedback loop. The result is a hyperinflammatory and hypercoagulable state producing acute immune-mediated lung injury and eventually, adult respiratory distress syndrome.


Subject(s)
Betacoronavirus/pathogenicity , Blood Coagulation , Coronavirus Infections/etiology , Cytokines/metabolism , Pneumonia, Viral/etiology , Renin-Angiotensin System , Animals , COVID-19 , Coronavirus Infections/metabolism , Coronavirus Infections/pathology , Coronavirus Infections/virology , Feedback, Physiological , Humans , Pandemics , Pneumonia, Viral/metabolism , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , SARS-CoV-2
8.
J Stroke Cerebrovasc Dis ; 29(8): 104989, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-622312

ABSTRACT

OBJECTIVE: Identify clinical and radiographic features of venous infarct as a presenting feature of COVID-19 in the young. BACKGROUND: SARS-CoV-2 infection causes hypercoagulability and inflammation leading to venous thrombotic events (VTE). Although elderly patients with comorbidities are at higher risk, COVID-19 may also cause VTE in a broader patient population without these risks. Neurologic complications and manifestations of COVID-19, including neuropathies, seizures, strokes and encephalopathy usually occur in severe established cases of COVID-19 infection who primarily present with respiratory distress. CASE DESCRIPTION: Case report of a 29-year-old woman, with no significant past medical history or comorbidities, presenting with new onset seizures. Further questioning revealed a one-week history of headaches, low-grade fever, mild cough and shortness of breath, diagnosed as COVID-19. Imaging revealed a left temporoparietal hemorrhagic venous infarction with left transverse and sigmoid sinus thrombosis treated with full dose anticoagulation and antiepileptics. CONCLUSION: Although elderly patients with comorbidities are considered highest risk for COVID-19 neurologic complications, usually when systemic symptoms are severe, this case report emphasizes that young individuals are at risk for VTE with neurologic complications even when systemic symptoms are mild, likely induced by COVID-19 associated hypercoagulable state.


Subject(s)
Betacoronavirus/pathogenicity , Brain Infarction/virology , Coronavirus Infections/virology , Pneumonia, Viral/virology , Sinus Thrombosis, Intracranial/virology , Venous Thrombosis/virology , Adult , Age Factors , Anticoagulants/therapeutic use , Anticonvulsants/therapeutic use , Brain Infarction/diagnostic imaging , Brain Infarction/drug therapy , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/diagnosis , Coronavirus Infections/drug therapy , Female , Host Microbial Interactions , Humans , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Pneumonia, Viral/drug therapy , Risk Factors , SARS-CoV-2 , Sinus Thrombosis, Intracranial/diagnostic imaging , Sinus Thrombosis, Intracranial/drug therapy , Treatment Outcome , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/drug therapy
9.
Diabetes Res Clin Pract ; 164: 108214, 2020 Jun.
Article in English | MEDLINE | ID: covidwho-262340

ABSTRACT

BACKGROUND: Diabetes is a risk factor for the progression and prognosis of coronavirus disease (COVID-19), but the relationship between glycosylated hemoglobin (HbA1c) level, inflammation, and prognosis of COVID-19 patients has not been explored. METHODS: This was a retrospective study of COVID-19 patients who underwent an HbA1c test. Their demographic data, medical history, signs and symptoms of COVID-19, laboratory test results, and final outcomes of COVID-19 treatment were collected and analyzed. RESULTS: A total of 132 patients were included and divided into three groups based on their blood glucose status. There were significant differences in SaO2, serum ferritin level, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen (Fbg) level, and IL6 level among the three groups. A pairwise comparison of the groups showed that groups B and C were significantly different from group A in terms of CRP, ESR, and Fbg, IL6, and serum ferritin levels (P < 0.05). Correlation analysis showed that there was a linear negative correlation between SaO2 and HbA1c (r = -0.22, P = 0.01), while there was a linear positive correlation between serum ferritin, CRP, Fbg, and ESR levels and HbA1c (P < 0.05). CONCLUSIONS: High HbA1c level is associated with inflammation, hypercoagulability, and low SaO2 in COVID-19 patients, and the mortality rate (27.7%) is higher in patients with diabetes. Determining HbA1c level after hospital admission is thus helpful assessing inflammation, hypercoagulability, and prognosis of COVID-19 patients.


Subject(s)
Coronavirus Infections/blood , Glycated Hemoglobin A/metabolism , Inflammation/blood , Inflammation/virology , Pneumonia, Viral/blood , Thrombophilia/virology , Aged , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/mortality , Coronavirus Infections/pathology , Female , Humans , Inflammation/pathology , Male , Middle Aged , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/pathology , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Survival Analysis , Thrombophilia/blood , Thrombophilia/pathology
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