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1.
Int J Biol Macromol ; 193(Pt A): 948-955, 2021 Dec 15.
Article in English | MEDLINE | ID: covidwho-1471998

ABSTRACT

The severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) keeps on destroying normal social integrity worldwide, bringing about extraordinary medical services, cultural and financial interruption. Individuals with diabetes have been demonstrated to be at higher risk of complications and even death when exposed to SARS-CoV-2. Regardless of pandemic scale infection, there is presently limited comprehension on the potential impact of SARS-CoV-2 on individuals with diabetes. Human serum albumin (HSA) is the most abundant circulating plasma protein in human serum and attracted more interest from researchers because most susceptible to non-enzymatic glycation reactions. Albumin down-regulates the expression of ACE2 that is the target receptor of COVID-19. Hypoalbuminemia, coagulopathy, and vascular disease have been connected in COVID-19 and appear to predict outcomes independent of age and morbidity. This review discusses the most recent evidence that the ACE/ACE2 ratio could influence by human serum albumin both the susceptibility of individuals to SARS-CoV-2 infection and the outcome of the COVID-19 disease.


Subject(s)
Angiotensin-Converting Enzyme 2/blood , COVID-19 , SARS-CoV-2/metabolism , Serum Albumin, Human/metabolism , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/therapy , COVID-19/blood , COVID-19/diagnosis , COVID-19/therapy , Disease Susceptibility , Humans , Vascular Diseases/blood , Vascular Diseases/diagnosis , Vascular Diseases/therapy
2.
Int J Immunopathol Pharmacol ; 35: 20587384211042115, 2021.
Article in English | MEDLINE | ID: covidwho-1430368

ABSTRACT

BACKGROUND: Hypercoagulability is a risk factor of thromboembolic events in COVID-19. Anti-phospholipid (aPL) antibodies have been hypothesized to be involved. Typical COVID-19 dermatological manifestations of livedo reticularis and digital ischemia may resemble cutaneous manifestations of anti-phospholipid syndrome (APS). OBJECTIVES: To investigate the association between aPL antibodies and thromboembolic events, COVID-19 severity, mortality, and cutaneous manifestations in patients with COVID-19. METHODS: aPL antibodies [anti-beta2-glycoprotein-1 (B2GP1) and anti-cardiolipin (aCL) antibodies] were titered in frozen serum samples from hospitalized COVID-19 patients and the patients' clinical records were retrospectively analyzed. RESULTS: 173 patients were enrolled. aPL antibodies were detected in 34.7% of patients, anti-B2GP1 antibodies in 30.1%, and aCL antibodies in 10.4%. Double positivity was observed in 5.2% of patients. Thromboembolic events occurred in 9.8% of patients, including 11 pulmonary embolisms, 1 case of celiac tripod thrombosis, and six arterial ischemic events affecting the cerebral, celiac, splenic, or femoral-popliteal arteries or the aorta. aPL antibodies were found in 52.9% of patients with vascular events, but thromboembolic events were not correlated to aPL antibodies (adjusted OR = 1.69, p = 0.502). Ten patients (5.8%) had cutaneous signs of vasculopathy: nine livedo reticularis and one acrocyanosis. No significant association was observed between the presence of cutaneous vasculopathy and aPL antibodies (p = 0.692). CONCLUSIONS: Anti-phospholipid antibodies cannot be considered responsible for hypercoagulability and thrombotic events in COVID-19 patients. In COVID-19 patients, livedo reticularis and acrocyanosis do not appear to be cutaneous manifestations of APS.


Subject(s)
Antibodies, Antiphospholipid/blood , COVID-19/complications , SARS-CoV-2 , Skin Diseases/blood , Vascular Diseases/blood , Adult , Aged , Aged, 80 and over , Antibodies, Anticardiolipin/blood , COVID-19/blood , COVID-19/immunology , COVID-19/mortality , Female , Hospitalization , Humans , Italy/epidemiology , Male , Middle Aged , Retrospective Studies , Seroepidemiologic Studies , Skin Diseases/immunology , Skin Diseases/mortality , Vascular Diseases/immunology , Vascular Diseases/mortality , beta 2-Glycoprotein I/immunology
3.
Nat Rev Cardiol ; 18(3): 194-209, 2021 03.
Article in English | MEDLINE | ID: covidwho-936141

ABSTRACT

The core pathology of coronavirus disease 2019 (COVID-19) is infection of airway cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that results in excessive inflammation and respiratory disease, with cytokine storm and acute respiratory distress syndrome implicated in the most severe cases. Thrombotic complications are a major cause of morbidity and mortality in patients with COVID-19. Patients with pre-existing cardiovascular disease and/or traditional cardiovascular risk factors, including obesity, diabetes mellitus, hypertension and advanced age, are at the highest risk of death from COVID-19. In this Review, we summarize new lines of evidence that point to both platelet and endothelial dysfunction as essential components of COVID-19 pathology and describe the mechanisms that might account for the contribution of cardiovascular risk factors to the most severe outcomes in COVID-19. We highlight the distinct contributions of coagulopathy, thrombocytopathy and endotheliopathy to the pathogenesis of COVID-19 and discuss potential therapeutic strategies in the management of patients with COVD-19. Harnessing the expertise of the biomedical and clinical communities is imperative to expand the available therapeutics beyond anticoagulants and to target both thrombocytopathy and endotheliopathy. Only with such collaborative efforts can we better prepare for further waves and for future coronavirus-related pandemics.


Subject(s)
Blood Coagulation Disorders/blood , Blood Platelet Disorders/blood , COVID-19/blood , Endothelium, Vascular/physiopathology , Inflammation/blood , Thrombosis/blood , Administration, Inhalation , Anticoagulants/therapeutic use , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/physiopathology , Blood Platelet Disorders/drug therapy , Blood Platelet Disorders/etiology , Blood Platelet Disorders/physiopathology , COVID-19/complications , COVID-19/drug therapy , COVID-19/physiopathology , Endothelium-Dependent Relaxing Factors/therapeutic use , Epoprostenol/therapeutic use , Heart Disease Risk Factors , Humans , Iloprost/therapeutic use , Inflammation/etiology , Inflammation/physiopathology , Nitric Oxide/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/blood , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/physiopathology , Thrombosis/etiology , Thrombosis/immunology , Thrombotic Microangiopathies/blood , Thrombotic Microangiopathies/drug therapy , Thrombotic Microangiopathies/etiology , Thrombotic Microangiopathies/physiopathology , Vascular Diseases/blood , Vascular Diseases/drug therapy , Vascular Diseases/etiology , Vascular Diseases/physiopathology , Vasodilator Agents/therapeutic use , Venous Thromboembolism/blood , Venous Thromboembolism/drug therapy , Venous Thromboembolism/etiology , Venous Thromboembolism/physiopathology
4.
Cell ; 183(5): 1354-1366.e13, 2020 11 25.
Article in English | MEDLINE | ID: covidwho-871817

ABSTRACT

The COVID-19 pandemic has led to extensive morbidity and mortality throughout the world. Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details underlying these processes remain to be determined. In this study, we demonstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from both humans and rhesus macaques infected with SARS-CoV-2. To define key molecular pathways associated with SARS-CoV-2 pathogenesis in macaques, we performed transcriptomic analyses of bronchoalveolar lavage and peripheral blood and proteomic analyses of serum. We observed macrophage infiltrates in lung and upregulation of macrophage, complement, platelet activation, thrombosis, and proinflammatory markers, including C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFα, and NF-κB. These results suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2-induced vascular disease. Our findings suggest potential therapeutic targets for COVID-19.


Subject(s)
COVID-19/complications , COVID-19/immunology , SARS-CoV-2/genetics , Thrombosis/complications , Vascular Diseases/complications , Aged, 80 and over , Animals , Bronchoalveolar Lavage , C-Reactive Protein/analysis , COVID-19/blood , COVID-19/pathology , Complement Activation , Cytokines/blood , Female , Humans , Inflammation/blood , Inflammation/immunology , Inflammation/virology , Lung/pathology , Macaca mulatta , Macrophages/immunology , Male , Platelet Activation , Thrombosis/blood , Thrombosis/pathology , Transcriptome , Vascular Diseases/blood , Vascular Diseases/pathology
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