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1.
authorea preprints; 2024.
Preprint in English | PREPRINT-AUTHOREA PREPRINTS | ID: ppzbmed-10.22541.au.170668043.30668238.v1

ABSTRACT

Objective: Covid-19 may cause thrombosis in both venous and arterial systems. Familiarity with the signs and symptoms of thrombosis and their treatment plays an important role in treating Covid-19 infection and its complications. D-Dimer and Mean platelet volume (MPV) are measurements related to the development of thrombosis. This study investigates whether MPV and D-Dimer values could be used to determine the risk of thrombosis and mortality in Covid-19 early stages. Methods: 424 patients were randomly and retrospectively included in the study, Covid 19 positive according to the World Health Organization (WHO) guidelines. Demographic and clinical characteristics such as age, gender, and length of hospitalization were obtained from the digital records of participants. Participants were divided into living and deceased groups. Results: WBC, neutrophils, and monocytes were significantly different in the two groups (p <0.001), and its values were lower in the living group than in the deceased group. MPV median values do not differ according to prognosis (p = 0.994). Creatinine, Procalcitonin, Ferritin, and the number of hospitalization days in living patients were significantly lower than in patients who died (p <0.001). Median values of D-dimer (mg / L) differ according to prognosis (p <0.001). While the median value was 0.63 in the survivors, it was found as 4.38 in the deceased. Conclusion: Our results did not show any significant relationship between the mortality of Covid-19 patients and their MPV levels. However, a significant association of D-Dimer and mortality in Covid-19 patients was observed. Keywords: COVID-19, MPV, D-Dimer, prognosis, mortality


Subject(s)
Thrombosis , COVID-19
2.
authorea preprints; 2024.
Preprint in English | PREPRINT-AUTHOREA PREPRINTS | ID: ppzbmed-10.22541.au.170668400.07102481.v1

ABSTRACT

The novel coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is a global pandemic which is primarily considered a respiratory illness. However, emerging reports show that the virus exhibits both pulmonary and extra-pulmonary manifestations in humans, with the kidney as a major extra-pulmonary target due to its abundant expression of angiotensin-converting enzyme 2 and transmembrane protease serine 2, which facilitate entry of the virus into cells. Acute kidney injury has become prevalent in COVID-19 patients without prior any history of kidney dysfunction. In addition, the virus also worsens kidney conditions and increases mortality of COVID-19 patients with pre-existing chronic kidney disease, renal cancer, diabetic nephropathy, end-stage kidney disease as well as dialysis and kidney transplant patients. In the search for antiviral agents for the treatment of COVID-19, hydrogen sulfide (H2S), the third established member of gasotransmitter family, is emerging as a potential candidate, possessing important therapeutic properties including antiviral, anti-inflammatory, anti-thrombotic and antioxidant properties. A recent clinical study revealed higher serum H2S levels in survivors of COVID-19 pneumonia with reduced interleukin-6 levels compared to fatal cases. In this review, we summarize the global impact of COVID-19 on kidney conditions and discuss the emerging role of H2S as a potential COVID-19 therapy.


Subject(s)
Renal Insufficiency, Chronic , Kidney Failure, Chronic , Thrombosis , Kidney Neoplasms , Pneumonia , Kidney Diseases , Diabetic Nephropathies , Respiratory Insufficiency , Acute Kidney Injury , COVID-19
3.
researchsquare; 2024.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3893183.v1

ABSTRACT

Sars-CoV2 associated coagulopathy is a complex entity. Platelets, coagulation factors, fibrinolysis, inflammatory cytokines, immunothrombosis, antiphospholipd antibodies, von Willebrand factor/ADAMTS13 axis, complement system have all been demonstrated to be actively involved in the determination of thrombotic events. Til now retrospective studies have analyzed the activaction of vWF/ADAMTS13 axis and complement involvement. We performed a prospective study with the aim of describing clinical and laboratoristic features of Sars-CoV2 associated coagulopathy and its relationship with complement activation. Biochemical variables, vWF/ADAMTS13 axis, complement factors of the enrolled patients have been analyzed. These variables have been correlated to clinical outcome of the disease. Covid associated coagulopathy is neither a Trombotic Trombocitopenc Purpura (TTP) nor and atypical hemolytic uremic syndrome (aSEU). Nevertheless, imbalance of vWF/Adamts13 axis and complement activation simultaneously occurre and are significantly higher in the severe form of disease.


Subject(s)
Thrombosis , Purpura , Hemolytic-Uremic Syndrome , Blood Coagulation Disorders
4.
researchsquare; 2024.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3891055.v1

ABSTRACT

Background and aim: Millions of people worldwide have suffered from coronavirus disease 2019 (COVID-19). COVID-19 can lead to coagulopathy and thrombosis, presenting as pulmonary artery thromboembolism, deep vein thrombosis, and thrombotic microangiopathy (TMA), the latter being a rare finding in affected patients’ kidneys. Prior reports have rarely addressed the pathophysiology, clinical presentations, and therapeutic options in patients with COVID-19-associated TMA. Case presentation: We herein described a case of renal biopsy-proven TMA after COVID-19 in a 36-year-old woman. Initial examination revealed inflammation, acute kidney injury (AKI), anemia, and thrombocytopenia. She was diagnosed with hemolytic uremic syndrome, pulmonary infection, and COVID-19. After treatment, her condition stabilized but remained hemodialysis-dependent after discharge. One week later, she was re-hospitalized, and physical examination showed anemia and bilateral lower extremity edema. Abdominal ultrasound showed increased bilateral kidney echogenicity. Whole-exome sequencing detected an unknown variant of the C3 gene associated with hemolytic uremic syndrome susceptibility type 5/complement C3 deficiency. Kidney biopsy showed renal artery lesions, including small arteriole endothelial swelling, intimal thickening, mucinous degeneration, luminal occlusion, and small arterial wall necrosis. She received plasma exchange and steroids with significant renal function recovery. Conclusion: TMA likely contributed to AKI after COVID-19,thus supporting the notion that TMA plays an important role in the pathogenesis of COVID-19-related kidney injury. When diagnosing and treating COVID-19 patients with abnormal renal function, clinicians should incorporate kidney biopsy and genetic testing for the complement system, identify renal-limited and systemic TMA, and treat accordingly, which can improve patient outcomes.


Subject(s)
Necrosis , Thrombosis , Edema , Acute Kidney Injury , Adenocarcinoma, Mucinous , Anemia , Kidney Diseases , Thrombotic Microangiopathies , Thrombocytopenia , Inflammation , Venous Thrombosis , Coronary Occlusion , COVID-19 , Hemolytic-Uremic Syndrome , Pulmonary Embolism
5.
researchsquare; 2024.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3846901.v1

ABSTRACT

Background Association of Coronavirus disease 2019 vaccines with thrombosis has raised concerns among patients with coronary atherosclerosis disease (CAD).Objectives After vaccination against SARS-CoV-2, to detect thrombosis formation in atherosclerosis ApoE−/− mice, and platelet activation, coagulation, the profile of prothrombotic antibodies, and the production of platelet factor 4 (PF4) antibodies in patients with CAD.Methods Atherosclerotic ApoE−/− mice were immunized with saline or inactivated SARS-CoV vaccines. We investigated FeCl3-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo. Inpatients undergoing percutaneous coronary intervention (PCI) were consecutively enrolled and defined according to vaccination status. We evaluated coagulation by thrombelastograph (TEG), platelet activation makers by flow cytometry, PF4 antibody and antiphospholipid antibodies by ELISA, and SARS-CoV-2 neutralizing antibody.Results In atherosclerotic ApoE−/− mice, FeCl3-induced thrombus formation and thrombus formation under flow conditions were similar between saline-treated and inactivated SARS-CoV-2 vaccines-treated groups. A total of 182 patients undergoing PCI were included in the final analysis, of whom 92 had been vaccinated. Baseline characteristics were well balanced between unvaccinated and vaccinated groups. The expression of PAC-1 and P-selectin, the prevalence of positivity for PF4 antibodies and antiphospholipid antibodies were similar between these two groups.Conclusions Inactivated SARS-CoV-2 vaccines did not potentiate thrombosis formation in atherosclerotic mice. Inactivated SARS-CoV-2 vaccines did not enhance platelet activation, or trigger the production of PF4 and antiphospholipid antibodies in patients with CAD. Our data adds evidence to the safety profile of the inactivated SARS-CoV-2 vaccines.


Subject(s)
Thrombosis , Coronary Artery Disease , Severe Acute Respiratory Syndrome , COVID-19 , Atherosclerosis
6.
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.11.21.568132

ABSTRACT

SARS-CoV-2, the coronavirus responsible for the COVID-19 pandemic, is associated with a range of neurological manifestations including haemorrhage, thrombosis and ischaemic necrosis and encephalitits. However, the mechanism by which this occurs is unclear. Neurological disease associated with SARS-CoV-2 infection has been proposed to occur following direct infection of the central nervous system and/or indirect sequelae as a result of peripheral inflammation. We profiled ACE2 and TMPRSS2 in brain tissue from five healthy human donors, and observed expression of these proteins in astrocytes, neurons and choroid plexus epithelium within frontal cortex and medulla. Primary human astrocytes, neurons and choroid plexus epithelial cells supported productive SARS-CoV-2 infection in an ACE2- dependent manner. Infected cells supported the full viral lifecycle, releasing infectious virus particles. In contrast, primary brain microvascular endothelial cells, pericytes and microglia were refractory to SARS-CoV-2 infection. These data support a model whereby SARS-CoV-2 is neurotropic, and this may in part explain the neurological sequelae of infection. ImportanceA subset of patients with COVID-19 develop neurological symptoms, but the underlying cause is poorly understood. We observed that cells within normal human brain express the SARS-CoV-2 entry factors ACE-2 and TMPRRS2, with expression mainly observed within astrocytes, neurons and choroid plexus epithelium. Primary human astrocytes, neurons and choroid plexus epithelial cells cultured in vitro supported the full SARS-CoV-2 life cycle with a range of SARS-CoV-2 variants. This study demonstrates that cells of the human central nervous system express SARS-CoV-2 entry factors in vivo and support viral infection in vitro, thus supporting a model where neurological symptoms seen in some COVID-19 patients may be as a result of direct viral infection of the central nervous system. Furthermore, these data highlight the importance of investigating the ability of therapeutics to clear virus from this potential reservoir of infection.


Subject(s)
Necrosis , Thrombosis , Virus Diseases , Severe Acute Respiratory Syndrome , Heredodegenerative Disorders, Nervous System , Hemorrhage , Inflammation , COVID-19
7.
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.10.25.563806

ABSTRACT

The clinical manifestations of acute severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection and COVID-19 suggest a dysregulation of the host immune response that leads to inflammation, thrombosis, and organ dysfunction. It is less clear whether these dysregulated processes persist during the convalescent phase of disease or during long COVID. We investigated the effects of SARS-CoV-2 infection on the proportions of classical, intermediate, and non-classical monocytes, their activation status, and their functional properties in convalescent COVID-19 patients and uninfected control subjects. We found that the percentage of total monocytes was decreased in convalescent COVID-19 patients compared to uninfected controls. This was due to decreased intermediate and non-classical monocytes. Classical monocytes from convalescent COVID-19 patients demonstrated a decrease in activation markers, such as CD56, in response to stimulation with bacterial lipopolysaccharide (LPS). In addition, classical monocytes from convalescent COVID-19 patients showed decreased expression of CD142 (tissue factor), which can initiate the extrinsic coagulation cascade, in response to LPS stimulation. Finally, we found that monocytes from convalescent COVID-19 patients produced less TNF- and IL-6 in response to LPS stimulation, than those from uninfected controls. In conclusion, SARS-CoV-2 infection exhibits a clear effect on the relative proportions of monocyte subsets, the activation status of classical monocytes, and proinflammatory cytokine production that persists during the convalescent phase of disease.


Subject(s)
Thrombosis , Inflammation , Coronavirus Infections , COVID-19
8.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.09.08.23295024

ABSTRACT

Linking clinical biomarkers and lung pathology still is necessary to understand COVID-19 pathogenesis and the basis of progression to lethal outcomes. Resolving these knowledge gaps enables optimal treatment approaches of severe COVID-19. We present an integrated analysis of longitudinal clinical parameters, blood biomarkers and lung pathology in COVID-19 patients from the Brazilian Amazon. We identified core signatures differentiating severe recovered patients and fatal cases with distinct disease trajectories. Progression to early death was characterized by rapid and intense endothelial and myeloid activation, presence of thrombi, mostly driven by SARS-CoV-2 + macrophages. Progression to late death was associated with systemic cytotoxicity, interferon and Th17 signatures and fibrosis, apoptosis, and abundant SARS-CoV-2 + epithelial cells in the lung. Progression to recovery was associated with pro-lymphogenic and Th2-mediated responses. Integration of antemortem clinical and blood biomarkers with post-mortem lung-specific signatures defined predictors of disease progression, identifying potential targets for more precise and effective treatments.


Subject(s)
Fibrosis , Thrombosis , Drug-Related Side Effects and Adverse Reactions , Death , COVID-19
9.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.08.22.23294400

ABSTRACT

BackgroundCOVID-19 vaccines have played a critical role in controlling the COVID-19 pandemic. Although overall considered safe, COVID-19 vaccination has been associated with rare but severe thrombotic events, occurring mainly in the context of adenoviral vectored vaccines. A better understanding of mechanisms underlying vaccine-induced hypercoagulability and prothrombotic state is needed to improve vaccine safety profile. MethodsWe assessed changes to the biomarkers of endothelial function (endothelin, ET-1), coagulation (thrombomodulin, THBD and plasminogen activator inhibitor, PAI) and platelet activation (platelet activating factor, PAF, and platelet factor 4 IgG antibody, PF4 IgG) within a three-week period after the first (prime) and second (boost) doses of Gam-Covid-Vac, an AdV5/AdV26-vectored COVID-19 vaccine. Blood plasma collected from vaccinees (n=58) was assayed using ELISA assays. Participants were stratified by prior COVID-19 exposure based on their baseline SARS-CoV-2-specific serology results. ResultsWe observed a significant post-prime increase in circulating ET-1, with levels sustained after the boost dose compared to baseline. ET-1 elevation following dose 2 was most pronounced in vaccinees without prior COVID-19 exposure. Prior COVID-19 was also associated with a mild increase in post-dose 1 PAI. ConclusionsVaccination was associated with elevated ET-1 up to day 21 after the second vaccine dose, while no marked alterations to other biomarkers, including PF4 IgG, were seen. A role of persistent endothelial activation followingCOVID-19 vaccination warrants further investigation.


Subject(s)
Thrombophilia , Thrombosis , Blood Coagulation Disorders, Inherited , COVID-19
10.
preprints.org; 2023.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202307.1113.v1

ABSTRACT

Background: We studied the outcomes of SARS-CoV-2 (COVID) hospitalizations and their association with myocardial injury and thrombosis. Methods: Retrospective analysis of the National Inpatient Sample 2020 database. Results: We identified 335,799 hospitalizations with COVID. Of these, 1.6% (5,355) were diagnosed with non-ST-segment myocardial infarction (COVNSTEMI). The mean age of COVID hospitalizations was 71.7, with 60.50% being males. The population prevalence included 53.10% Whites, 17.80% Blacks, 19.20% Hispanics, and 4.10% Asians. The average length of stay (LOS) was 10 days, and 37.60% of patients died during their hospitalization. The average cost of hospitalization (TOTCHG) was $156,633. The COVSTEMI group comprised 1,364 cases, with a mean age of 67.4, in-hospital mortality of 47.4%, and the mean TOTCHG was $177,600. The DVTCOV group comprised 2,869 cases, while the PECOV group had 4,828 cases. Male predominance was observed in both groups, with mean ages of 66 years in the DVTCOV group and 64 years in the PECOV group. The DVTCOV group had a LOS of 16 days, with 24.71% mortality, while the PECOV group had a LOS of 11 days, with 19.20% mortality. The average TOTCHG in the DVTCOV group was $248,900, whereas it was $145,378 in the PECOV group. Conclusion: Our study revealed significant mortality rates across different groups, including 38% in COVNSTEMI, 47% in COVSTEMI, 25% in DVTCOV, and 19% in PECOV. These findings highlight the severity of COVID-related complications and the substantial financial burden of hospitalization.


Subject(s)
Myocardial Infarction , Thrombosis , Cardiomyopathies , Venous Thrombosis , Pulmonary Embolism
11.
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.07.14.549113

ABSTRACT

Despite more than 90% of total plasma fucosylated IgG, specific IgGs with low core fucosylation are found sporadically in response to enveloped virus infections and to alloantigens on blood cells. IgG responses with low core fucosylation are directly pathogenic in SARS-CoV-2 and dengue infections. In COVID-19, formation of IgG with low core fucosylation (afucosylated IgG) against spike protein (S) predicts and directly mediates disease progression to severe form. Low fucosylation of IgG causes increased antibody-dependent cellular toxicity mediated by intense Fc{gamma}R-mediated stimulation of platelets, monocytes, macrophages, and natural killer cells. The mechanism of afucosylated IgG formation has remained elusive thus far in COVID-19, dengue infection, and other disorders. This study demonstrates that infection of megakaryocytes by SARS-CoV-2 drives the formation of pathogenic anti-S afucosylated IgGs, causing pulmonary vascular thrombosis, acute lung injury, and death in Fc{gamma}-expressing mice.


Subject(s)
Thrombosis , Drug-Related Side Effects and Adverse Reactions , Dengue , Death , Tumor Virus Infections , COVID-19 , Acute Lung Injury
12.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.07.05.23292278

ABSTRACT

Background: COronaVIrus Disease 2019 (COVID-19) has been observed to be associated with a hypercoagulable state. Intracardiac thrombosis is a serious complication but has seldom been evaluated in COVID-19 patients. We assessed the incidence, associated factors, and outcomes of COVID-19 patients with intracardiac thrombosis. Methods: COVID-19 inpatients during 2020 were retrospectively identified from the national inpatient sample (NIS) database, and data retrieved regarding clinical characteristics, intracardiac thrombosis, and adverse outcomes. Multivariable logistic regression was performed to identify the clinical factors associated with intracardiac thrombosis and in-hospital mortality and morbidities. Results: A total of 1,683,785 COVID-19 inpatients were identified in 2020 from NIS, with a mean age of 63.8 {+/-} 1.6 years, and 32.2% females. Intracardiac thrombosis was present in 0.001% (1,830) patients. Overall, in-hospital outcomes include all-cause mortality 13.2% (222,695/1,683,785), cardiovascular mortality 3.5%, cardiac arrest 2.6%, acute coronary syndrome (ACS) 4.4%, heart failure 16.1%, stroke 1.3% and acute kidney injury (AKI) 28.3%. The main factors associated with intracardiac thrombosis were a history of congestive heart failure and coagulopathy. Intracardiac thrombosis was independently associated with a higher risk of in-hospital all-cause mortality (OR: 3.32, 95% CI: 2.42-4.54, p<0.001), cardiovascular mortality (OR: 2.95, 95% CI: 1.96-4.44, p<0.001), cardiac arrest (OR: 2.04, 95% CI: 1.22-3.43, p=0.006), ACS (OR: 1.62, 95% CI: 1.17-2.22, p=0.003), stroke (OR: 3.10, 95% CI: 2.11-4.56, p<0.001), and AKI (OR: 2.13 95% CI: 1.68-2.69, p<0.001), but not incident heart failure (p=0.27). Conclusion: Although intracardiac thrombosis is rare in COVID-19 inpatients, its presence was independently associated with higher risks of in-hospital mortality and most morbidities. Prompt investigations and treatments for intracardiac thrombosis are warranted when there is a high index of suspicion and a confirmed diagnosis respectively.


Subject(s)
Heart Failure , Thrombosis , Stroke , Acute Coronary Syndrome , Acute Kidney Injury , Heart Arrest , COVID-19 , Blood Coagulation Disorders
14.
Br J Hosp Med (Lond) ; 84(5): 1-11, 2023 May 02.
Article in English | MEDLINE | ID: covidwho-20238129

ABSTRACT

Hospitalised patients with coronavirus disease 2019 (COVID-19) are at a significantly higher risk of having thromboembolic events while in hospital and in the immediate post-hospital discharge period. Based on early data from observational studies, multiple high quality randomised controlled trials have been conducted worldwide to evaluate optimal thromboprophylaxis regimens to reduce thromboembolism and other COVID-19-related adverse outcomes in hospitalised patients. The International Society on Thrombosis and Haemostasis has published evidence-based guideline recommendations using established methodology for the management of antithrombotic therapy of COVID-19 patients, both in-hospital and in the immediate post-hospital discharge period. A good clinical practice statement supplemented these guidelines based on topics for which there was no or limited high-quality evidence. This review summarises the main recommendations of these documents to serve as a quick access tool for hospital doctors to use in their everyday practice when treating COVID-19 patients.


Subject(s)
COVID-19 , Thrombosis , Venous Thromboembolism , Humans , Anticoagulants/therapeutic use , Fibrinolytic Agents/therapeutic use , Venous Thromboembolism/drug therapy , Venous Thromboembolism/prevention & control , Thrombosis/drug therapy , Thrombosis/prevention & control
15.
Front Immunol ; 14: 1186000, 2023.
Article in English | MEDLINE | ID: covidwho-20236819

ABSTRACT

Coronavirus disease 2019 (COVID-19) is known to commonly induce a thrombotic diathesis, particularly in severely affected individuals. So far, this COVID-19-associated coagulopathy (CAC) has been partially explained by hyperactivated platelets as well as by the prothrombotic effects of neutrophil extracellular traps (NETs) released from neutrophils. However, precise insight into the bidirectional relationship between platelets and neutrophils in the pathophysiology of CAC still lags behind. Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare autoimmune disorder caused by auto-antibody formation in response to immunization with adenoviral vector vaccines. VITT is associated with life-threatening thromboembolic events and thus, high fatality rates. Our concept of the thrombophilia observed in VITT is relatively new, hence a better understanding could help in the management of such patients with the potential to also prevent VITT. In this review we aim to summarize the current knowledge on platelet-neutrophil interplay in COVID-19 and VITT.


Subject(s)
COVID-19 , Thrombocytopenia , Thrombosis , Vaccines , Humans , Blood Platelets , Neutrophils , COVID-19/complications , Thrombocytopenia/chemically induced , Thrombosis/etiology , Rare Diseases
16.
Neurol Neuroimmunol Neuroinflamm ; 10(4)2023 07.
Article in English | MEDLINE | ID: covidwho-20235895

ABSTRACT

OBJECTIVES: Vaccine-induced immune thrombotic thrombocytopenia (VITT), a recently described entity characterized by thrombosis at unusual locations such as cerebral venous sinus and splanchnic vein, has been rarely described after adenoviral-encoded COVID-19 vaccines. In this study, we report the immunohistological correlates in 3 fatal cases of cerebral venous thrombosis related to VITT analyzed at an academic medical center. METHODS: Detailed neuropathologic studies were performed in 3 cases of cerebral venous thrombosis related to VITT after adenoviral COVID-19 vaccination. RESULTS: Autopsy revealed extensive cerebral vein thrombosis in all 3 cases. Polarized thrombi were observed with a high density of neutrophils in the core and a low density in the tail. Endothelial cells adjacent to the thrombus were largely destroyed. Markers of neutrophil extracellular trap and complement activation were present at the border and within the cerebral vein thrombi. SARS-CoV-2 spike protein was detected within the thrombus and in the adjacent vessel wall. DISCUSSION: Data indicate that neutrophils and complement activation associated with antispike immunity triggered by the vaccine is probably involved in the disease process.


Subject(s)
COVID-19 , Thrombocytopenia , Thrombosis , Vaccines , Venous Thrombosis , Humans , COVID-19 Vaccines/adverse effects , Endothelial Cells , SARS-CoV-2 , Venous Thrombosis/etiology
17.
J Cardiovasc Pharmacol Ther ; 28: 10742484221145010, 2023.
Article in English | MEDLINE | ID: covidwho-20233025

ABSTRACT

Fondaparinux sodium is a chemically synthesized selective factor Xa inhibitor approved for the prevention and treatment of venous thromboembolic events, that is, deep vein thrombosis, pulmonary embolism, and superficial vein thrombosis, in acutely ill (including those affected by COVID-19 or cancer patients) and those undergoing surgeries. Since its approval in 2002, the efficacy and safety of fondaparinux is well demonstrated by many clinical studies, establishing the value of fondaparinux in clinical practice. Some of the advantages with fondaparinux are its chemical nature of synthesis, minimal risk of contamination, 100% absolute bioavailability subcutaneously, instant onset of action, a long half-life, direct renal excretion, fewer adverse reactions when compared with direct oral anticoagulants, and being an ideal alternative in conditions where oral anticoagulants are not approved for use or in patients intolerant to low molecular weight heparins (LMWH). In the last decade, the real-world use of fondaparinux has been explored in other conditions such as acute coronary syndromes, bariatric surgery, in patients developing vaccine-induced immune thrombotic thrombocytopenia (VITT) and in pregnant women with heparin-induced thrombocytopenia (HIT), or those intolerant to LMWH. The emerging data from these studies have culminated in recent updates in the guidelines that recommend the use of fondaparinux under various conditions. This paper aims to review the recent data and the subsequent updates in the recommendations of various guidelines on the use of fondaparinux sodium.


Subject(s)
COVID-19 , Thrombosis , Venous Thrombosis , Pregnancy , Humans , Female , Fondaparinux/adverse effects , Heparin, Low-Molecular-Weight/adverse effects , Polysaccharides/adverse effects , Anticoagulants/adverse effects , Thrombosis/drug therapy , Thrombosis/prevention & control , Venous Thrombosis/drug therapy , Heparin
18.
Med. lab ; 26(3): 219-236, 2022. Tabs, ilus, Grafs
Article in Spanish | WHO COVID, LILACS (Americas) | ID: covidwho-20244331

ABSTRACT

El virus SARS-CoV-2 continúa infectando a millones de individuos en el mundo. Aunque los síntomas más frecuentes observados en los pacientes con COVID-19 son fiebre, fatiga y tos, en los casos severos la hipercoagulabilidad y la inflamación son dos condiciones que pueden producir complicaciones y causar daño en órganos, poniendo en riesgo la vida del paciente. Con el fin de clasificar a los pacientes durante el triaje, se han explorado diferentes marcadores hematológicos, incluidos el recuento de plaquetas, linfocitos y eosinófilos, y la relación neutrófilos/ linfocitos, entre otros. Por su parte, para la evaluación de las coagulopatías, se vienen determinando marcadores como el dímero D y el fibrinógeno. En esta revisión se abordan las coagulopatías y los parámetros hematológicos en pacientes con COVID-19, al igual que las anormalidades en la coagulación como la trombocitopenia trombótica inmune inducida por las vacunas contra el SARS-CoV-2


The SARS-CoV-2 virus continues to infect millions of individuals around the world. Although the most frequent symptoms observed in patients with COVID-19 are fever, fatigue and cough, in severe cases hypercoagulability and inflammation are two conditions that can cause complications and organ failure, putting the patient's life at risk. In order to classify patients during triage, different hematological markers have been explored, including platelet, lymphocyte, and eosinophil counts, and the neutrophil/lymphocyte ratio, among others. Furthermore, for the evaluation of coagulopathies, markers such as D-dimer and fibrinogen are being evaluated. This review addresses the coagulopathies and hematological parameters in patients with COVID-19, as well as coagulation abnormalities such as immune thrombotic thrombocytopenia induced by SARS-CoV-2 vaccines


Subject(s)
Humans , COVID-19 , Prognosis , Reference Standards , Thrombosis , Blood Coagulation , Blood Coagulation Disorders , Blood Platelets , Vaccines , Antigens, Differentiation , SARS-CoV-2 , Hematology
19.
Kardiologiia ; 63(1): 29-35, 2023 Jan 31.
Article in Russian, English | MEDLINE | ID: covidwho-20232462

ABSTRACT

Aim      To evaluate the incidence and characteristic features of left atrial appendage (LAA) thrombosis in patients with persistent nonvalvular atrial fibrillation (AF) after COVID-19.Material and methods  Transesophageal echocardiography (TEE) was performed for 469 patients (57.4 % males; mean age, 64.0 [58.0; 70.0] years) with persistent nonvalvular AF before scheduled sinus rhythm restoration. In 131 of these patients (27.9 %), the most recent episode of arrhythmia developed during the coronavirus infection. The time from the onset of COVID-19 to TEE was 145 [62; 303] days. All patients received an adequate anticoagulant therapy, in most cases, with direct oral anticoagulants for at least 3 weeks preceding the study.Results A LAA thrombus was detected in 20 (5.9 %) patients who have had no coronavirus infection and in 19 (14.5 %) patients after COVID-19 (р=0.0045). 18 of 19 (94.7 %) thrombi found in patients who have had COVID-19 were mural whereas only 5 (25.0 %) of such thrombi were found in patients who have had no COVID-19 (p<0.0001). In the absence of LAA thrombus, the LAA emptying velocity was 32.0 [25.0; 40.0] cm/sec whereas in the presence of a mural thrombus, it was 25.0 [20.0; 32.3] cm/sec, and in the presence of a typical thrombus, it was 17.0 [13.5; 20.0] cm/sec (р<0.0001). A Kaplan-Meier analysis showed that the median time of mural thrombus dissolution was 35.0 (95 % confidence interval (CI), 24.0-55.0) days and for a typical thrombus, this time was 69.0 (95 % CI, 41.0-180.0) days (р=0.0018).Conclusion      Patients with persistent AF who have had COVID-19 had LAA thrombosis 2,5 times more frequently and, in most cases, the thrombus was mural. Mural thrombi, in contrast to typical, are not associated with a pronounced decrease in LAA emptying velocity and dissolve twice as fast as typical thrombi with an adequate anticoagulant treatment.


Subject(s)
Atrial Appendage , Atrial Fibrillation , COVID-19 , Heart Diseases , Thrombosis , Male , Humans , Middle Aged , Female , Atrial Fibrillation/complications , Atrial Appendage/diagnostic imaging , COVID-19/complications , Anticoagulants , Thrombosis/etiology , Echocardiography, Transesophageal/adverse effects , Heart Diseases/complications
20.
Indian J Med Res ; 157(4): 281-292, 2023 04.
Article in English | MEDLINE | ID: covidwho-20243533

ABSTRACT

Venous thromboembolism (VTE), which entails the formation of a thrombus (blood clot) in a vein, has a significant disease burden worldwide. While VTE has traditionally been considered to predominantly affect Caucasian populations, recent studies have indicated a gradual shift in the disease burden towards Asian populations, with added significance of it being a key driver of post-operative mortality. It is imperative to develop a sound understanding of the various factors that affect VTE in stratified local populations. However, there is a glaring paucity of quality data on VTE and its ramifications among Indians - both in terms of quality of life and cost of healthcare. This review aims to throw light on the disease burden, epidemiology, risk factors, environmental factors, food and nutrition that plays a key role in VTE. We also explored the association of VTE with coronavirus disease 2019 to grasp the interplay between the two most significant public health crises of our time. It is vital to place a special emphasis on future research on VTE in India to plug the gaps, which exist in our current knowledge of the disease, particularly with respect to Indian population.


Subject(s)
COVID-19 , Pulmonary Embolism , Thrombosis , Venous Thromboembolism , Venous Thrombosis , Humans , Venous Thromboembolism/epidemiology , Quality of Life , Risk Factors
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