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1.
authorea preprints; 2024.
Preprint in English | PREPRINT-AUTHOREA PREPRINTS | ID: ppzbmed-10.22541.au.170667762.25200980.v1

ABSTRACT

Objective: Cytokine storm and Coagulopathy have been implicated as major causes of morbidity and mortality in COVID-19 patients. A black yeast Aureobasidium pullulans AFO-202 strain produced beta 1,3-1,6 glucan has been reported to offer potential immune enhancement and metabolism balancing, as well as mitigation of coagulopathy risks. The N-163 strain produced beta glucan is an efficient anti-inflammatory immune modulator. In this pilot clinical study, we report the beneficial effects of these two beta glucans on the biomarkers for cytokine storm and coagulopathy in COVID-19 patients. Methods: : A total of 24 RT-PCR positive COVID-19 patients were recruited (Age range: 18~62; 17 males and 7 females). Patients were randomly divided into three groups (Gr): Gr. 1 control (n=8); Gr. 2: AFO-202 beta glucan (n=8); and Gr. 3, a combination of AFO-202 and N-163 beta glucans (n=8). All three groups received the standard care while groups 2 and 3 received additional supplementation of beta glucans for 30 days. In addition to basic clinical parameters, we periodically evaluated D-Dimer, IL-6, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), the neutrophil to lymphocyte ratio (NLR), the lymphocyte to CRP ratio (LCR) and the leukocyte-CRP ratio (LeCR). Results: : The duration of hospital stay for all three groups was nearly equivalent. There was no mortality of the subjects in any of the groups. Intermittent oxygen was administered from day of admission for up to four to five days with mask (two to four Lpm) to two subjects in Gr. 2 and one subject in Gr. 3. None of the subjects required ventilation. The D-Dimer values in Gr. 1, which was on average 751 ng/ml at baseline, decreased to 143.89 ng/ml on day 15, but increased to 202.5 ng/ml on day 30, which in groups 2 and 3 decreased on day 15 and continued to remain at normal levels until day 30. IL-6 levels decreased on day 15 from an average of 7.395 pg/ml to 3.16 pg/ml in the control, 26.18 pg/ml to 6.94 pg/ml in Gr. 2 and 6.25 pg/ml to 5.22 pg/ml in Gr. 3. However, when measured on day 30, in Gr. 1, the IL-6 increased to 55.37 pg/ml while there was only slight marginal increase in Gr. 2 but within normal range, and the levels further decreased to less than 0.5 pg/ml in Gr. 3. The same trend was observed with ESR. LCR and LeCR increased significantly in Gr. 3. NLR decreased significantly in groups 2 and 3. There was no difference in CRP within the groups. Conclusion: In this exploratory study, consumption of Aureobasidium pullulans produced beta glucans for thirty days, results in a significant control of IL6, D-Dimer and NLR, a significant increase in LCR, LeCR and marginal control of ESR in COVID-19 patients. As these beta glucans are well known food supplements with decades of a track record for safety, based on these results, we recommend larger multi-centric clinical studies to validate their use as an adjunct in the management of COVID-19 and the ensuing long COVID-19 syndrome.


Subject(s)
Blood Coagulation Disorders , COVID-19
2.
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)
Hemolytic-Uremic Syndrome , Blood Coagulation Disorders , Purpura , Thrombosis
3.
preprints.org; 2023.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202310.0001.v2

ABSTRACT

The host glycosylation mechanism synthesizes the carbohydrates of glycoproteins of viral envelopes. Due to the loss of the Cytidine Monophospho-N-Acetylneuraminic Acid Hydroxylase gene by some mammalian species, including humans (negative-CMAH), Neu5Gc is no longer synthesized. Uptake of Neu5Gc by negative-CMAH species, through the intake of food products derived from positive-CMAH mammals, leads to incorporating Neu5Gc-glycans in the glycocalyx (xenosialylation). Neu5Gc, being a Mammalian-associated Carbohydrate Antigen (MCA), acts as a non-self-antigen, inducing an inflammatory reaction (Xenosialitis), and triggering the production of circulating antiNeu5Gc antibodies to attack/remove all incorporated Neu5Gc. In the state of Xenosialitis, the virus-neutralizing antibodies produced by a heavily xenosialylated patient following exposure to viral infection (including SarsCoV2) or anti SarsCoV2 vaccination cross-react against all incorporated non-self Neu5Gc-MCA glycans due to their resemblance with viral envelope antigens synthesized by the host glycosylation mechanism. In addition, the circulating anti-XeSias antibodies determine the massive removal of the circulating neutralizing FC-xeno-contaminated antibodies by the serum, living only the hyper-inflammatory agalattosylated antiviral IgG antibodies. Therefore, we hypothesize that the combination of antibody cross-reaction against non-self Neu5Gc-MCA glycans and the massive removal of the xeno-contaminated newly formed neutralizing antibodies in favor of hyper reactive antibodies, could be the cause of the massive inflammatory reaction (cytokine storm, coagulopathies, neuropathies) observed in Covid 19 patients or after anti-SarsCoV2 vaccination. This analysis is an invitation to investigate the post-infectious and/or post-vaccination adverse phenomena in the light of xenosialization as a key to understanding the severe post viral and post vaccine complications, including SARS-CoV2 infection or related vaccination.


Subject(s)
Virus Diseases , Nervous System Diseases , Hyper-IgM Immunodeficiency Syndrome, Type 1 , Severe Acute Respiratory Syndrome , Blood Coagulation Disorders , Autoimmune Diseases
4.
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)
Stroke , Acute Coronary Syndrome , COVID-19 , Heart Failure , Heart Arrest , Acute Kidney Injury , Thrombosis , Blood Coagulation Disorders
5.
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
7.
Viruses ; 15(5)2023 04 25.
Article in English | MEDLINE | ID: covidwho-20234853

ABSTRACT

The benefits of SARS-CoV-2 spike mRNA vaccines are well known, including a significant decline in COVID-19 morbidity and a decrease in the mortality rate of SARS-CoV-2 infected persons. However, pharmacovigilance studies have revealed the existence of rare cases of cardiovascular complications after mass vaccination using such formulations. Cases of high blood pressure have also been reported but were rarely documented under perfectly controlled medical supervision. The press release of these warning signals triggered a huge debate over COVID-19 vaccines' safety. Thereby, our attention was quickly focused on issues involving the risk of myocarditis, acute coronary syndrome, hypertension and thrombosis. Rare cases of undesirable post-vaccine pathophysiological phenomena should question us, especially when they occur in young subjects. They are more likely to occur with inappropriate use of mRNA vaccine (e.g., at the time when the immune response is already very active during a low-noise infection in the process of healing), leading to angiotensin II (Ang II) induced inflammation triggering tissue damage. Such harmful effects observed after the COVID-19 vaccine evoke a possible molecular mimicry of the viral spike transiently dysregulating angiotensin converting enzyme 2 (ACE2) function. Although the benefit/risk ratio of SARS-CoV-2 spike mRNA vaccine is very favorable, it seems reasonable to suggest medical surveillance to patients with a history of cardiovascular diseases who receive the COVID-19 vaccine.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Hypertension , Humans , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , SARS-CoV-2/metabolism , Angiotensin-Converting Enzyme 2/genetics , Renin-Angiotensin System/physiology , Peptidyl-Dipeptidase A/metabolism , Molecular Mimicry , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism
8.
Int J Mol Sci ; 24(10)2023 May 18.
Article in English | MEDLINE | ID: covidwho-20241658

ABSTRACT

Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thrombophilia , Thrombosis , Humans , COVID-19/complications , SARS-CoV-2 , Blood Coagulation Disorders/complications , Blood Coagulation Disorders/drug therapy , Inflammation/drug therapy , Thrombosis/etiology , Thrombophilia/complications , Anticoagulants/therapeutic use
9.
preprints.org; 2023.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202306.0473.v1

ABSTRACT

Background: The manifestations, severity, and mortality of COVID-19 are considered to be associated with the changes in various hematological parameters and in immunity. Associations of immunoglobulin G antibodies against severe acute respiratory syndrome-linked coronavirus (IgG-SARS)-positive status with cardiac function and hematological and biochemical parameters in apparently health subjects are poorly understood. Methods: The present cross-sectional study included 307 healthy volunteers (24-69 years of age; 44.8±8.6 years; 80.4% men) and was initiated in 2019 before the COVID-19 pandemic. COVID-19 episodes were confirmed by detection of IgG-SARS against SARS-CoV-2 S1 RBD to reveal 70 IgG-SARS-positive and 237 negative participants. Numerous ultrasound characteristics were assessed by echocardiography, and 15 hematological and biochemical parameters were assayed in the blood. Descriptive and comparative analysis was based on the IgG-SARS status of the participants. Results: The left ventricular mass index, mitral ratio of peak early to late diastolic filling velocity or flow velocity across the mitral valve, and deceleration time of early mitral inflow were decreased (P<0.05) in IgG-SARS-positive participants versus those in IgG-SARS-negative participants according to multivariate logistic regression analysis. Erythrocyte sedimentation rate and platelet count were slightly increased, and blood hemoglobin was decreased in IgG-SARS-positive participants compared with those in IgG-SARS-negative participants. Conclusions: LV filling, inflammation, blood coagulation, and hemoglobin appear to be influenced by COVID-19 infection in healthy participants. These observations contribute to the development of a population recovery strategy after the episodes of COVID-19.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Coronavirus Infections , Inflammation
10.
preprints.org; 2023.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202305.1487.v1

ABSTRACT

Long COVID (LC) encompasses a constellation of long-term symptoms experienced by at least 10% of people after the initial SARS-CoV-2 infection, and so far has affected about 65 million people. The etiology of LC remains unclear; however, many pathophysiological pathways may be involved, including viral persistence; chronic, low grade inflammatory response; immune dysregulation and defective immune response; reactivation of latent viruses; autoimmunity; persistent endothelial dysfunction and coagulopathy; gut dysbiosis; hormonal dysregulation, mitochondrial dysfunction; and autonomic nervous system dysfunction. There are no specific tests for the diagnosis of LC, and clinical features including laboratory findings and biomarkers may not specifically relate to LC. Therefore, it is of paramount importance to develop and validate biomarkers that can be employed for the prediction, diagnosis and prognosis of LC and its therapeutic response. Promising candidate biomarkers that are found in some patients are markers of systemic inflammation including acute phase proteins, cytokines and chemokines; biomarkers reflecting SARS-CoV-2 persistence, reactivation of herpesviruses and immune dysregulation; biomarkers of endotheliopathy, coagulation and fibrinolysis; microbiota alterations; diverse proteins and metabolites; hormonal and metabolic biomarkers; as well as cerebrospinal fluid biomarkers. At present, there are only two reviews summarizing relevant biomarkers; however, they do not cover the entire umbrella of current biomarkers or their link to etiopathogenetic mechanisms, and the diagnostic work-up in a comprehensive manner. Herein, we aim to appraise and synopsize the available evidence on the typical laboratory manifestations and candidate biomarkers of LC, their classification based on main LC symptomatology in the frame of the epidemiological and pathogenetic aspects of the syndrome, and furthermore assess limitations and challenges as well as potential implications in candidate therapeutic interventions.


Subject(s)
COVID-19 , Nervous System Diseases , Mitochondrial Diseases , Dysbiosis , Blood Coagulation Disorders, Inherited , Blood Coagulation Disorders , Inflammation
11.
Monaldi Arch Chest Dis ; 92(4)2022 Jan 26.
Article in English | MEDLINE | ID: covidwho-2310092

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can vary on a spectrum of asymptomatic disease to rarer manifestations like hypercoagulability especially among elderly patients admitted in the intensive care unit (ICU) and those with preexisting comorbidities. The exact mechanism behind this phenomenon is still unclear, however studies have shown an association with elevated cytokines and severe inflammatory response which encompasses this disease. Hypercoagulability can be limited to the lungs, or present as systemic manifestations of arterial and venous thrombosis leading to mortal outcomes. Thus, careful evaluation of risk factors should be performed by physicians and treatment with anticoagulants should be modified accordingly. All Coronavirus Disease 2019 (COVID-19) in-patients should receive thromboprophylactic therapy, with increased dosages administered to patients with increased disease severity or those with a high risk. D-dimer levels and sepsis-induced coagulopathy (SIC) score aid in identifying high risk patients and predicting outcome. This article highlights the pathophysiology behind hypercoagulability, its clinical associations and discusses therapeutic modalities to combat this fatal consequence of SARS-CoV-2.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thrombophilia , Aged , Anticoagulants/therapeutic use , Blood Coagulation Disorders/etiology , COVID-19/complications , Cytokines , Humans , SARS-CoV-2 , Thrombophilia/chemically induced , Thrombophilia/etiology
12.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2939263.v1

ABSTRACT

Long COVID describes an array of often debilitating symptoms in the aftermath of SARS-CoV-2 infection, with similar symptomatology affecting some people post-vaccination. With an estimated > 200 million Long COVID patients worldwide and cases still rising, the effects on quality of life and the economy are significant, thus warranting urgent attention to understand the pathophysiology. Herein we describe our perspective that Long COVID is a continuation of acute COVID-19 pathology, whereby coagulopathy is the main driver of disease and can cause or exacerbate other pathologies common in Long COVID, such as mast cell activation syndrome and dysautonomia. Considering the SARS-CoV-2 spike protein can independently induce fibrinaloid microclots, platelet activation, and endotheliitis, we predict that persistent spike protein will be a key mechanism driving the continued coagulopathy in Long COVID. We discuss several treatment targets to address the coagulopathy, and predict that (particularly early) treatment with combination anticoagulant and antiplatelet drugs will bring significant relief to many patients, supported by a case study. To help focus attention on such treatment targets, we propose Long COVID should be referred to as Spike protein Induced Thrombotic Vasculitis (SITV). These ideas require urgent testing, especially as the world tries to co-exist with COVID-19.


Subject(s)
COVID-19 , Vasculitis , Mastocytosis , Primary Dysautonomias , Blood Coagulation Disorders
13.
Ann Hematol ; 102(6): 1589-1598, 2023 Jun.
Article in English | MEDLINE | ID: covidwho-2293303

ABSTRACT

COVID-19 is characterized by a predominantly prothrombotic state, which underlies severe disease and poor outcomes. Imbalances of the gut microbiome have been linked with abnormal hemostatic processes. Understanding the relationship between the gut microbiome and abnormal coagulation parameters in COVID-19 could provide a novel framework for the diagnosis and management of COVID-related coagulopathies (CRC). This cross-sectional study used shotgun metagenomic sequencing to examine the gut microbiota of patients with CRC (n = 66) and compared it to COVID control (CCs) (n = 27) and non-COVID control (NCs) (n = 22) groups. Three, 1, and 3 taxa were found enriched in CRCs, CCs, and NCs. Next, random forest models using 7 microbial biomarkers and differential clinical characteristics were constructed and achieved strong diagnostic potential in distinguishing CRC. Specifically, the most promising biomarker species for CRC were Streptococcus thermophilus, Enterococcus faecium, and Citrobacter portucalensis. Conversely, Enterobacteriaceae family and Fusicatenibacter genus are potentially protective against CRC in COVID patients. We further identified 4 species contributing to 20 MetaCyc pathways that were differentially abundant among groups, with S. thermophilus as the main coding species in CRCs. Our findings suggest that the alterations of gut microbiota compositional and functional profiles may influence the pathogenesis of CRC and that microbiota-based diagnosis and treatment could potentially benefit COVID patients in preventing and alleviating thrombosis-related clinical outcomes.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Gastrointestinal Microbiome , Microbiota , Humans , Cross-Sectional Studies , COVID-19/complications , Blood Coagulation Disorders/etiology
14.
Wiad Lek ; 76(3): 634-639, 2023.
Article in English | MEDLINE | ID: covidwho-2303896

ABSTRACT

OBJECTIVE: The aim: To investigate the features of coagulation homeostasis in patients with liver cirrhosis (LC) in COVID-19 infection. PATIENTS AND METHODS: Materials and methods: At the clinical base of the Department of Propaedeutics of Internal Medicine, 32 patients with LC infected with COVID-19 were examined - 1 Group of patients. The study also included 30 patients with LC who were not infected with COVID-19 (2 Group of patients). RESULTS: Results: The analysis of the obtained data indicates disorders of the hemostasis system in patients with LC without the COVID-19 infection (Group 2), as well as in patients with LC at the time of being infected with COVID-19. The violation of the protein synthesis function of the liver is manifested through a decrease in the level of fibrinogen in blood serum (up to 2.0±0.5 gr/l in patients of Group 1 at the time of admission for inpatient care) and up to 21.9±0.5 gr/l in patients of group ІІ - р<0.05. This was accompanied by an acceleration of prothrombin time, thrombin time and activated partial thromboplastic time in patients with LC, as well as an increase in the level of antithrombin III. The level of D-dimer was reduced both in patients of group II and in patients of group I at the time of being infected with COVID-19. CONCLUSION: Conclusions: Changes in coagulation homeostasis characteristic of hypocoagulation syndrome have been established in patients with LC. COVID-19 infection in patients with LC leads to hypercoagulation, especially in patients with complicated stage of LC (ascites, encephalopathy, hepatorenal syndrome).


Subject(s)
Blood Coagulation Disorders , COVID-19 , Humans , COVID-19/complications , Blood Coagulation , Hemostasis , Blood Coagulation Disorders/complications , Liver Cirrhosis/complications
15.
Ann Hematol ; 102(6): 1307-1322, 2023 Jun.
Article in English | MEDLINE | ID: covidwho-2303196

ABSTRACT

The coagulation, fibrinolytic, anticoagulation, and complement systems are in delicate balance with the vessel wall endothelium ensuring appropriate hemostasis. Coagulopathy in coronavirus disease 2019 (COVID-19) is not a simple disorder of one hemostatic component but a complicated process affecting most of the hemostasis system. COVID-19 disturbs the balance between the procoagulant systems and the regulatory mechanisms. Here, we investigate the effect of COVID-19 on key hemostatic components, including platelets, endothelial cells, coagulation factors, fibrinolytic system, anticoagulant protein system, and complement system, to improve our understanding of the pathophysiological processes underlying COVID-19 coagulopathy based on evidence.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Hemostatics , Humans , Hemostatics/pharmacology , Endothelial Cells/metabolism , Hemostasis , Blood Coagulation Factors/metabolism , Blood Platelets/metabolism , Endothelium, Vascular/metabolism , Fibrinolysis
16.
Anatol J Cardiol ; 27(5): 232-239, 2023 05.
Article in English | MEDLINE | ID: covidwho-2305229

ABSTRACT

Since severe acute respiratory syndrome coronavirus 2 led to a world pandemic, extensive research has been conducted to identify its characteristics and form an appropriate management plan. One recognized complication of COVID-19 is coagulation defects that can lead to thromboembolic events. We have reviewed the literature to summarize and present the latest research about the pathophysiology, clinical manifestations, anticoagulation use and appropriate dose in COVID-19 patients, as well as the effect of anticoagulation in outpatient and post-hospital settings. The pathophysiology of coagulation abnormalities in COVID-19 is not fully understood yet, but multiple mechanisms appear to be involved, such as a direct viral attack, hyperinflammation, increased immune response, blood stasis, and endothelial injury. Clinical manifestations are mainly venous thromboembolism (deep vein thrombosis and pulmonary embolism), arterial thromboembolism, ischemic stroke, central venous sinus thrombosis, and central retinal vein occlusion. Anticoagulation is widely used in hospitalized patients with COVID-19, unless it is contraindicated. Heparinoid is the main anticoagulant used. However, the appropriate dosage is still debated as research is trying to find a balance between benefits and risks. In outpatients, it appears that anticoagulation has no benefit in contrast to post-hospitalization use, where benefit could be observed in severely affected patients. We concluded that thromboprophylaxis should be used in treating hospitalized COVID-19 patients, but the dosage is still a matter of debate. More research needs to be done on outpatient and post-hospitalized patients to derive accurate conclusions.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Venous Thromboembolism , Humans , COVID-19/complications , Anticoagulants/therapeutic use , Outpatients , Venous Thromboembolism/drug therapy , Venous Thromboembolism/prevention & control , Venous Thromboembolism/complications , Hospitalization
17.
Int J Lab Hematol ; 44(5): 823-830, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-2295313

ABSTRACT

BACKGROUND: COVID-19 associated coagulopathy (CAC) can either be localized or systemic hypercoagulable state with increased risk of thromboembolism. This study looked into the usefulness of Thromboelastography (TEG) and the velocity curve (V-curve) derivative from TEG in diagnosing and differentiating different stages of CAC. MATERIALS AND METHODS: A prospective single cohort study of RT-PCR confirmed COVID-19 patients was carried out for 2 weeks. Severe COVID-19 patients in the adult critical care units with a TEG report were recruited for the study. Citrated kaolin TEG was performed on the day of admission before anticoagulation. TEG parameters included were R and K time, alpha angle, maximum amplitude, clotting index, lysis at 30 min. The first-degree velocity curve of TEG is plotted as V-curve which extrapolates thrombus generation potential. Parameters analyzed were the maximum rate of thrombus generation as well as thrombus generated (TG). RESULTS: The study included 43 patients with an average age of 58.34 (±15.35). TEG as well as V-curve of all the patients were hypercoagulable compared with age-matched reference range. We had 79.06% of patients in hypercoagulable stage. The mortality rate was 32.56% and 30.23% developed thrombotic incidents. Patients who succumbed to death had prolonged PT, aPTT, MA, Ly30, with a reduced TG (p < .05). The presence of fibrinolysis was associated with thromboembolism (OR = 6.76, CI = 1.48-25.82). Repeat TEG was done randomly in 11 patients and revealed a persistent hypercoagulable stage with increasing fibrinolysis activity. CONCLUSION: TEG is a useful tool in diagnosing and categorizing Coagulopathy associated with COVID-19.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thromboembolism , Thrombophilia , Adult , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/etiology , COVID-19/complications , COVID-19/diagnosis , COVID-19 Testing , Cohort Studies , Humans , Middle Aged , Prospective Studies , Thrombelastography , Thrombophilia/complications , Thrombophilia/etiology
18.
Intern Med ; 62(5): 717-722, 2023 Mar 01.
Article in English | MEDLINE | ID: covidwho-2287359

ABSTRACT

Objectives Coronavirus disease 2019 (COVID-19) reportedly causes thromboembolic complications due to coagulopathy with hypercoagulability and a hypofibrinolytic state. We evaluated the time-course of coagulopathy in patients with severe COVID-19 from admission to discharge from our intensive-care unit (ICU). Methods We conducted a retrospective study of adults with severe COVID-19 admitted to our ICU between January 20, 2021, and March 31, 2022. We obtained clinical information, laboratory data, and rotational thromboelastometry (ROTEM) parameters at admission and discharge. Results Fifteen patients were included. Fibrinogen and D-dimer values did not change significantly but were above the normal ranges at admission and discharge. Regarding ROTEM parameters, the maximum clot firmness in fibrinogen function (FIBTEM), a marker of hypercoagulability, did not change significantly but was above the normal range at admission and discharge [median (interquartile range), admission vs. discharge: 31 (25-34) mm vs. 31 (27-32) mm, p=0.589]. The maximum lysis at 60 minutes in the extrinsic coagulation pathway (EXTEM) and intrinsic coagulation pathway (INTEM), as markers of the fibrinolytic function, were both significantly lower at discharge than at admission [median (interquartile range), admission vs. discharge: EXTEM, 3 (2-4) vs. 1 (0-2), p=0.011; INTEM, 3 (1-6) vs. 1 (0-2), p=0.008]. Conclusion This study revealed a persistent hypercoagulable state at ICU discharge and a worse hypofibrinolytic state at discharge than at admission. These results may contribute to a better understanding of coagulopathies in the acute to subacute phases of severe COVID-19.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thrombophilia , Adult , Humans , Thrombelastography/methods , Retrospective Studies , Blood Coagulation Tests , Fibrinogen
19.
Int J Mol Sci ; 24(6)2023 Mar 14.
Article in English | MEDLINE | ID: covidwho-2277759

ABSTRACT

During the acute phase of COVID-19, many patients experience a complex coagulopathy characterized by a procoagulant pattern. The present study investigates the persistence of hemostatic changes in post-COVID patients at a long-term follow up, and the link with the persistence of physical and neuropsychological symptoms. We completed a prospective cohort study on 102 post-COVID patients. Standard coagulation and viscoelastic tests were performed, along with an assessment of persistent symptoms and recording of acute phase details. A procoagulant state was adjudicated in the presence of fibrinogen > 400 mg/dL, or D-dimer > 500 ng/mL, or platelet count > 450,000 cells/µL, or a maxim clot lysis at viscoelastic test < 2%. A procoagulant state was identified in 75% of the patients at 3 months follow up, 50% at 6 months, and 30% at 12-18 months. Factors associated with the persistence of a procoagulant state were age, severity of the acute phase, and persistence of symptoms. Patients with major physical symptoms carry a procoagulant state relative risk of 2.8 (95% confidence interval 1.17-6.7, p = 0.019). The association between persistent symptoms and a procoagulant state raises the hypothesis that an ongoing process of thrombi formation and/or persistent microthrombosis may be responsible for the main physical symptoms in long-COVID patients.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thrombosis , Humans , COVID-19/complications , Prospective Studies , Post-Acute COVID-19 Syndrome , Blood Coagulation
20.
Curr Med Imaging ; 19(14): 1616-1627, 2023.
Article in English | MEDLINE | ID: covidwho-2268327

ABSTRACT

Coronavirus (COVID-19) is a global pandemic with over 600 million cases identified. In addition to extensive pulmonary complications of COVID-19, one feature unique to many patients with severe COVID-19 infections is coagulopathy with a rising prevalence of multi-systemic thromboembolic manifestations. Global data suggests a relationship between coagulopathy and mortality. In this review, we highlight multiple COVID-19 thromboembolic complications with emphasis on pathophysiology, clinical management, and radiological manifestations.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Humans , SARS-CoV-2 , Blood Coagulation Disorders/epidemiology , Blood Coagulation Disorders/etiology
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