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1.
Shock ; 57(1): 1-6, 2022 01 01.
Article in English | MEDLINE | ID: covidwho-2191212

ABSTRACT

BACKGROUND: The pathomechanisms of hypoxemia and treatment strategies for type H and type L acute respiratory distress syndrome (ARDS) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced coronavirus disease 2019 (COVID-19) have not been elucidated. MAIN TEXT: SARS-CoV-2 mainly targets the lungs and blood, leading to ARDS, and systemic thrombosis or bleeding. Angiotensin II-induced coagulopathy, SARS-CoV-2-induced hyperfibrin(ogen)olysis, and pulmonary and/or disseminated intravascular coagulation due to immunothrombosis contribute to COVID-19-associated coagulopathy. Type H ARDS is associated with hypoxemia due to diffuse alveolar damage-induced high right-to-left shunts. Immunothrombosis occurs at the site of infection due to innate immune inflammatory and coagulofibrinolytic responses to SARS-CoV-2, resulting in microvascular occlusion with hypoperfusion of the lungs. Lung immunothrombosis in type L ARDS results from neutrophil extracellular traps containing platelets and fibrin in the lung microvasculature, leading to hypoxemia due to impaired blood flow and a high ventilation/perfusion (VA/Q) ratio. COVID-19-associated ARDS is more vascular centric than the other types of ARDS. D-dimer levels have been monitored for the progression of microvascular thrombosis in COVID-19 patients. Early anticoagulation therapy in critical patients with high D-dimer levels may improve prognosis, including the prevention and/or alleviation of ARDS. CONCLUSIONS: Right-to-left shunts and high VA/Q ratios caused by lung microvascular thrombosis contribute to hypoxemia in type H and L ARDS, respectively. D-dimer monitoring-based anticoagulation therapy may prevent the progression to and/or worsening of ARDS in COVID-19 patients.


Subject(s)
COVID-19/physiopathology , Hemostasis/physiology , Hypoxia/physiopathology , Respiratory Distress Syndrome/physiopathology , Thrombosis/physiopathology , Anticoagulants/therapeutic use , Biomarkers/blood , Blood Platelets/metabolism , COVID-19/drug therapy , Extracellular Traps/metabolism , Fibrin/metabolism , Fibrin Fibrinogen Degradation Products/analysis , Fibrinolysis , Humans , Lung/blood supply , Microvessels/physiopathology , Phenotype , Respiratory Distress Syndrome/drug therapy , SARS-CoV-2 , Thrombosis/drug therapy
2.
QJM ; 114(11): 810-811, 2022 Jan 05.
Article in English | MEDLINE | ID: covidwho-2190228
5.
J Ayub Med Coll Abbottabad ; 34(3): 557-562, 2022.
Article in English | MEDLINE | ID: covidwho-2207192

ABSTRACT

BACKGROUND: Coronavirus disease 19 (COVID-19) is a viral disease caused by SARS-CoV-2. There is an increased incidence of a thromboembolic phenomenon in patients with COVID-19 infection. Pulmonary embolism is the most common thrombotic presentation in COVID-19 patients. Extra-pulmonary thrombosis is an unusual thrombotic complication of COVID-19 disease. METHODS: This study was conducted at The Aga Khan University Hospital from June-July'2021. Patients clinical and laboratory findings, treatment, and outcomes were recorded. RESULTS: We report three cases with the diagnosis of COVID-19 pneumonia associated with extra-pulmonary thrombosis from June to July 2021. The mean age of the patients were 66.3 and two of them (66.6%) were male. The diagnosis of COVID-19 was confirmed by real-time reverse transcriptase-polymerase chain reaction analysis in all the three patients. Extra-pulmonary thrombosis was identified in the celiac artery and splenic veins in case 1, left common iliac artery in case 2, and left ventricular apical thrombus in case 3. All the patients were treated with anticoagulation. In total, two patients were discharged home after total recovery, while the third patient died. CONCLUSIONS: The take-home message is that COVID-19 infection is a pro-thrombotic condition that can provoke arterial and venous thrombosis. Extra-pulmonary thrombosis is increasingly identified with COVID-19 infection. It is important to remember that the patient might have no potential risk factor for thromboses, as COVID-19 infection per se is a risk to induce thrombosis.


Subject(s)
COVID-19 , Thrombosis , Venous Thrombosis , Humans , Male , Female , COVID-19/complications , SARS-CoV-2 , Anticoagulants/therapeutic use , Venous Thrombosis/etiology , Thrombosis/etiology
6.
Pol Arch Intern Med ; 132(11)2022 Nov 25.
Article in English | MEDLINE | ID: covidwho-2204737
7.
Indian J Med Res ; 155(1): 178-188, 2022 01.
Article in English | MEDLINE | ID: covidwho-2201748

ABSTRACT

Background & objectives: Autopsy study has been considered the gold standard method for studying the effects of any disease on the body. Since COVID-19 is a novel disease, autopsy is crucial to understand its pathophysiology. This study was conducted to analyze the microscopic and macroscopic findings of various organs in COVID-19 and to associate those findings with clinical observations and laboratory findings. Methods: Conventional invasive autopsies were performed on 33 patients with COVID-19 from September 7, 2020 to December 23, 2020. All the organs were removed by routine dissection techniques and preserved in 10 per cent formalin. The tissues were processed and stained according to standard practices using haematoxylin-eosin (H & E) and periodic acid-schiff (PAS) stain. Results: The study included 28 males and 5 females with a median age of 61 yr (range 30-90 yr). Massive pulmonary oedema and thrombi in the lungs were the characteristic features macroscopically. On microscopic examination, diffuse alveolar damage in the exudative/proliferative phase was found in 29 (87.88%) cases. Among the other notable microscopic findings were bronchopneumonia and lung abscesses due to secondary bacterial infection (n=17, 51.52%), acute tubular injury (n=21, 63.64%) and thrombi in the lungs, heart, and kidneys. Interpretation & conclusions: COVID-19 primarily affected the respiratory and the renal systems in the vast majority of severely affected patients in our study. We also found signs of hypercoagulability, as evidenced by widespread thrombi in multiple organs, along with a raised d-dimer level and a hyperinflammatory state manifested by elevated inflammatory markers. Our autopsy findings and altered laboratory investigations support the role of immune-mediated cellular injury along with direct virus-mediated cellular damage.


Subject(s)
COVID-19 , Thrombosis , Autopsy , Female , Humans , India/epidemiology , Lung/pathology , Male , SARS-CoV-2 , Thrombosis/pathology
8.
Dtsch Arztebl Int ; 119(25): 429-435, 2022 06 24.
Article in English | MEDLINE | ID: covidwho-2198562

ABSTRACT

BACKGROUND: The COVID-19 pandemic is the third worldwide coronavirus-associated disease outbreak in the past 20 years. Lung involvement, with acute respiratory distress syndrome (ARDS) in severe cases, is the main clinical feature of this disease; the cardiovascular system, the central nervous system, and the gastrointestinal tract can also be affected. The pathophysiology of both pulmonary and extrapulmonary organ damage was almost completely unknown when the pandemic began. METHODS: This review is based on pertinent publications retrieved by a selective search concerning the structural changes and pathophysiology of COVID-19, with a focus on imaging techniques. RESULTS: Immunohistochemical, electron-microscopic and molecular pathological analyses of tissues obtained by autopsy have improved our understanding of COVID-19 pathophysiology, including molecular regulatory mechanisms. Intussusceptive angiogenesis (IA) has been found to be a prominent pattern of damage in the affected organs of COVID-19 patients. In IA, an existing vessel changes by invagination of the endothelium and formation of an intraluminal septum, ultimately giving rise to two new lumina. This alters hemodynamics within the vessel, leading to a loss of laminar flow and its replacement by turbulent, inhomogeneous flow. IA, which arises because of ischemia due to thrombosis, is itself a risk factor for the generation of further microthrombi; these have been detected in the lungs, heart, liver, kidneys, brain, and placenta of COVID-19 patients. CONCLUSION: Studies of autopsy material from various tissues of COVID-19 patients have revealed ultrastructural evidence of altered microvascularity, IA, and multifocal thrombi. These changes may contribute to the pathophysiology of post-acute interstitial fibrotic organ changes as well as to the clinical picture of long COVID.


Subject(s)
COVID-19 , Thrombosis , COVID-19/complications , Humans , Lung/diagnostic imaging , Pandemics , SARS-CoV-2
9.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.01.13.23284524

ABSTRACT

COVID-19 syndrome does not occur in all who are infected with SARS-CoV-2, and symptoms vary. The anti-SARS CoV-2 Spike immune responses is confounded by the Spike proteins ability to bind Ig{gamma}3 heavy chains. This appears to be via sialic acid glycans found on the O-Linked glycosylation moieties of this heavy chain extended neck domain. Furthermore glycosylation of light chains, particularly Kappa ({kappa}), is an associated feature of antibodies binding to SARS-CoV-2 antigens nucleocapsid and Spike protein. COVID-19 recovered patients had increased IgG1 and IgM levels and un-glycosylated {kappa} {lambda} light chains; possibly In order to counter this immune system subjugation of IgG3. These molecular finding, together with our previous finding that Spike protein binds glycated human serum albumin (HSA), may explain the micro-vascular inflammatory clots that are a causative feature of COVID-19 acute respiratory syndrome (ARDS). The postulated molecular sequelae are that SARS-CoV-2 virion, entering the blood circulation, being coated with IgG3 and glycated HSA forms a colloid and deposits into micro-focal clots which are also inflammatory. It is not that all IgG3 and albumin is being bound by the virus; this depends on the affinity the SARS-CoV2 virion has for binding an individual IgG3 and albumin due to glycosylation and glycation status. The degree of glycosylation and terminal sialyation of an individuals antibodies is both a genetic and age-maturity dependant feature of the immune system. The degree of HSA glycation is also age related feature particularly related to type 2 diabetes. Thereby establishing the molecular basis of the association of severe COVID-19 disease syndrome and deaths with diabetes, metabolic disorders, and old age. Furthermore, already having cardiovascular disease, with hardened arteries, SARS-CoV2-glycated HSA-IgG3 deposition is going to exacerbate an already compromised circulatory physiology. The binding of IgG3 might also drives a shift in the immune repertoire response to SAR-CoV-2 anti-spike antibodies of increased IgG1 and prolonged IgM levels. This may be associated with Long Covid. In summary, SARS-CoV-2 Spike protein binding of IgG3, via sialic acid glycan residues, along with increased glycosylated {kappa}-light chains and glycated-HSA may form a focal amyloid-like precipitate within blood vessels which in turn leads to the inflammatory micro-thrombosis characteristic of COVID-19 immuno-pathology.


Subject(s)
Cardiovascular Diseases , COVID-19 , Congenital Disorders of Glycosylation , Death , Thrombosis , Severe Acute Respiratory Syndrome , Metabolic Diseases , Diabetes Mellitus
10.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2473292.v1

ABSTRACT

Background: Due to the high risk of COVID-19 patients to the formation of thrombosis in the circulating blood, atherosclerosis, and myocardial infarction, it was necessary to study the lipidomic of the erythrocytes. The aim of this work was to analyze the pathogenic oxysterols and acylcarnitines in the erythrocyte’s homogenate of COVID-19 patients and to estimate the case severity from the level of oxysterols. Methods: A linear ion trap mass spectrometry coupled with high-performance liquid chromatography was used to investigate the extract of erythrocytes homogenate. The toxic biomarkers that primarily induce the generation of dead red blood cells, were characterized, and quantified in the erythrocytes of COVID-19 patients and matched with healthy volunteers. Results: A total of 30 patients and 30 healthy volunteers were enrolled. The concentration of five oxysterols and six acylcarnitines in the erythrocyte’s homogenate of COVID-19 patients was significantly upregulated matching with healthy subjects at p <0.05. The average total concentration of oxysterols was 23.36 ± 13.47 μg/mL in the erythrocytes of COVID-19 patients, while samples of healthy volunteers showed a total concentration of 4.92 ± 1.61 μg/mL. The average concentration level of 7-ketocholesterol and 4-cholestenone in the COVID-19 patients was higher by five and ten-fold compared to the healthy subjects. Also, the average concentration of acylcarnitines in the erythrocyte's homogenate of COVID-19 patients was high by 2-to-4-fold in comparison with the healthy volunteers. Conclusions: The abnormally high levels of oxysterols and acylcarnitines found in the erythrocytes of COVID-19 patients were associated with the severity of the case's complications and substantial risk of thrombosis. The concentration of oxysterols in the erythrocyte homogenate could be useful as a diagnostic biomarker to stand on the COVID-19 case severity.


Subject(s)
COVID-19 , Atherosclerosis , Thrombosis , Myocardial Infarction
11.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2441808.v1

ABSTRACT

Background Thrombosis after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination is a serious complication for patients with a thrombophilic predisposition. Factors that predict the risk of post-vaccination thrombosis should be explored. We report a case in which a patient with pediatric antiphospholipid syndrome (APS) developed deep vein thrombosis (DVT) six months after receiving a second dose of the BNT162b2 vaccine.Case presentation: A 17-year-old girl with no family history of thrombophilia developed DVT at six years of age. The thrombus was found in the right common iliac vein and the inferior vena cava, with concomitant left pulmonary infarction. After treatment with warfarin, the pulmonary infarction was resolved, but the thrombus became organized and persisted for the next 11 years. The patient was treated with anticoagulants for six years after DVT onset, with subsequent cessation of treatment for five years without thrombosis recurrence. She received the BNT162b2 vaccine at 17 years of age, one week before a routine outpatient visit. Elevation of platelet factor 4 level was detected 14 days after the first vaccination and remained for five months after that, but without thrombotic symptoms. A second dose of the BNT162b2 vaccine was administered; six months later, the DVT in the right common iliac vein recurred and was treated with a direct oral anticoagulant.Conclusions The BNT162b2 vaccine exacerbated her antiphospholipid antibody syndrome by activating the coagulation system, thereby exacerbating her thrombosis. Platelet factor 4 may be a useful indicator of the coagulation system. The persistence of high platelet factor 4 levels after vaccination suggests that the vaccine caused DVT by exacerbating the patient’s APS. After vaccination of patients with a predisposition to thrombosis, coagulation status and platelet activation markers should be monitored to prevent the development of DVT.


Subject(s)
Thrombophilia , Coronavirus Infections , Venous Thrombosis , Pulmonary Infarction , Blood Coagulation Disorders, Inherited , Thrombosis , Antiphospholipid Syndrome , Nystagmus, Pathologic
12.
preprints.org; 2022.
Preprint in English | PREPRINT-PREPRINTS.ORG | ID: ppzbmed-10.20944.preprints202209.0430.v2

ABSTRACT

Objectives Assess rates of adverse events (AE) after COVID-19 vaccines experienced by women of reproductive age, focusing on pregnancy and menstruation, using data collected by the US Centers for Disease Control and Prevention (CDC) Vaccine Adverse Events Reporting System (VAERS) database. Design Population-based retrospective cohort study. Setting US and global entries in US Centers for Disease Control and Prevention (CDC) Vaccine Adverse Events Reporting System (VAERS). Participants CDC VAERS entries from January 1, 1998 to June 30, 2022. Interventions None. Main Outcome Measures A proportional reporting ratio analysis is performed using data in the VAERS system comparing adverse events (AE) reported post-COVID-19 vaccines with that of post-Influenza vaccines. Results COVID-19 vaccines, when compared to the Influenza vaccines, are associated with a significant increase in AE with all proportional reporting ratios of > 2.0: menstrual abnormalities, miscarriage, fetal chromosomal abnormalities, fetal malformation, fetal cystic hygroma, fetal cardiac disorders, fetal arrhythmias, fetal cardiac arrest, fetal vascular malperfusion, fetal growth abnormalities, fetal abnormal surveillance, fetal placental thrombosis, low amniotic fluid, preeclampsia, premature delivery, preterm premature rupture of membrane, fetal death/stillbirth, and premature baby death (all p values were much smaller than 0.05). When normalized by time-available, doses-given, or persons-received, all COVID-19 vaccine AE far exceed the safety signal on all recognized thresholds. Conclusions Pregnancy complications and menstrual abnormalities are significantly more frequent following COVID-19 vaccinations than Influenza vaccinations. A worldwide moratorium on the use of COVID-19 vaccines in pregnancy is advised until randomized prospective trials document safety in pregnancy and long-term follow-up in offspring.


Subject(s)
Heart Arrest , Heart Diseases , COVID-19 , Stillbirth , Death , Thrombosis , Fetal Growth Retardation , Fetal Diseases , Arrhythmias, Cardiac , Menstruation Disturbances
13.
Int J Mol Sci ; 23(14)2022 Jul 16.
Article in English | MEDLINE | ID: covidwho-2163420

ABSTRACT

Platelet-derived extracellular vesicles (PEVs) play important roles in hemostasis and thrombosis. There are three major types of PEVs described based on their size and characteristics, but newer types may continue to emerge owing to the ongoing improvement in the methodologies and terms used to define various types of EVs. As the literature on EVs is growing, there are continuing attempts to standardize protocols for EV isolation and reach consensus in the field. This review provides information on mechanisms of PEV production, characteristics, cellular interaction, and their pathological role, especially in autoimmune and infectious diseases. We also highlight the mechanisms through which PEVs can activate parent cells in a feedback loop.


Subject(s)
Extracellular Vesicles , Thrombosis , Blood Platelets , Hemostasis , Humans
14.
Front Immunol ; 13: 941742, 2022.
Article in English | MEDLINE | ID: covidwho-2154719

ABSTRACT

Background: Thromboinflammation may influence disease outcome in COVID-19. We aimed to evaluate complement and endothelial cell activation in patients with confirmed COVID-19 compared to controls with clinically suspected but excluded SARS-CoV-2 infection. Methods: In a prospective, observational, single-center study, patients presenting with clinically suspected COVID-19 were recruited in the emergency department. Blood samples on presentation were obtained for analysis of C5a, sC5b-9, E-selectin, Galectin-3, ICAM-1 and VCAM-1. Results: 153 cases and 166 controls (suffering mainly from non-SARS-CoV-2 respiratory viral infections, non-infectious inflammatory conditions and bacterial pneumonia) were included. Hospital admission occurred in 62% and 45% of cases and controls, respectively. C5a and VCAM-1 concentrations were significantly elevated and E-selectin concentrations decreased in COVID-19 out- and inpatients compared to the respective controls. However, relative differences in outpatients vs. inpatients in most biomarkers were comparable between cases and controls. Elevated concentrations of C5a, Galectin-3, ICAM-1 and VCAM-1 on presentation were associated with the composite outcome of ICU- admission or 30-day mortality in COVID-19 and controls, yet more pronounced in COVID-19. C5a and sC5b-9 concentrations were significantly higher in COVID-19 males vs. females, which was not observed in the control group. Conclusions: Our data indicate an activation of the complement cascade and endothelium in COVID-19 beyond a nonspecific inflammatory trigger as observed in controls (i.e., "over"-activation).


Subject(s)
COVID-19 , Thrombosis , Biomarkers , Complement System Proteins , E-Selectin , Endothelial Cells , Female , Galectin 3 , Humans , Inflammation , Intercellular Adhesion Molecule-1 , Male , Prospective Studies , SARS-CoV-2 , Vascular Cell Adhesion Molecule-1
15.
Thromb Res ; 220: 100-106, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2150681

ABSTRACT

INTRODUCTION: COVID-19 disease, which has recently become an important cause of mortality and morbidity all over the world, is remarkably associated with thrombotic complications. Although many factors are responsible for these increased thrombotic complications in COVID-19 disease, its relationship with a marker that increases the risk of thrombosis such as Signal peptide-CUB-EGF domain-containing protein 1 (SCUBE1) has not yet been clarified. This is the first study to examine the potential diagnostic and prognostic value of SCUBE1 levels in patients with COVID-19. In this study, we aimed to clarify the relationship between the increased risk of thrombosis and SCUBE1 in the course of COVID-19 disease. MATERIALS AND METHODS: 553 patients with COVID-19 and 553 healthy controls were compared in terms of SCUBE1 levels. Additionally, patients with COVID-19 were divided into two groups according to their SCUBE1 levels and compared in terms of severity of disease, thrombotic complications and in-hospital mortality. RESULTS: SCUBE1 levels were significantly higher in patients with COVID-19 compared to the control group (p < 0.001). Plasma SCUBE1 levels were significantly higher in patients with severe disease and thrombotic complications, those with mild to moderate disease, and those without thrombotic complications (p < 0.001, for both). In addition, SCUBE1 was found to be an independent predictor of in-hospital mortality (p < 0.001). CONCLUSIONS: SCUBE1 may be one of the major determinants of thrombotic complications, which is an increased cause of mortality and morbidity in COVID-19 patients so inhibition of this peptide may be among the therapeutic targets in patients with COVID-19.


Subject(s)
COVID-19 , Thrombosis , Humans , Hospital Mortality , COVID-19/complications , Thrombosis/etiology , Plasma , Severity of Illness Index , Calcium-Binding Proteins
16.
biorxiv; 2022.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2022.12.20.521247

ABSTRACT

Previously, we and others have shown that SARS-CoV-2 spike-specific IgG antibodies play a major role in disease severity in COVID-19 by triggering macrophage hyperactivation, disrupting endothelial barrier integrity, and inducing thrombus formation. This hyperinflammation is dependent on high levels of anti-spike IgG with aberrant Fc tail glycosylation, leading to Fc{gamma} receptor hyperactivation. For development of immune-regulatory therapeutics, drug specificity is crucial to counteract excessive inflammation while simultaneously minimizing inhibition of antiviral immunity. We here developed an in vitro activation assay to screen for small molecule drugs that specifically counteract antibody-induced pathology. We identified that anti-spike induced inflammation is specifically blocked by small molecule inhibitors against SYK and PI3K. We identified SYK inhibitor entospletinib as the most promising candidate drug, which also counteracted anti-spike-induced endothelial dysfunction and thrombus formation. Moreover, entospletinib blocked inflammation by different SARS-CoV-2 variants of concern. Combined, these data identify entospletinib as a promising treatment for severe COVID-19.


Subject(s)
COVID-19 , Thrombosis , Inflammation
17.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2402533.v1

ABSTRACT

Introduction: COVID - 19 viruses are responsible for endemic respiratory tract infection in the wide world. Following vaccination with the nCoV-19 vaccine, however, cases of thrombosis and thrombocytopenia, to detect these cases D-dimer test should be done. Aims: this study aims to detect the relation between D- dimer and vaccination of COVID19 Methods: This study that done by vaccinated patients from the special labs in Amman the capital of Jordan between January 2022 to October 2022 using PCR tests for detecting the virus. XL-FDP level estimated by using Atlas D-Dimer Latex Kit (Atlas Medical, Cowley Rd, Cambridge) Following manufacturing instruction. Discussion/Conclusion. We conclude that the vaccinated COVID-19 patients suffer from elevated baseline D-dimer. thrombosis can occur in different organs, leading to organ failure in serious COVID-19 cases.


Subject(s)
Respiratory Tract Infections , COVID-19 , Thrombocytopenia , Thrombosis
18.
Clin Hemorheol Microcirc ; 82(2): 149-155, 2022.
Article in English | MEDLINE | ID: covidwho-2141600

ABSTRACT

BACKGROUND: Elevated estimated blood viscosity (EBV), derived from hematocrit and globulins, is associated with thrombotic complications, organ failure, and higher mortality in COVID-19 patients. Although informative, EBV does not account for cellular interactions or fibrinogen. OBJECTIVE: Investigate whether patients with acute and recent COVID-19 have altered whole blood viscosity (WBV) when measured at both high and low shear rates using in vitro blood samples from patients. METHODS: Cross-sectional study of 58 patients: 15 in the intensive care unit with acute COVID-19, 32 convalescent (9 < 8weeks [W] from acute infection, 23 > 8 W), and 11 controls without COVID-19. WBV was measured at high (300 s-1) and low (5 s-1) shear rates (HSR, LSR) using a scanning capillary viscometer.RESULTSAcute and convalescent patients < 8 W had mean WBV at LSR (16.0 centipoise [cP] and 15.1 cP) and HSR (5.1 cP and 4.7 cP). Mean WBV of convalescent > 8 W and control patients were 12.3 cP and 13.0 cP at LSR, and 4.1 cP and 4.2 cP at HSR. Acute and < 8 W patients had significantly higher WBV at both HSR and LSR compared to patients > 8 W (all p≤0.01). No significant differences in WBV were observed between acute and < 8 W patients, or between patients > 8 W and controls. CONCLUSIONS: Hyperviscosity provides a possible explanation for thrombotic risk in acute and convalescent (< 8 W) patients. These findings have important implications for thromboprophylaxis.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Venous Thromboembolism , Humans , Cross-Sectional Studies , Anticoagulants , Venous Thromboembolism/complications , Blood Viscosity , Thrombosis/etiology
19.
Curr Med Imaging ; 18(13): 1439-1442, 2022.
Article in English | MEDLINE | ID: covidwho-2141254

ABSTRACT

INTRODUCTION: Paragangliomas are tumors of neuroendocrine origin, may appear in different localizations, and are related to the autonomic nervous system. Paragangliomas are generally asymptomatic and may rarely appear with adrenergic symptoms, and clinical findings depend on the catecholamines they secrete. Extra-adrenal paragangliomas are mostly benign, like all paragangliomas. Malignancy criteria consist of local recurrence, metastasis after total resection, and presence of distant metastasis during primary diagnosis. CASE PRESENTATION: This report presents the case of a 31-year-old man with jugular paraganglioma, multiple skeletal metastases, and a long-segment tumor thrombus. Imaging procedures showed a continuous tumor thrombus extending from the posterior fossa to the right atrium and metastases in C2, T1, T6, T8, L5, and right humerus. Histopathological assessment of the metastasis in C2 identified malignant paraganglioma. Curative surgery was not an option for this patient, hence combined chemotherapy was given. CONCLUSION: In cases of malignant paraganglioma with multiple distant metastases, chemotherapy and radiotherapy are feasible treatment methods.


Subject(s)
Paraganglioma , Thrombosis , Male , Humans , Adult , Paraganglioma/diagnostic imaging , Paraganglioma/surgery , Heart Atria/diagnostic imaging , Heart Atria/pathology , Thrombosis/diagnostic imaging , Catecholamines , Adrenergic Agents
20.
Immunol Rev ; 312(1): 61-75, 2022 11.
Article in English | MEDLINE | ID: covidwho-2136897

ABSTRACT

Tissue factor (TF) is a procoagulant protein released from activated host cells, such as monocytes, and tumor cells on extracellular vesicles (EVs). TF + EVs are observed in the circulation of patients with various types of diseases. In this review, we will summarize the association between TF + EVs and activation of coagulation and survival in different types of diseases, including cancer, sepsis, and infections with different viruses, such as human immunodeficiency virus (HIV), influenza A virus (IAV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We will also discuss the source of TF + EVs in various diseases. EVTF activity is associated with thrombosis in pancreatic cancer patients and coronavirus disease 2019 patients (COVID-19) and with disseminated intravascular coagulation in cancer patients. EVTF activity is also associated with worse survival in patients with cancer and COVID-19. Monocytes are the major sources of TF + EVs in sepsis, and viral infections, such as HIV, Ebola virus, and SARS-CoV-2. In contrast, alveolar epithelial cells are the major source of TF + EVs in bronchoalveolar lavage fluid in COVID-19 and influenza A patients. These studies indicate that EVTF activity could be used as a biomarker to identify patients that have an increased risk of coagulopathy and mortality.


Subject(s)
COVID-19 , Extracellular Vesicles , Pancreatic Neoplasms , Sepsis , Thrombosis , Biomarkers/metabolism , Extracellular Vesicles/metabolism , Extracellular Vesicles/pathology , Humans , Pancreatic Neoplasms/complications , Pancreatic Neoplasms/metabolism , Pancreatic Neoplasms/pathology , SARS-CoV-2 , Thromboplastin/metabolism
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