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2.
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
3.
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
4.
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
5.
Thromb Res ; 222: 102-108, 2023 02.
Article in English | MEDLINE | ID: covidwho-2326956

ABSTRACT

BACKGROUND: An association between thrombotic events and SARS-CoV-2 infection and the adenovirus-based COVID-19 vaccines has been established, leading to concern over the risk of thrombosis after BNT162b2 COVID-19 vaccination. OBJECTIVES: To evaluate the risk of arterial thrombosis, cerebral venous thrombosis (CVT), splanchnic thrombosis, and venous thromboembolism (VTE) following BNT162b2 vaccination in New Zealand. METHODS: This was a self-controlled case series using national hospitalisation and immunisation records to calculate incidence rate ratios (IRR). The study population included individuals aged ≥12 years, unvaccinated, or vaccinated with BNT162b2, who were hospitalised with one of the thrombotic events of interest from 19 February 2021 through 19 February 2022. The risk period was 0-21 days after receiving a primary or booster dose of BNT162b2. RESULTS: 6039 individuals were hospitalised with one of the thrombotic events examined, including 5127 with VTE, 605 with arterial thrombosis, 272 with splanchnic thrombosis, and 35 with CVT. The proportion of individuals vaccinated with at least one dose of BNT162b2 ranged from 82.7 % to 91.4 %. Compared with the control unexposed period, the IRR (95 % CI) of VTE, arterial thrombosis, splanchnic thrombosis, and CVT were 0.87 (0.76-1.00), 0.73 (0.56-0.95), 0.71 (0.43-1.16), and 0.87 (0.31-2.50) in the 21 days after BNT162b2 vaccination, respectively. There was no statistically significant increased risk of thrombosis following BNT162b2 in different ethnic groups in New Zealand. CONCLUSION: The BNT162b2 vaccine was not found to be associated with thrombosis in the general population or different ethnic groups in New Zealand, providing reassurance for the safety of the BNT162b2 vaccine.


Subject(s)
COVID-19 Vaccines , COVID-19 , Intracranial Thrombosis , Thrombosis , Venous Thromboembolism , Humans , BNT162 Vaccine , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , New Zealand/epidemiology , Research Design , RNA, Messenger , SARS-CoV-2 , Thrombosis/etiology , Venous Thromboembolism/epidemiology , Venous Thromboembolism/etiology
6.
Methods Mol Biol ; 2663: 463-477, 2023.
Article in English | MEDLINE | ID: covidwho-2324173

ABSTRACT

The serotonin release assay (SRA) has been the gold-standard assay for detection of heparin-dependent platelet-activating antibodies and integral for the diagnosis for heparin-induced thrombotic thrombocytopenia (HIT). In 2021, a thrombotic thrombocytopenic syndrome was reported after adenoviral vector COVID-19 vaccination. This vaccine-induced thrombotic thrombocytopenic syndrome (VITT) proved to be a severe immune platelet activation syndrome manifested by unusual thrombosis, thrombocytopenia, very elevated plasma D-dimer, and a high mortality even with aggressive therapy (anticoagulation and plasma exchange). While the platelet-activating antibodies in both HIT and VITT are directed toward platelet factor 4 (PF4), important differences have been found. These differences have required modifications to the SRA to improve detection of functional VITT antibodies. Functional platelet activation assays remain essential in the diagnostic workup of HIT and VITT. Here we detail the application of SRA for the assessment of HIT and VITT antibodies.


Subject(s)
COVID-19 , Thrombocytopenia , Thrombosis , Humans , Heparin/adverse effects , Serotonin , Anticoagulants/adverse effects , COVID-19 Vaccines/adverse effects , Thrombocytopenia/chemically induced , Thrombocytopenia/diagnosis , Antibodies , Thrombosis/diagnosis , Thrombosis/etiology , Platelet Factor 4/adverse effects
7.
J Thromb Thrombolysis ; 56(2): 241-252, 2023 Aug.
Article in English | MEDLINE | ID: covidwho-2325921

ABSTRACT

Heparin-induced thrombocytopenia (HIT) occurs in approximately 3% of patients receiving heparinoids. About 30-75% of patients with type 2 of HIT develop thrombosis as a result of platelet activation. The most important clinical symptom is thrombocytopenia. Patients with severe COVID-19 are among those receiving heparinoids. This meta-analysis performed to picture the current knowledge and results of published studies in this field. Three search engines were searched and 575 papers were found. After evaluation, 37 articles were finally selected of which 13 studies were quantitatively analyzed. The pooled frequency rate of suspected cases with HIT in 13 studies with 11,241 patients was 1.7%. The frequency of HIT was 8.2% in the extracorporeal membrane oxygenation subgroup with 268 patients and 0.8% in the hospitalization subgroup with 10,887 patients. The coincidence of these two conditions may increase the risk of thrombosis. Of the 37 patients with COVID-19 and confirmed HIT, 30 patients (81%) were treated in the intensive care unit or had severe COVID-19. The most commonly used anticoagulants were UFH in 22 cases (59.4%). The median platelet count before treatment was 237 (176-290) x 103/µl and the median nadir platelet count was 52 (31-90.5) x 103/µl.


Subject(s)
COVID-19 , Heparinoids , Thrombocytopenia , Thrombosis , Humans , Heparin/adverse effects , Heparinoids/adverse effects , COVID-19/complications , Thrombocytopenia/diagnosis , Anticoagulants/adverse effects , Thrombosis/etiology
8.
Int J Mol Sci ; 24(9)2023 Apr 28.
Article in English | MEDLINE | ID: covidwho-2320242

ABSTRACT

Coronavirus disease 2019 (COVID-19) has spread, with thrombotic complications being increasingly frequently reported. Although thrombosis is frequently complicated in septic patients, there are some differences in the thrombosis noted with COVID-19 and that noted with bacterial infections. The incidence (6-26%) of thrombosis varied among reports in patients with COVID-19; the incidences of venous thromboembolism and acute arterial thrombosis were 4.8-21.0% and 0.7-3.7%, respectively. Although disseminated intravascular coagulation (DIC) is frequently associated with bacterial infections, a few cases of DIC have been reported in association with COVID-19. Fibrin-related markers, such as D-dimer levels, are extremely high in bacterial infections, whereas soluble C-type lectin-like receptor 2 (sCLEC-2) levels are high in COVID-19, suggesting that hypercoagulable and hyperfibrinolytic states are predominant in bacterial infections, whereas hypercoagulable and hypofibrinolytic states with platelet activation are predominant in COVID-19. Marked platelet activation, hypercoagulability and hypofibrinolytic states may cause thrombosis in patients with COVID-19.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Humans , COVID-19/complications , SARS-CoV-2 , Thrombosis/etiology , Thrombophilia/complications , Platelet Activation
9.
Front Immunol ; 13: 977443, 2022.
Article in English | MEDLINE | ID: covidwho-2316329

ABSTRACT

Thrombosis is a major clinical complication of COVID-19 infection. COVID-19 patients show changes in coagulation factors that indicate an important role for the coagulation system in the pathogenesis of COVID-19. However, the multifactorial nature of thrombosis complicates the prediction of thrombotic events based on a single hemostatic variable. We developed and validated a neural net for the prediction of COVID-19-related thrombosis. The neural net was developed based on the hemostatic and general (laboratory) variables of 149 confirmed COVID-19 patients from two cohorts: at the time of hospital admission (cohort 1 including 133 patients) and at ICU admission (cohort 2 including 16 patients). Twenty-six patients suffered from thrombosis during their hospital stay: 19 patients in cohort 1 and 7 patients in cohort 2. The neural net predicts COVID-19 related thrombosis based on C-reactive protein (relative importance 14%), sex (10%), thrombin generation (TG) time-to-tail (10%), α2-Macroglobulin (9%), TG curve width (9%), thrombin-α2-Macroglobulin complexes (9%), plasmin generation lag time (8%), serum IgM (8%), TG lag time (7%), TG time-to-peak (7%), thrombin-antithrombin complexes (5%), and age (5%). This neural net can predict COVID-19-thrombosis at the time of hospital admission with a positive predictive value of 98%-100%.


Subject(s)
COVID-19 , Hemostatics , Thrombosis , Antithrombins , C-Reactive Protein , COVID-19/complications , Fibrinolysin , Humans , Immunoglobulin M , Neural Networks, Computer , Predictive Value of Tests , Thrombin/metabolism , Thrombosis/etiology
10.
J Am Podiatr Med Assoc ; 113(2)2023.
Article in English | MEDLINE | ID: covidwho-2313005

ABSTRACT

Plantar thrombophlebitis is a rare abnormality with few cases reported in the literature. Coexistence with severe acute respiratory syndrome coronavirus 2 infection increases its relevance. The disease is generally classified as idiopathic, and it is suggested that it is attributed to conditions that lead to hypercoagulability. We present the case of a 68-year-old female patient with thrombosis of the lateral plantar veins and a diagnosis of coronavirus disease of 2019. The plantar vein thrombosis diagnosis was made by means of Doppler ultrasonography and magnetic resonance imaging. Severe acute respiratory syndrome coronavirus 2 infection was suspected per clinical information and confirmed with reverse-transcriptase polymerase chain reaction technique. Treatment was successful using rivaroxaban and nonsteroidal antiinflammatory drugs.


Subject(s)
COVID-19 , Thrombosis , Venous Thrombosis , Female , Humans , Aged , COVID-19/complications , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/etiology , Thrombosis/etiology , Ultrasonography , Magnetic Resonance Imaging
11.
J R Coll Physicians Edinb ; 53(1): 55-56, 2023 03.
Article in English | MEDLINE | ID: covidwho-2293459

ABSTRACT

Inflammatory bowel disease and paroxysmal nocturnal hemoglobinuria (PNH) are both well-known prothrombotic states. However, ongoing thromboprophylaxis is usually effective in such conditions. We report an imbalance that was triggered by COVID-19 infection. There is evidence that COVID-19 infection leads to thrombosis of vessels. The thrombosis of mesenteric vessels can be multifocal and without respiratory symptoms and leads to devastating consequences like resection of large segments of the bowel and lifelong requirement of parenteral nutritional support. We report about a case of ulcerative colitis (in remission) and PNH where COVID-19 resulted in mesenteric ischemia.


Subject(s)
COVID-19 , Colitis, Ulcerative , Hemoglobinuria, Paroxysmal , Mesenteric Ischemia , Thrombosis , Venous Thromboembolism , Humans , Anticoagulants/therapeutic use , Mesenteric Ischemia/etiology , Mesenteric Ischemia/drug therapy , Hemoglobinuria, Paroxysmal/complications , Hemoglobinuria, Paroxysmal/diagnosis , Hemoglobinuria, Paroxysmal/drug therapy , Colitis, Ulcerative/complications , Colitis, Ulcerative/drug therapy , COVID-19/complications , Venous Thromboembolism/drug therapy , Thrombosis/etiology , Thrombosis/drug therapy
12.
J Med Vasc ; 48(1): 31-35, 2023 Feb.
Article in English | MEDLINE | ID: covidwho-2292493

ABSTRACT

The occurrence of arterial and venous thrombosis during coronavirus infection has been widely reported since the beginning of the epidemic. Floating carotid thrombus (FCT) in the common carotid artery is exceptional and its main known cause is atherosclerosis. We describe the case of a 54-year-old man who developed, one week after the onset symptomatology of related to COVID-19 infection, an ischemic stroke, complicating a large intraluminal floating thrombus in the left common carotid artery. Despite surgery and anticoagulation, a local recurrence with other thrombotic complications occurred and the patient died.


Subject(s)
COVID-19 , Thrombosis , Male , Humans , Middle Aged , COVID-19/complications , Carotid Artery, Common/diagnostic imaging , Carotid Artery, Common/surgery , Thrombosis/diagnostic imaging , Thrombosis/drug therapy , Thrombosis/etiology , Carotid Arteries , Blood Coagulation
13.
Cardiovasc Pathol ; 64: 107524, 2023.
Article in English | MEDLINE | ID: covidwho-2305846

ABSTRACT

BACKGROUND: Histopathological studies have shown inflammation, cardiomyocyte injury, and microvascular thrombosis in the ventricular myocardium of patients with coronavirus disease 2019 (COVID-19). However, although atrial dysfunction is common in COVID-19, little is known about histopathological changes in the atria of the heart. We therefore analyzed inflammation, cardiomyocyte injury, and microvascular thrombogenicity in the atria of deceased patients with COVID-19. METHODS: Atrial tissue was obtained from autopsied COVID-19 (n=16) patients and control patients (n=10) and analyzed using immunohistochemistry. The infiltration of CD45+ leukocytes, CD3+ T lymphocytes, CD68+ macrophages, MPO+ neutrophils, and Tryptase+ mast cells were quantified as well as cardiomyocyte damage and microvascular thrombosis. In addition, Tissue Factor (TF) and Factor XII (FXII) were quantified as markers of microvascular thrombogenicity. RESULTS: The numbers of lymphocytes, macrophages, and neutrophils were significantly increased in the atrial myocardium and epicardial atrial adipose tissue of COVID-19 patients compared with the control group. This was accompanied by dispersed cardiomyocyte injury, the occasional presence of microvascular thrombosis, and an increased presence of TF and FXII in the microvascular endothelium. CONCLUSIONS: Severe COVID-19 induces inflammation, cardiomyocyte injury, and microvascular thrombosis in the atria of the heart.


Subject(s)
Atrial Fibrillation , COVID-19 , Thrombosis , Humans , COVID-19/complications , COVID-19/pathology , Inflammation/pathology , Heart Atria/pathology , Thrombosis/etiology , Thrombosis/pathology
14.
J Investig Med High Impact Case Rep ; 11: 23247096231166672, 2023.
Article in English | MEDLINE | ID: covidwho-2305300

ABSTRACT

We present an adolescent male with a single intracardiac mass and pulmonary emboli, complicated by peripheral venous thrombosis and subsequent development of pulmonary pseudoaneurysms, leading to diagnosis of Hughes-Stovin syndrome. Remission was achieved with cyclophosphamide, corticosteroids, and pseudoaneurysm resection and maintained with infliximab and methotrexate.


Subject(s)
Aneurysm, False , Aneurysm , Thrombosis , Vasculitis , Male , Humans , Adolescent , Aneurysm, False/complications , Aneurysm, False/therapy , Syndrome , Pulmonary Artery , Aneurysm/complications , Aneurysm/diagnosis , Vasculitis/complications , Thrombosis/drug therapy , Thrombosis/etiology
15.
Viruses ; 15(4)2023 04 10.
Article in English | MEDLINE | ID: covidwho-2304688

ABSTRACT

SARS-CoV-2 (COVID-19) infection is responsible for causing a disease with a wide spectrum of clinical presentations. Predisposition to thromboembolic disease due to excessive inflammation is also attributed to the disease. The objective of this study was to characterize the clinical and laboratory aspects of hospitalized patients, in addition to studying the pattern of serum cytokines, and associate them with the occurrence of thromboembolic events. METHODOLOGY: A retrospective cohort study with 97 COVID-19 patients hospitalized from April to August 2020 in the Triângulo Mineiro macro-region was carried out. A review of medical records was conducted to evaluate the clinical and laboratory aspects and the frequency of thrombosis, as well as the measurement of cytokines, in the groups that presented or did not present a thrombotic event. RESULTS: There were seven confirmed cases of thrombotic occurrence in the cohort. A reduction in the time of prothrombin activity was observed in the group with thrombosis. Further, 27.8% of all patients had thrombocytopenia. In the group that had thrombotic events, the levels of IL1b, IL-10, and IL2 were higher (p < 0.05). CONCLUSIONS: In the studied sample, there was an increase in the inflammatory response in patients with thrombotic events, confirmed by the increase in cytokines. Furthermore, in this cohort, a link was observed between the IL-10 percentage and an increased chance of a thrombotic event.


Subject(s)
COVID-19 , Thrombosis , Humans , COVID-19/complications , SARS-CoV-2 , Interleukin-10 , Retrospective Studies , Thrombosis/etiology , Cytokines
16.
J Cardiothorac Surg ; 18(1): 158, 2023 Apr 21.
Article in English | MEDLINE | ID: covidwho-2303639

ABSTRACT

BACKGROUND: Nearly half of the patients with hypereosinophilic syndrome (HES) have cardiovascular involvement, a major cause of mortality. COVID-19 infection can lead to cardiac involvement, negatively impacting the clinical course and prognosis. We reported two patients with HES complicated by COVID-19, with cardiac involvement and valve replacement. CASE PRESENTATION: Our first patient was a 27-year-old woman admitted due to dyspnea and signs of heart failure. She had severe mitral stenosis and mitral regurgitation on the echocardiogram. Corticosteroid therapy improved her symptoms initially, but she deteriorated following a positive COVID-19 test. A repeated echocardiogram showed right ventricular failure, severe mitral regurgitation, and torrential tricuspid regurgitation and, she underwent mitral and tricuspid valve replacement. Our second patient was a 43-year-old man with HES resulted in severe tricuspid stenosis, which was improved with corticosteroid treatment. He underwent tricuspid valve replacement due to severe valvular regurgitation. He was admitted again following tricuspid prosthetic mechanical valve thrombosis. Initial workups revealed lung involvement in favor of COVID-19 infection, and his PCR test was positive. CONCLUSION: COVID-19 infection can change the clinical course of HES. It may result in a heart failure exacerbation due to myocardial injury and an increased risk of thrombosis in prosthetic valves or native vessels due to hypercoagulability.


Subject(s)
COVID-19 , Heart Failure , Heart Valve Diseases , Heart Valve Prosthesis Implantation , Heart Valve Prosthesis , Mitral Valve Insufficiency , Thrombosis , Tricuspid Valve Insufficiency , Humans , Male , Female , Adult , Mitral Valve Insufficiency/etiology , Mitral Valve Insufficiency/surgery , Heart Valve Prosthesis Implantation/methods , COVID-19/complications , Heart Valve Diseases/surgery , Tricuspid Valve Insufficiency/etiology , Tricuspid Valve Insufficiency/surgery , Syndrome , Heart Failure/surgery , Thrombosis/etiology , Disease Progression , Heart Valve Prosthesis/adverse effects
18.
Front Immunol ; 14: 1151926, 2023.
Article in English | MEDLINE | ID: covidwho-2306444

ABSTRACT

Thrombosis is a frequent cause of cardiovascular mortality and hospitalization. Current antithrombotic strategies, however, target both thrombosis and physiological hemostasis and thereby increase bleeding risk. In recent years the pathophysiological understanding of thrombus formation has significantly advanced and inflammation has become a crucial element. Neutrophils as most frequent immune cells in the blood and their released mediators play a key role herein. Neutrophil-derived cathelicidin next to its strong antimicrobial properties has also shown to modulates thrombosis and thus presents a potential therapeutic target. In this article we review direct and indirect (immune- and endothelial cell-mediated) effects of cathelicidin on platelets and the coagulation system. Further we discuss its implications for large vessel thrombosis and consecutive thromboinflammation as well as immunothrombosis in sepsis and COVID-19 and give an outlook for potential therapeutic prospects.


Subject(s)
COVID-19 , Thrombosis , Humans , Thrombosis/drug therapy , Thrombosis/etiology , Thromboinflammation , Inflammation/drug therapy , Cathelicidins
19.
Immun Inflamm Dis ; 11(4): e838, 2023 04.
Article in English | MEDLINE | ID: covidwho-2291080

ABSTRACT

Coronavirus disease 2019 (Covid-19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS-CoV-2) leading to the global pandemic worldwide. Systemic complications in Covid-19 are mainly related to the direct SARS-CoV-2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and the development of cytokine storm (CS). As well, Covid-19 complications are developed due to the propagation of oxidative and thrombotic events which may progress to a severe state called oxidative storm and thrombotic storm (TS), respectively. In addition, inflammatory and lipid storms are also developed in Covid-19 due to the activation of inflammatory cells and the release of bioactive lipids correspondingly. Therefore, the present narrative review aimed to elucidate the interrelated relationship between different storm types in Covid-19 and the development of the mixed storm (MS). In conclusion, SARS-CoV-2 infection induces various storm types including CS, inflammatory storm, lipid storm, TS and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the MS seems to be more appropriate to be related to severe Covid-19 than CS, since it develops in Covid-19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway.


Subject(s)
COVID-19 , Thrombosis , Humans , SARS-CoV-2 , Cytokines/metabolism , Cytokine Release Syndrome , Thrombosis/etiology , Lipids
20.
Am J Case Rep ; 24: e938730, 2023 Apr 23.
Article in English | MEDLINE | ID: covidwho-2300844

ABSTRACT

BACKGROUND Vaccine-induced thrombosis and thrombocytopenia is a rare immune disorder documented after adenoviral vector ChAdOx1 nCOV-19 (AstraZeneca) and Ad26.COV2-S (Janssen) vaccine administration against severe acute respiratory syndrome coronavirus 2. It is a rare adverse effect with an incidence of 1 case per 100 000 exposures. The disorder represents altered immune response with proliferation of antibodies that bind to platelet factor 4 (PF4), leading to formation of thrombi and consumptive coagulopathy. Thrombosis combined with thrombocytopenia generally occurs in the first month following vaccination and can lead to fatal outcome, even in young, previously healthy individuals. These young adults ultimately may become solid organ donors. The main concerns with vaccine-induced thrombosis and thrombocytopenia solid organ donors are anti-PF4 antibodies transmission potential, risk of early major graft thrombosis, and serious bleeding. CASE REPORT In our center, 2 kidney transplantations were performed from a single brain-dead vaccine-induced thrombosis and thrombocytopenia donor following Ad26.COV2-S COVID-19 (Janssen) vaccine in October 2021, which represents the first 2 cases of kidney transplantation from a deceased vaccine-induced thrombosis and thrombocytopenia donor after immunization with Ad26.COV2-S (Janssen) vaccine. Both recipients were closely monitored in the early post-transplantation period and after discharge from the hospital. To date, both recipients have a good functioning allograft, without any evidence of vaccine-induced thrombosis and thrombocytopenia transmission. CONCLUSIONS Our results are consistent with those of previously published cases of successful vaccine-induced thrombosis and thrombocytopenia donor solid organ transplantation. Kidney allografts transplanted from vaccine-induced thrombosis and thrombocytopenia donors can have a good overall function with favorable outcomes.


Subject(s)
COVID-19 , Kidney Transplantation , Thrombocytopenia , Thrombosis , Young Adult , Humans , COVID-19 Vaccines/adverse effects , Ad26COVS1 , Kidney Transplantation/adverse effects , ChAdOx1 nCoV-19 , Tissue Donors , Thrombocytopenia/chemically induced , Thrombosis/etiology
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