Arterial and Venous Thrombosis Complicated in COVID-19: A Retrospective Single Center Analysis in Japan DOI Creative Commons
Seiya Oba, Tadashi Hosoya,

Miki Amamiya

и другие.

Frontiers in Cardiovascular Medicine, Год журнала: 2021, Номер 8

Опубликована: Ноя. 19, 2021

Background: Thrombosis is a characteristic complication in coronavirus disease 2019 (COVID-19). Since coagulopathy has been observed over the entire clinical course, thrombosis might be clue to understanding specific pathology COVID-19. Currently, there limited epidemiological data of COVID-19-associated Japanese population and none regarding variant strains SARS-CoV-2. Here, we elucidate risk factors pattern COVID-19 patients. Methods: The patients consecutively admitted Tokyo Medical Dental University Hospital with were retrospectively analyzed. SARS-CoV-2 variants concern/interest (VOC/VOI) carrying spike protein mutants E484K, N501Y, or L452R identified by PCR-based analysis. All thrombotic events diagnosed symptoms, ultrasonography, and/or radiological tests. Results: Among 516 patients, 32 experienced 42 thromboembolic events. Advanced age, severe respiratory conditions, several abnormal laboratory markers associated development thrombosis. While occurred 13% condition, those still 2.5% who did not require oxygen therapy. Elevated D-dimer ferritin levels on admission independent (adjusted odds ratio 9.39 3.11, 95% confidence interval 2.08-42.3, 1.06-9.17, respectively). Of events, 22 venous, whereas 20 arterial. received anticoagulation antiinflammatory therapies higher proportion, mortality rate, organ dysfunctions, bleeding complications these than without incidence became less frequent time, such as during replacement earlier VOC/VOI increased use anticoagulatory therapeutics. Conclusion: This study elucidated that elevated are useful biomarkers comparable arterial venous required further considerations for management Further studies would identify high-risk populations establish appropriate interventions

Язык: Английский

The pulmonary pathology of COVID-19 DOI Creative Commons
Hans Bösmüller, Matthias S. Matter, Falko Fend

и другие.

Virchows Archiv, Год журнала: 2021, Номер 478(1), С. 137 - 150

Опубликована: Янв. 1, 2021

The lung is the main affected organ in severe coronavirus disease 2019 (COVID-19) caused by novel SARS-CoV-2, and damage leading cause of death vast majority patients. Mainly based on results obtained autopsies, seminal features fatal COVID-19 have been described many groups worldwide. Early changes encompass edema, epithelial damage, capillaritis/endothelialitis, frequently combined with microthrombosis. Subsequently, patients manifest respiratory insufficiency exhibit exudative diffuse alveolar (DAD) hyaline membrane formation pneumocyte type 2 hyperplasia, variably complicated superinfection, which may progress to organizing/fibrotic stage DAD. These features, however, are not specific for can be found other disorders including viral infections. Clinically, early characterized high load, lymphopenia, massive secretion pro-inflammatory cytokines hypercoagulability, documented elevated D-dimers an increased frequency thrombotic thromboembolic events, whereas virus loads cytokine levels tend decrease late stages, when tissue repair angiogenesis prevails. present review describes spectrum pathology current literature authors' personal experience derived from clinical tries summarize our understanding open questions pathophysiology pulmonary COVID-19.

Язык: Английский

Процитировано

168

Mechanisms of Immunothrombosis in Vaccine-Induced Thrombotic Thrombocytopenia (VITT) Compared to Natural SARS-CoV-2 Infection DOI Open Access
Dennis McGonagle, Gabriele De Marco, Charlie Bridgewood

и другие.

Journal of Autoimmunity, Год журнала: 2021, Номер 121, С. 102662 - 102662

Опубликована: Май 19, 2021

Язык: Английский

Процитировано

156

Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein DOI Open Access
Gerard J. Nuovo, Cynthia M. Magro,

Toni Shaffer

и другие.

Annals of Diagnostic Pathology, Год журнала: 2020, Номер 51, С. 151682 - 151682

Опубликована: Дек. 24, 2020

Язык: Английский

Процитировано

141

Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome? DOI Open Access
Theoharis C. Theoharides

Molecular Neurobiology, Год журнала: 2022, Номер 59(3), С. 1850 - 1861

Опубликована: Янв. 13, 2022

Язык: Английский

Процитировано

129

Role of SARS-CoV-2 Spike-Protein-Induced Activation of Microglia and Mast Cells in the Pathogenesis of Neuro-COVID DOI Creative Commons
Theoharis C. Theoharides, Duraisamy Kempuraj

Cells, Год журнала: 2023, Номер 12(5), С. 688 - 688

Опубликована: Фев. 22, 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes disease 2019 (COVID-19). About 45% of COVID-19 patients experience several symptoms a few months after the initial infection and develop post-acute sequelae SARS-CoV-2 (PASC), referred to as “Long-COVID,” characterized by persistent physical mental fatigue. However, exact pathogenetic mechanisms affecting brain are still not well-understood. There is increasing evidence neurovascular inflammation in brain. precise role neuroinflammatory response that contributes severity long COVID pathogenesis clearly understood. Here, we review reports spike protein can cause blood–brain barrier (BBB) dysfunction damage neurons either directly, or via activation mast cells microglia release various molecules. Moreover, provide recent novel flavanol eriodictyol particularly suited for development an effective treatment alone together with oleuropein sulforaphane (ViralProtek®), all which have potent anti-viral anti-inflammatory actions.

Язык: Английский

Процитировано

56

COVID-19 Vasculopathy: Mounting Evidence for an Indirect Mechanism of Endothelial Injury DOI Creative Commons

Roberto F. Nicosia,

Giovanni Ligresti, Nunzia Caporarello

и другие.

American Journal Of Pathology, Год журнала: 2021, Номер 191(8), С. 1374 - 1384

Опубликована: Май 23, 2021

Язык: Английский

Процитировано

97

A scoping review of the pathophysiology of COVID-19 DOI Creative Commons
Paul E. Marik, José Iglesias, Joseph Varón

и другие.

International Journal of Immunopathology and Pharmacology, Год журнала: 2021, Номер 35

Опубликована: Янв. 1, 2021

COVID-19 is a highly heterogeneous and complex medical disorder; indeed, severe probably amongst the most of conditions known to science. While enormous strides have been made in understanding molecular pathways involved patients infected with coronaviruses an overarching comprehensive pathogenesis lacking. Such essential formulation effective prophylactic treatment strategies. Based on clinical, proteomic, genomic studies as well autopsy data disease can be considered connection three basic pathologic processes, namely pulmonary macrophage activation syndrome uncontrolled inflammation, complement-mediated endothelialitis together procoagulant state thrombotic microangiopathy. In addition, platelet release serotonin degranulation mast cells contributes hyper-inflammatory state. Auto-antibodies demonstrated large number hospitalized which adds end-organ damage pro-thrombotic This paper provides clinical overview major pathogenetic mechanism leading disease.

Язык: Английский

Процитировано

65

The histologic and molecular correlates of COVID-19 vaccine-induced changes in the skin DOI Creative Commons
Cynthia M. Magro, A. Neil Crowson,

Linda Franks

и другие.

Clinics in Dermatology, Год журнала: 2021, Номер 39(6), С. 966 - 984

Опубликована: Июль 25, 2021

A total of 22 patients who had developed an adverse cutaneous reaction to the Moderna or Pfizer vaccine underwent biopsies. Each patient was assessed light microscopically, and, in select biopsies, spike glycoprotein and cytokine assessment were also conducted. The self-limited reactions often described clinically as urticarial eczematous within 1 day 4 weeks after receiving first second dose vaccine. Classic clinical morphologic depictions type IV hypersensitivity with features dermatitis, interface granulomatous inflammation, and/or lymphocytic vasculitic component observed. Clinical histologic perniosis, pityriasis rosea, rubra pilaris, guttate psoriasis seen cases. In 2 cases dominant picture vasculitis, possibly reflective Arthus III immune complex action. biopsy specimens normal skin post affected by post-vaccine eruption showed rare deep microvessels positive for no complement deposition contrasting greater vascular protein biopsies from experiencing severe coronavirus disease 2019 (COVID-19). It is concluded that occur owing a substance found vehicle (eg, polyethylene glycol). An response directed against human-manufactured has be considered because some histologically closely resemble mild COVID-19. Finally, vaccine-associated enhancement largely attributable adjuvant properties may unmask certain inflammatory milieus operational psoriasis, atopic subclinical hypersensitivity.

Язык: Английский

Процитировано

57

The pathogenesis of coronavirus-19 disease DOI Creative Commons
Alain Borczuk, Rhonda K. Yantiss

Journal of Biomedical Science, Год журнала: 2022, Номер 29(1)

Опубликована: Окт. 26, 2022

Abstract Severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2) is the causal agent of coronavirus disease-2019 (COVID-19), a systemic illness characterized by variably severe pulmonary symptoms, cardiac conduction abnormalities, diarrhea, and gastrointestinal bleeding, as well neurologic deficits, renal insufficiency, myalgias, endocrine other perturbations that reflect widespread microvascular injury pro-inflammatory state. The mechanisms underlying various manifestations viral infection are incompletely understood but most data suggest COVID-19 results from virus-driven in immune system resultant tissue injury. Aberrant interferon-related responses lead to alterations cytokine elaboration deplete resident cells while simultaneously recruiting hyperactive macrophages functionally altered neutrophils, thereby tipping balance adaptive immunity innate immunity. Disproportionate activation these neutrophils further depletes normal activity B-cells, T-cells, natural killer (NK) cells. In addition, this state stimulates uncontrolled complement development neutrophil extracellular traps (NETS), both which promote coagulation cascade induce “thrombo-inflammation”. These have similar multiple organ systems, frequently show pathologic findings related thrombosis large small vessels. However, patients with generally more pronounced than those organs. Not only do they feature inflammatory thromboses endothelial injury, much parenchymal damage stems failed maturation alveolar pneumocytes, interactions between type 2 pneumocytes non-resident macrophages, greater degree NET formation. purpose review discuss pathogenesis can occur SARS-CoV-2 infection. Understanding important future therapies for COVID-19, many will likely target specific components system, particularly induction, cytokines, subpopulations

Язык: Английский

Процитировано

57

Systematic Review of Microthrombi in COVID-19 Autopsies DOI Creative Commons
Rafael Parra‐Medina,

Sabrina Herrera,

Jaime Piracoca Mejìa

и другие.

Acta Haematologica, Год журнала: 2021, Номер 144(5), С. 476 - 483

Опубликована: Янв. 1, 2021

Background: Histopathological analysis can provide additional clues in COVID-19 understanding. During the last year, autopsy reports have revealed that diffuse alveolar damage (DAD) is most significant observed finding. The aim of this study to review cases literature about autopsies reported microthrombi different organs. Methods: We performed a systematic PubMed, Virtual Health Library (VHL), and Google Scholar. Results: In total, 151 were included, 91 presented lung (73%), heart (11.2%), kidney (24%), liver (16.3%). age range was between 27 96 years. Males 64.8%. patients with had more comorbidities such as arterial hypertension (62%), obesity or overweight (64%), diabetes mellitus type 2 (51%), disease (53%). common histopathological changes found microthrombosis DAD exudative phase (78%), pulmonary embolism (59%), infarct (81%). Presence associated (p < 0.0001) proliferative phases = 0.02). Discussion: these results shows may be organs are frequent comorbidities, embolism, infarct.

Язык: Английский

Процитировано

57