Autoimmune post-COVID vaccine syndromes: does the spectrum of autoimmune/inflammatory syndrome expand?

Clinical Rheumatology, Journal Year: 2022, Volume and Issue: 41(5), P. 1603 - 1609

Published: April 5, 2022

Language: Английский

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Postural orthostatic tachycardia syndrome as a sequela of COVID-19

Heart Rhythm, Journal Year: 2022, Volume and Issue: 19(11), P. 1880 - 1889

Published: July 16, 2022

Language: Английский

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Role of SARS-CoV-2 Spike-Protein-Induced Activation of Microglia and Mast Cells in the Pathogenesis of Neuro-COVID

Cells, Journal Year: 2023, Volume and Issue: 12(5), P. 688 - 688

Published: Feb. 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.

Language: Английский

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COVID-19 Induced Postural Orthostatic Tachycardia Syndrome (POTS): A Review

Cureus, Journal Year: 2023, Volume and Issue: unknown

Published: March 31, 2023

POTS (Postural Orthostatic Tachycardia Syndrome) is a multisystem disorder characterized by the abnormal autonomic response to an upright posture, causing orthostatic intolerance and excessive tachycardia without hypotension. Recent reports suggest that significant percentage of COVID-19 survivors develop within 6 8 months infection. Prominent symptoms include fatigue, intolerance, tachycardia, cognitive impairment. The exact mechanisms post-COVID-19 are unclear. Still, different hypotheses have been given, including autoantibody production against nerve fibers, direct toxic effects SARS-CoV-2, or sympathetic nervous system stimulation secondary Physicians should high suspicion in survival when presented with dysfunction conduct diagnostic tests like Tilt table others confirm it. management COVID-19-related requires comprehensive approach. Most patients respond initial non-pharmacological options, but become more severe they do not approach, pharmacological options considered. We limited understanding knowledge POTS, further research warranted improve our formulate better plan.

Language: Английский

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Pathophysiological, immunological, and inflammatory features of long COVID

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 28, 2024

The COVID-19 pandemic continues to cause severe global disruption, resulting in significant excess mortality, overwhelming healthcare systems, and imposing substantial social economic burdens on nations. While most of the attention therapeutic efforts have concentrated acute phase disease, a notable proportion survivors experience persistent symptoms post-infection clearance. This diverse set symptoms, loosely categorized as long COVID, presents potential additional public health crisis. It is estimated that 1 5 exhibit clinical manifestations consistent with COVID. Despite this prevalence, mechanisms pathophysiology COVID remain poorly understood. Alarmingly, evidence suggests cases within condition develop debilitating or disabling symptoms. Hence, urgent priority should be given further studies equip systems for its management. review provides an overview available information emerging condition, focusing affected individuals’ epidemiology, pathophysiological mechanisms, immunological inflammatory profiles.

Language: Английский

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Larger gray matter volumes in neuropsychiatric long-COVID syndrome

Psychiatry Research, Journal Year: 2022, Volume and Issue: 317, P. 114836 - 114836

Published: Sept. 6, 2022

Neuropsychiatric symptoms are the most common sequelae of long-COVID. As accumulating evidence suggests an impact survived SARS-CoV-2-infection on brain physiology, it is necessary to further investigate structural changes in relation course and neuropsychiatric symptom burden To this end, present study investigated 3T-MRI scans from long-COVID patients suffering (n = 30), healthy controls 20). Whole-brain comparison gray matter volume (GMV) was conducted by voxel-based morphometry. determine whether GMV predicted and/or initial severity COVID-19 time since onset stepwise linear regression analysis performed. Significantly enlarged several clusters (spanning fronto-temporal areas, insula, hippocampus, amygdala, basal ganglia, thalamus both hemispheres) when compared controls. Time a significant regressor four these with inverse relationship. No associations clinical were found. alterations limbic secondary olfactory areas might be dynamic over time. Larger samples longitudinal data required clarify mediating mechanisms between COVID-19, symptoms.

Language: Английский

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COVID-19 and Long COVID: Disruption of the Neurovascular Unit, Blood-Brain Barrier, and Tight Junctions

The Neuroscientist, Journal Year: 2023, Volume and Issue: 30(4), P. 421 - 439

Published: Sept. 11, 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of disease 2019 (COVID-19), could affect brain structure and function. SARS-CoV-2 can enter through different routes, including olfactory, trigeminal, vagus nerves, blood immunocytes. may also from peripheral a disrupted blood-brain barrier (BBB). The neurovascular unit in brain, composed neurons, astrocytes, endothelial cells, pericytes, protects parenchyma by regulating entry substances blood. astrocytes highly express angiotensin converting enzyme (ACE2), indicating that BBB be disturbed lead to derangements tight junction adherens proteins. This leads increased permeability, leakage components, movement immune cells into parenchyma. cross microvascular an ACE2 receptor–associated pathway. exact mechanism dysregulation COVID-19/neuro-COVID is not clearly known, nor development long COVID. Various biomarkers indicate severity neurologic complications COVID-19 help objectively diagnose those developing review highlights importance disruption, as well some potentially useful COVID-19, COVID/neuro-COVID.

Language: Английский

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Cardiovascular autonomic dysfunction in “Long COVID”: pathophysiology, heart rate variability, and inflammatory markers

Frontiers in Cardiovascular Medicine, Journal Year: 2023, Volume and Issue: 10

Published: Sept. 1, 2023

Long COVID is characterized by persistent signs and symptoms that continue or develop for more than 4 weeks after acute COVID-19 infection. Patients with experience a cardiovascular autonomic imbalance known as dysautonomia. However, the underlying pathophysiological mechanisms behind this remain unclear. Current hypotheses include neurotropism, cytokine storms, inflammatory persistence. Certain immunological factors indicate autoimmune dysfunction, which can be used to identify patients at higher risk of COVID. Heart rate variability imbalances in individuals suffering from COVID, measurement non-invasive low-cost method assessing modulation. Additionally, biochemical markers are diagnosing monitoring These improve understanding driving response its effects on sympathetic parasympathetic pathways nervous system. Autonomic may result lower heart variability, impaired vagal activity, substantial sympathovagal imbalance. New research subject must encouraged enhance long-term risks cause

Language: Английский

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Gut-brain pathogenesis of post-acute COVID-19 neurocognitive symptoms

Frontiers in Neuroscience, Journal Year: 2023, Volume and Issue: 17

Published: Sept. 28, 2023

Approximately one third of non-hospitalized coronavirus disease 2019 (COVID-19) patients report chronic symptoms after recovering from the acute stage severe respiratory syndrome 2 (SARS-CoV-2) infection. Some most persistent and common complaints this post-acute COVID-19 (PACS) are cognitive in nature, described subjectively as “brain fog” also objectively measured deficits executive function, working memory, attention, processing speed. The mechanisms these sequelae currently not understood. SARS-CoV-2 inflicts damage to cerebral blood vessels intestinal wall by binding angiotensin-converting enzyme (ACE2) receptors evoking production high levels systemic cytokines, compromising brain’s neurovascular unit, degrading barrier, potentially increasing permeability both harmful substances. Such substances hypothesized be produced gut pathogenic microbiota that, given profound effects has on gastrointestinal system, may fourish a result post-COVID-19 dysbiosis. therefore create scenario which neurotoxic neuroinflammatory readily proliferate lumen encounter weakened gaining access brain subsequently producing deficits. Here, we review proposed PACS pathogenesis along gut-brain axis, while identifying specific methodologies that available experimentally measure each individual component model.

Language: Английский

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Acute Myocardial Infarction during the COVID-19 Pandemic: Long-Term Outcomes and Prognosis—A Systematic Review

Life, Journal Year: 2024, Volume and Issue: 14(2), P. 202 - 202

Published: Jan. 31, 2024

Coronavirus disease 2019 (COVID-19) was a global pandemic with high mortality and morbidity that led to an increased health burden all over the world. Although virus mostly affects pulmonary tract, cardiovascular implications are often observed among COVID-19 patients predictive of poor outcomes. Increased values myocardial biomarkers such as troponin I or NT-proBNP were proven be risk factors for respiratory failure. acute coronary syndromes (ACSs) greater in phase COVID-19, there lower rates hospitalization ACSs, due patients’ hesitation presenting at hospital. Hospitalized ACSs infection had prolonged symptom-to-first-medical-contact time, longer door-to-balloon time. The mechanisms injury still not entirely clear; however, most frequently implicated include downregulation ACE2 receptors, endothelial dysfunction, pro-coagulant status, levels pro-inflammatory cytokines. aim this paper is evaluate long-term outcomes prognosis survivors presented infarction, by reviewing existing data. importance association between infectious infarction arises from SARS-CoV-2 AMI (10–76%, compared 4.6% NSTEMI 7% STEMI without COVID-19). literature review showed events general population, even after disease, poorer

Language: Английский

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