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Investigating the possible mechanisms of autonomic dysfunction post-COVID-19.
Jammoul, Maya; Naddour, Judith; Madi, Amir; Reslan, Mohammad Amine; Hatoum, Firas; Zeineddine, Jana; Abou-Kheir, Wassim; Lawand, Nada.
Afiliação
  • Jammoul M; Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Lebanon.
  • Naddour J; Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Lebanon.
  • Madi A; Department of Biomedicine, Neuroscience and Advanced Diagnostics (BIND), University of Palermo, 90127 Palermo, Italy.
  • Reslan MA; Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
  • Hatoum F; Faculty of Medicine, American University of Beirut, Lebanon.
  • Zeineddine J; Faculty of Medicine, American University of Beirut, Lebanon.
  • Abou-Kheir W; Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Lebanon.
  • Lawand N; Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Lebanon; Department of Neurology, Faculty of Medicine, American University of Beirut, Lebanon. Electronic address: Alchaer@sbcglobal.net.
Auton Neurosci ; 245: 103071, 2023 03.
Article em En | MEDLINE | ID: mdl-36580747
Patients with long COVID suffer from many neurological manifestations that persist for 3 months following infection by SARS-CoV-2. Autonomic dysfunction (AD) or dysautonomia is one complication of long COVID that causes patients to experience fatigue, dizziness, syncope, dyspnea, orthostatic intolerance, nausea, vomiting, and heart palpitations. The pathophysiology behind AD onset post-COVID is largely unknown. As such, this review aims to highlight the potential mechanisms by which AD occurs in patients with long COVID. The first proposed mechanism includes the direct invasion of the hypothalamus or the medulla by SARS-CoV-2. Entry to these autonomic centers may occur through the neuronal or hematogenous routes. However, evidence so far indicates that neurological manifestations such as AD are caused indirectly. Another mechanism is autoimmunity whereby autoantibodies against different receptors and glycoproteins expressed on cellular membranes are produced. Additionally, persistent inflammation and hypoxia can work separately or together to promote sympathetic overactivation in a bidirectional interaction. Renin-angiotensin system imbalance can also drive AD in long COVID through the downregulation of relevant receptors and formation of autoantibodies. Understanding the pathophysiology of AD post-COVID-19 may help provide early diagnosis and better therapy for patients.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças do Sistema Nervoso Autônomo / Intolerância Ortostática / COVID-19 Tipo de estudo: Screening_studies Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças do Sistema Nervoso Autônomo / Intolerância Ortostática / COVID-19 Tipo de estudo: Screening_studies Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article