COVID-19 and its sequelae: a platform for optimal patient care, discovery and training

Becker, Richard C.

doi:10.1007/s11239-021-02375-w

Cited by 50 publications

(34 citation statements)

References 13 publications

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“…It has been recently estimated (May 2021) that between 10% to 35% of patients not requiring hospitalization for acute COVID-19 may develop post-COVID-19 symptoms, regardless of co-morbidities [1,16,88], while incidence rates of up to 70% have been reported among hospitalized patients and among patients with severe illnesses [89]. The true prevalence of LC/PASC syndrome is currently unknown; however, it has been stated that as many as one-in-three survivors or more depending on the depth and reliability of investigation may develop LC/PASC [89].…”

Section: Discussionmentioning

confidence: 99%

Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID

Hayden

2021

Neuroglia

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The COVID-19 pandemic has paralleled the great Spanish flu pandemic of 1918–1919 in the United States. Previous historical accounts have strongly suggested a post-viral syndrome and, currently, a post-COVID-19 viral syndrome is unquestionable, which shares many of the characteristics of myalgic encephalomyelitis/chronic fatigue syndrome that is present globally. The original term for this post-acute sequela of SARS-CoV-2 (PASC) was termed long haulers by those who were affected with this syndrome and it is now termed long COVID (LC) or PASC. International researchers and clinicians are desperately trying to better understand the pathobiological mechanisms possibly involved in this syndrome. This review aims to summarize many of the cumulated findings associated with LC/PASC and provides supportive and representative illustrations and transmission electron micrographic remodeling changes within brain tissues associated with a stress type of injury as occurs in the classic db/db and novel BTBR ob/ob obesity and diabetes mellitus mice models. These models are utilized to merely provide a response to metabolic stress injury wound healing mechanisms that are also present in humans. This review posits that neuroglial activation and chronic neuroinflammation may be a common denominator for the development of the complex LC/PASC syndrome following acute COVID-19 due to SARS-CoV-2.

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Section: Discussionmentioning

confidence: 99%

Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID

Hayden

2021

Neuroglia

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“…Based on the initial symptoms, duration of symptoms, period of quiescence and time of onset of symptoms long COVID (PCS) can be divided into five categories ( Table 1 ) [ 8 ]. As can be noted from the classifications, symptoms could last 3-12 months, and vary in severity from mild to severe, or even lead to death.…”

mentioning

confidence: 99%

Post COVID-19 Syndrome (“Long COVID”) and Diabetes: Challenges in Diagnosis and Management

Raveendran¹,

Misra

2021

Diabetes & Metabolic Syndrome: Clinical Research & Revi

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Presence of various health issues even after recovering from acute COVID19 is collectively called post COVID syndrome (PCS, or “long COVID”). The symptoms of PCS can be due to organ dysfunction, effects of hospitalisation and drugs, or unrelated to these. Type 2 diabetes mellitus has bidirectional relationship with COVID-19. Presence of diabetes also influences PCS via various pathophysiological mechanisms. COVID-19 can add to or exacerbate postural hypotension with tachycardia, sarcopenia (and muscle fatigue), and microvascular dysfunction in patients with diabetes. Strict control of diabetes and other co-morbidities, supervised rehabilitation and physical exercise, and optimal nutrition could help in reducing and managing PCS. Patients may suffer from several debilitating symptoms/signs that develop during or after an infection consistent with COVID-19, continue for more than 12 weeks after infection, and are not explained by an alternative diagnosis [ 1 ]. Common symptoms include fatigue, breathlessness, myalgia, weakness, headache, cognitive blunting etc. This conglomeration of symptoms is called “Long COVID” or more appropriately as “Post COVID-19 Syndrome (PCS)” [ 2 ]. The aim of the brief review is to summarise current knowledge of health events occurring after COVID-19 in brief and relate them for patients with diabetes.

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“…The prospective observational study of patients hospitalised with COVID-19 showed that 4 months after discharge, 51% (244 of 478) had at least one symptom that was not present before the illness, including (31%) reported fatigue, (21%) cognitive symptoms and dyspnoea [184]. In non-hospitalised patients after COVID-19, without comorbidities, it is estimated that 10% to 35% may present with symptoms of post-COVID syndrome [183,186,187], and in hospitalised patients with severe COVID-19, the incidence is up to 80% [182,188,189]. An Italian study of 238 patients hospitalised with severe COVID-19, 4 months after discharge, showed prolonged pulmonary dysfunction in 53.8%, which may account for many post-COVID symptoms [190].…”

Section: Post-covid Syndromementioning

confidence: 99%

Depressive and Neurocognitive Disorders in the Context of the Inflammatory Background of COVID-19

Dąbrowska

Galińska-Skok

Waszkiewicz

2021

Life

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The dysfunctional effects of the coronavirus disease 2019 (COVID-19) infection on the nervous system are established. The manifestation of neuropsychiatric symptoms during and after infection is influenced by the neuroinvasive and neurotrophic properties of SARS-CoV-2 as well as strong inflammation characterised by a specific “cytokine storm”. Research suggests that a strong immune response to a SARS-CoV-2 infection and psychological stressors related to the pandemic may cause chronic inflammatory processes in the body with elevated levels of inflammatory markers contributing to the intensification of neurodegenerative processes. It is suggested that neuroinflammation and associated central nervous system changes may significantly contribute to the etiopathogenesis of depressive disorders. In addition, symptoms after a COVID-19 infection may persist for up to several weeks after an acute infection as a post-COVID-19 syndrome. Moreover, previous knowledge indicates that among SSRI (selective serotonin reuptake inhibitor) group antidepressants, fluoxetine is a promising drug against COVID-19. In conclusion, further research, observation and broadening of the knowledge of the pathomechanism of a SARS-CoV-2 infection and the impact on potential complications are necessary. It is essential to continue research in order to assess the long-term neuropsychiatric effects in COVID-19 patients and to find new therapeutic strategies.

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COVID-19 and its sequelae: a platform for optimal patient care, discovery and training

Cited by 50 publications

References 13 publications

Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID

Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID

Post COVID-19 Syndrome (“Long COVID”) and Diabetes: Challenges in Diagnosis and Management

Depressive and Neurocognitive Disorders in the Context of the Inflammatory Background of COVID-19

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