May the Central Nervous System Be Fogged by the Cytokine Storm in COVID-19?: an Appraisal

Balcıoğlu, Yasin Hasan; Yeşilkaya, Ümit Haluk; Gokcay, Hasan; Kırlıoğlu, Simge Seren

doi:10.1007/s11481-020-09932-9

Cited by 21 publications

(17 citation statements)

References 7 publications

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“…In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.) in GBS tested cases may reinforce the hypothesis of a systemic inflammatory storm in COVID-19 [76,77]. However, given the limited data, we could not perform an accurate analysis of the distribution and, eventually, prognostic value of inflammatory markers in COVID-19-associated GBS.…”

Section: Discussionmentioning

confidence: 87%

“…the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [76,77]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.)…”

Section: Discussionmentioning

confidence: 99%

“…This feature, together with the frequently reported negative nasopharyngeal swab at GBS onset [ 22 , 24 , 36 , 44 , 45 , 52 ] and clinical improvement after IVIG therapy, seems to support the notion of a prominent post-infectious immune-mediated mechanism. However, in this context, the massive release of cytokines in COVID-19 may also contribute to the amplification of the dysimmune process underlying GBS [ 76 , 77 ]. In this regard, the increase of blood inflammatory markers (e.g., CRP, IL-6, TNF-α, IL-1, etc.)…”

Section: Discussionmentioning

confidence: 99%

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Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases

et al. 2020

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Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain-Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11-max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases

et al. 2020

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“…Following infection of respiratory cells, rapid production and release of cytokines and chemokines occur. Macrophages are in turn activated, as are other key components of the innate immune system, such as dendritic cells, which leads to a more extensive immune response initiating the cytokine storm [ 19 ]. It is therefore conceivable from our findings that only severe pulmonary infection and infiltration results in cytokine activation and proliferation, and neurological features are either a consequence or coincidence of COVID-19 infection in this cohort.…”

Section: Discussionmentioning

confidence: 99%

Laboratory biomarkers associated with COVID-19 severity and management

Keddie

Ziff

Chou

et al. 2020

Clinical Immunology

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The heterogeneous disease course of COVID-19 is unpredictable, ranging from mild self-limiting symptoms to cytokine storms, acute respiratory distress syndrome (ARDS), multi-organ failure and death. Identification of high-risk cases will enable appropriate intervention and escalation. This study investigates the routine laboratory tests and cytokines implicated in COVID-19 for their potential application as biomarkers of disease severity, respiratory failure and need of higher-level care. From analysis of 203 samples, CRP, IL-6, IL-10 and LDH were most strongly correlated with the WHO ordinal scale of illness severity, the fraction of inspired oxygen delivery, radiological evidence of ARDS and level of respiratory support ( p ≤ 0.001). IL-6 levels of ≥3.27 pg/ml provide a sensitivity of 0.87 and specificity of 0.64 for a requirement of ventilation, and a CRP of ≥37 mg/L of 0.91 and 0.66. Reliable stratification of high-risk cases has significant implications on patient triage, resource management and potentially the initiation of novel therapies in severe patients.

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“…With this regard, the emerging review article published in the Journal by Armocida et al has drawn our special attention to the possible involvement of a broad range of receptors in the neurotropism and neuronal cell entry of SARS-CoV-2 [1] . Despite the effects of SARS-CoV-2 on the central nervous system (CNS) currently remained inconclusive, a foregoing line of evidence supports the hermeneutical notion that the CNS transmission of SARS-CoV-2 might be via either direct viral infiltration or angiotensin-converting enzyme-2 receptors [2] , [3] . Alternatively and presumably, the recent interactome study by Gordon et al adumbrated that Sigma1 (σ1) and Sigma2 (σ2) receptors might play a role in the neuronal infectivity of SARS-CoV-2 [4] .…”

mentioning

confidence: 99%