Laboratory biomarkers associated with COVID-19 severity and management

Keddie, Stephen; Ziff, Oliver J.; Chou, Michael; Taylor, Robert; Heslegrave, Amanda; Garr, Edmund; Lakdawala, Neghat; Church, Andrew J.; Ludwig, Dalia; Manson, Jessica; Scully, Marie; Nastouli, Eleni; Chapman, Miles D.; Hart, Melanie; Lunn, Michael P.

doi:10.1101/2020.08.18.20168807

Cited by 18 publications

(24 citation statements)

References 12 publications

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“…In other studies from Finland, ICU patients had higher levels of IL‐6, C‐reactive protein, and procalcitonin compared with non‐ICU patients 30 . Keddie et al 31 also noted similar findings. The authors demonstrated that CRP, IL‐6, IL‐10, and lactate dehydrogenase significantly correlated with ARDS and respiratory support.…”

Section: Discussionmentioning

confidence: 62%

Relative expression of proinflammatory molecules in COVID‐19 patients who manifested disease severities

Nigar¹,

Shah

Setu³

et al. 2021

Journal of Medical Virology

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Aggressive immune response, due to overexpressed proinflammatory molecules, has been characterized in coronavirus disease 2019 (COVID‐19) patients. Some of those mediators have a dual and opposite role on immune systems at play behind differential disease severities. We investigated the expression of some cytokines and chemokines in COVID‐19 patients in Bangladesh. We diagnosed the patients by detecting severe acute respiratory syndrome coronavirus 2 RNA in nasal swab samples by the real‐time RT‐PCR method. Thirty adult patients were preselected based on their disease severities and grouped into mild, moderate, and severe cases. Nine healthy volunteers participated in this study as a control. Relative expression of nine cytokines/chemokine in total leukocytes was semi‐quantified in SYBRgreen‐based real‐time quantitative reverse‐transcriptase polymerase chain reaction. We performed statistical tests on transformed log data using SPSS 24.0. At the onset of symptoms (Day 1), angiotensin‐converting enzyme 2 (ACE2) ( p < 0.05) and interleukin (IL)‐6 ( p > 0.05) were upregulated in all COVID‐19 groups, although the expression levels did not significantly correlate with disease severities. However, expressions of IL‐6, monocyte chemotactic protein‐1, macrophage inflammatory protein‐1α, tumor necrosis factor‐α (TNF‐α), RANTES (regulated upon activation, normal T cell expressed and secreted), and ACE2, on Day 14, were positively correlated with disease severities. Relative viral load at Day 1 showed no significant correlation with cytokine expression but had a significant positive correlation with RANTES and ACE2 expression on Day 14 ( p < 0.05). Male patients had a higher level of IL‐6 than female patients on Day 1 ( p < 0.05). All COVID‐19 patients showed upregulated cytokines and chemokines on Day 14 compared to Day 1 except TNF‐α. Female patients had a higher expression of ACE2 and IL‐12 on Day 14. Upregulated cytokines/chemokines at the convalescent stage, especially IL‐6, may help in targeting anticytokine therapy in post‐COVID‐19 patients' management.

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Section: Discussionmentioning

confidence: 62%

Relative expression of proinflammatory molecules in COVID‐19 patients who manifested disease severities

Nigar¹,

Shah

Setu³

et al. 2021

Journal of Medical Virology

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“…Acute phase reactants such as ferritin, C-reactive protein (CRP) and coagulation markers including D-dimer, fibrinogen and factor VIII, have been associated to be markers of severe and critical COVID-19. (39-42) To investigate if they are associated with mechanisms of neurological involvement in COVID-19, we quantified such markers in the CSF of COVID-19 subjects and controls. Using a high-sensitive CRP (hsCRP) assay, we found that CRP was present almost exclusively in the CSF of COVID-19 subjects as it was detected in 7/18 subjects, 4 COVID-19 encephalopathy and 3 COVID-19 stroke, while only one CSF (from an autoimmune encephalitis subject) of the 82 CSF controls had detectable hsCRP (P= 0.001).…”

Section: Resultsmentioning

confidence: 99%

Cerebrospinal fluid in COVID-19 neurological complications: no cytokine storm or neuroinflammation

García

Barreras

Lewis

et al. 2021

Preprint

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BACKGROUNDNeurological complications occur in COVID-19. We aimed to examine cerebrospinal fluid (CSF) of COVID-19 subjects with neurological complications and determine presence of neuroinflammatory changes implicated in pathogenesis.METHODSCross-sectional study of CSF neuroinflammatory profiles from 18 COVID-19 subjects with neurological complications categorized by diagnosis (stroke, encephalopathy, headache) and illness severity (critical, severe, moderate, mild). COVID-19 CSF was compared with CSF from healthy, infectious and neuroinflammatory disorders and stroke controls (n=82). Cytokines (IL-6, TNFα, IFNγ, IL-10, IL-12p70, IL-17A), inflammation and coagulation markers (high-sensitivity-C Reactive Protein [hsCRP], ferritin, fibrinogen, D-dimer, Factor VIII) and neurofilament light chain (NF-L), were quantified. SARS-CoV2 RNA and SARS-CoV2 IgG and IgA antibodies in CSF were tested with RT-PCR and ELISA.RESULTSCSF from COVID-19 subjects showed a paucity of neuroinflammatory changes, absence of pleocytosis or specific increases in pro-inflammatory markers or cytokines (IL-6, ferritin, or D-dimer). Anti-SARS-CoV2 antibodies in CSF of COVID-19 subjects (77%) were observed despite no evidence of SARS-CoV2 viral RNA. A similar increase of pro-inflammatory cytokines (IL-6, TNFα, IL-12p70) and IL-10 in CSF of COVID-19 and non-COVID-19 stroke subjects was observed compared to controls. CSF-NF-L was elevated in subjects with stroke and critical COVID-19. CSF-hsCRP was present almost exclusively in COVID-19 cases.CONCLUSIONThe paucity of neuroinflammatory changes in CSF of COVID-19 subjects and lack of SARS-CoV2 RNA do not support the presumed neurovirulence of SARS-CoV2 or neuroinflammation in pathogenesis of neurological complications in COVID-19. Elevated CSF-NF-L indicates neuroaxonal injury in COVID-19 cases. The role of CSF SARS-CoV2 IgG antibodies is still undetermined.FUNDINGThis work was supported by NIH R01-NS110122 and The Bart McLean Fund for Neuroimmunology Research.

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“…In the severe group, WBC showed normal/increased values and decreased lymphocytes, while neutrophils, CRP, procalcitonin, D dimer, and ferritin increased. Biomarkers such as WBC, neutrophil procalcitonin lymphocytes, CRP, D-dimer, ferritin showed significant differences with the WHO severity [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Association of serum KL-6 levels on COVID-19 severity: A cross-sectional study design with purposive sampling

Suryananda

Yudhawati

2021

Annals of Medicine &Amp; Surgery

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Background The main target of SARS-CoV2 is the alveolar type II (AT2) cells of the lung. SARS-CoV2 evades the innate immune system resulting in the release of proinflammatory cytokines (IL-1β, IL-6, TNF-α) which causes AT2 cell damage. Krebs von den Lungen (KL-6) is a specific biomarker of AT2 cell damage. KL-6 is produced in AT2 cells that are injured/regenerated. Objective Research that discusses the role of KL-6 in COVID-19 is still being debated and not much has been done in Indonesia. Methods This study was an analytical study with a prospective design on 75 COVID-19 patients who were treated. Subjects were divided into two large groups according to their degree of severity, 57 subjects with severe degrees and 18 subjects with non-severe degrees. The serum KL-6 levels were measured on days 0 and 6. Data were analyzed using paired t -test and independent t -test for data were normally distributed and Wilcoxon test and Mann Whitney test for data that were not normally distributed. Result In this study, the mean serum KL-6 for day 0 in the severe group was higher than the non-severe group with values of 45.70 U/mL and 44.85 U/mL. On day 6, the mean serum KL-6 in the severe group was lower than that in the non-severe group with values of 41.3 U/mL and 41.95 U/mL. Serum KL-6 in the severe group experienced an even greater decrease than the non-severe group. Conclusion There was no significant association between serum KL-6 values on 0 days in the severity of COVID-19.

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Laboratory biomarkers associated with COVID-19 severity and management

Cited by 18 publications

References 12 publications

Relative expression of proinflammatory molecules in COVID‐19 patients who manifested disease severities

Relative expression of proinflammatory molecules in COVID‐19 patients who manifested disease severities

Cerebrospinal fluid in COVID-19 neurological complications: no cytokine storm or neuroinflammation

Association of serum KL-6 levels on COVID-19 severity: A cross-sectional study design with purposive sampling

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