Lactate dehydrogenase level as a COVID-19 severity marker

Szarpak, Łukasz; Ruetzler, Kurt; Safiejko, Kamil; Hampel, Michał; Pruc, Michał; Kańczuga‐Koda, Luiza; Filipiak‬, Krzysztof J.; Jaguszewski, Miłosz

doi:10.1016/j.ajem.2020.11.025

Cited by 87 publications

(76 citation statements)

References 4 publications

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“…The WHO ordinal scale, stratifying patients according to their oxygen therapy requirement, has been widely used as a correlate of COVID-19 severity. Additionally, a wide range of nonspecific indicators of systemic inflammation, including among others C-reactive protein (CRP), ferritin, serum amyloid A (SAA), procalcitonin, lactate dehydrogenase (LDH), D-dimer, IL-6, IL-10, white cell count (WCC), or neutrophil count, have been associated with adverse COVID-19 outcomes ( 36 – 39 ). Furthermore, higher levels of SARS-CoV-2–specific antibodies have been shown to associate with increased COVID-19 severity ( 40 , 41 ).…”

Section: Resultsmentioning

confidence: 99%

Relationship of SARS-CoV-2–specific CD4 response to COVID-19 severity and impact of HIV-1 and tuberculosis coinfection

Riou¹,

Bruyn²,

Stek³

et al. 2021

Journal of Clinical Investigation

135

105

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T cells are involved in control of coronavirus disease 2019 (COVID-19), but limited knowledge is available on the relationship between antigen-specific T cell response and disease severity. Here, we used flow cytometry to assess the magnitude, function, and phenotype of SARS coronavirus 2–specific (SARS-CoV-2–specific) CD4 + T cells in 95 hospitalized COVID-19 patients, 38 of them being HIV-1 and/or tuberculosis (TB) coinfected, and 38 non–COVID-19 patients. We showed that SARS-CoV-2–specific CD4 + T cell attributes, rather than magnitude, were associated with disease severity, with severe disease being characterized by poor polyfunctional potential, reduced proliferation capacity, and enhanced HLA-DR expression. Moreover, HIV-1 and TB coinfection skewed the SARS-CoV-2 T cell response. HIV-1–mediated CD4 + T cell depletion associated with suboptimal T cell and humoral immune responses to SARS-CoV-2, and a decrease in the polyfunctional capacity of SARS-CoV-2–specific CD4 + T cells was observed in COVID-19 patients with active TB. Our results also revealed that COVID-19 patients displayed reduced frequency of Mycobacterium tuberculosis –specific CD4 + T cells, with possible implications for TB disease progression. These results corroborate the important role of SARS-CoV-2–specific T cells in COVID-19 pathogenesis and support the concept of altered T cell functions in patients with severe disease.

show abstract

Section: Resultsmentioning

confidence: 99%

Relationship of SARS-CoV-2–specific CD4 response to COVID-19 severity and impact of HIV-1 and tuberculosis coinfection

Riou¹,

Bruyn²,

Stek³

et al. 2021

Journal of Clinical Investigation

135

105

View full text Add to dashboard Cite

show abstract

“…However, in addition to immune activation, we and others have shown that mtDAMPs induce functional tolerance, with neutrophils pre-treated with mtDAMPs or mtDAMP mimetics exhibiting significantly impaired calcium mobilisation, chemotaxis and NET generation upon secondary stimulation with inflammatory or pharmacological agonists ( 216 , 219 – 221 ). To date, whilst several studies have reported evidence of cellular injury and inflammatory cell death in patients with severe COVID-19 ( 23 , 26 , 222 ), few have directly screened blood samples for the presence of DAMPs. However, in those that have, significantly elevated levels of the nuclear-derived DAMPs high mobility group box-1 (HMGB-1) and extracellularly-secreted nicotinamide phosphoribosyl-transferase (eNAMPT), as well as mitochondrial-derived DNA (mtDNA) were detected in the plasma of severe COVID-19 patients when compared to HCs and/or mild to moderate COVID-19 cases ( 205 , 223 , 224 ).…”

Section: Neutrophil Tolerance In Severe Covid-19mentioning

confidence: 99%

Neutrophils and COVID-19: Active Participants and Rational Therapeutic Targets

Hazeldine

Lord

2021

Front. Immunol.

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Whilst the majority of individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative pathogen of COVID-19, experience mild to moderate symptoms, approximately 20% develop severe respiratory complications that may progress to acute respiratory distress syndrome, pulmonary failure and death. To date, single cell and high-throughput systems based analyses of the peripheral and pulmonary immune responses to SARS-CoV-2 suggest that a hyperactive and dysregulated immune response underpins the development of severe disease, with a prominent role assigned to neutrophils. Characterised in part by robust generation of neutrophil extracellular traps (NETs), the presence of immature, immunosuppressive and activated neutrophil subsets in the circulation, and neutrophilic infiltrates in the lung, a granulocytic signature is emerging as a defining feature of severe COVID-19. Furthermore, an assessment of the number, maturity status and/or function of circulating neutrophils at the time of hospital admission has shown promise as a prognostic tool for the early identification of patients at risk of clinical deterioration. Here, by summarising the results of studies that have examined the peripheral and pulmonary immune response to SARS-CoV-2, we provide a comprehensive overview of the changes that occur in the composition, phenotype and function of the neutrophil pool in COVID-19 patients of differing disease severities and discuss potential mediators of SARS-CoV-2-induced neutrophil dysfunction. With few specific treatments currently approved for COVID-19, we conclude the review by discussing whether neutrophils represent a potential therapeutic target for the treatment of patients with severe COVID-19.

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“…The WHO ordinal scale, stratifying patients according to their oxygen therapy requirement, has been widely used as correlate of COVID-19 severity. Additionally, a wide range of non-specific indicators of systemic inflammation (including amongst others: C-reactive protein (CRP), ferritin, serum amyloid A (SAA), procalcitonin, lactate dehydrogenase (LDH), D-dimer, IL-6, IL-10, white cell count or neutrophil count) have been associated with adverse COVID-19 outcome (Chen et al, 2020b; Izcovich et al, 2020; Szarpak et al, 2020; Zhang et al, 2020). Furthermore, higher levels of SARS-CoV-2-specific antibodies have been shown to associate with increased COVID-19 severity (Bosnjak et al, 2020; Klein et al, 2020).…”

Section: Resultsmentioning

confidence: 99%

Profile of SARS-CoV-2-specific CD4 T cell response: Relationship with disease severity and impact of HIV-1 and activeMycobacterium tuberculosisco-infection

Riou

Bruyn

Stek

et al. 2021

Preprint

View full text Add to dashboard Cite

T cells are involved in control of COVID-19, but limited knowledge is available on the relationship between antigen-specific T cell response and disease severity. Here, we assessed the magnitude, function and phenotype of SARS-CoV-2-specific CD4 T cells in 95 hospitalized COVID-19 patients (38 of them being HIV-1 and/or tuberculosis (TB) co-infected) and 38 non-COVID-19 patients, using flow cytometry. We showed that SARS-CoV-2-specific CD4 T cell attributes, rather than magnitude, associates with disease severity, with severe disease being characterized by poor polyfunctional potential, reduced proliferation capacity and enhanced HLA-DR expression. Moreover, HIV-1 and TB co-infection skewed the SARS-CoV-2 T cell response. HIV-1 mediated CD4 T cell depletion associated with suboptimal T cell and humoral immune responses to SARS-CoV-2; and a decrease in the polyfunctional capacity of SARS-CoV-2-specific CD4 T cells was observed in COVID-19 patients with active TB. Our results also revealed that COVID-19 patients displayed reduced frequency of Mtb-specific CD4 T cells, with possible implications for TB disease progression. There results corroborate the important role of SARS-CoV-2-specific T cells in COVID-19 pathogenesis and support the concept of altered T cell functions in patients with severe disease.

show abstract

Lactate dehydrogenase level as a COVID-19 severity marker

Cited by 87 publications

References 4 publications

Relationship of SARS-CoV-2–specific CD4 response to COVID-19 severity and impact of HIV-1 and tuberculosis coinfection

Relationship of SARS-CoV-2–specific CD4 response to COVID-19 severity and impact of HIV-1 and tuberculosis coinfection

Neutrophils and COVID-19: Active Participants and Rational Therapeutic Targets

Profile of SARS-CoV-2-specific CD4 T cell response: Relationship with disease severity and impact of HIV-1 and activeMycobacterium tuberculosisco-infection

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