No evidence of hemoglobin damage by SARS-CoV-2 infection

DeMartino, Anthony; Rose, Jason J.; Amdahl, Matthew B.; Dent, Matthew R.; Shah, Faraaz; Bain, William; McVerry, Bryan J.; Kitsios, Georgios D; Tejero, Jesús; Gladwin, Mark T.

doi:10.3324/haematol.2020.264267

Cited by 35 publications

(39 citation statements)

References 30 publications

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“…In the laboratory exams (Table 2), the hemoglobin levels did not change among the groups, which is consistent with more recent findings showing no evidence of hemoglobin damage by SARS-CoV-2 infection (22). In the present study, severe and critical patients had increased plasma ferritin levels compared to mild ones, as has been reported in other studies (23,24).…”

Section: Discussionsupporting

confidence: 92%

Quantitative plasma proteomics of survivor and non-survivor COVID-19 patients admitted to hospital unravels potential prognostic biomarkers and therapeutic targets

Flora

Dionízio

Pereira

et al. 2021

Preprint

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The development of new approaches that allow early assessment of which cases of COVID-19 will likely become critical and the discovery of new therapeutic targets are urgent demands. In this cohort study, we performed proteomic and laboratorial profiling of plasma from 163 patients admitted to Bauru State Hospital (Bauru, SP, Brazil) between May 4th and July 4th, 2020, who were diagnosed with COVID-19 by RT-PCR nasopharyngeal swab samples. Plasma samples were collected upon admission for routine laboratory analyses and shotgun quantitative label-free proteomics. Based on the course of the disease, the patients were further divided into 3 groups: a) mild symptoms, discharged without admission to an intensive care unit (ICU) (n=76); b) severe symptoms, discharged after admission to an ICU (n=56); c) critical, died after admission to an ICU (n=31). White cells and neutrophils were significantly higher in severe and critical patients compared to mild ones. Lymphocytes were significantly lower in critical patients compared to mild ones and platelets were significantly lower in critical patients compared to mild and severe ones. Ferritin, TGO, urea and creatinine were significantly higher in critical patients compared to mild and severe ones. Albumin, CPK, LDH and D-dimer were significantly higher in severe and critical patients compared to mild ones. PCR was significantly higher in severe patients compared to mild ones. Proteomic analysis revealed marked changes between the groups in plasma proteins related to complement activation, blood coagulation, antimicrobial humoral response, acute inflammatory response, and endopeptidase inhibitor activity. Higher levels of IREB2, GELS, POLR3D, PON1 and ULBP6 upon admission to hospital were found in patients with mild symptoms, while higher levels of Gal-10 were found in critical and severe patients. This needs to be validated in further studies. If confirmed, pathways involving these proteins might be potential new therapeutic targets for COVID-19.

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Section: Discussionsupporting

confidence: 92%

Quantitative plasma proteomics of survivor and non-survivor COVID-19 patients admitted to hospital unravels potential prognostic biomarkers and therapeutic targets

Flora

Dionízio

Pereira

et al. 2021

Preprint

View full text Add to dashboard Cite

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“…Although hemoglobin-related biomarkers such as serum ferritin, progressively increase as the severity of COVID-19 increases [134][135][136], there is very limited evidence supporting this hypothesis [133]. This hypothesis has subsequently been refuted by DeMartino and colleagues, confirming that disease markers such as hemoglobin, iron and ferritin did not differ between critically ill COVID-19 patients and non-COVID ARDS patients [137].…”

Section: Hyperferritinemia As a Results Of Hyperinflammation Can Induce A Cytokine Stormmentioning

confidence: 99%

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Demeulemeester¹,

Punder²,

Heijningen³

et al. 2021

Cells

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Emerging data suggest that obesity is a major risk factor for the progression of major complications such as acute respiratory distress syndrome (ARDS), cytokine storm and coagulopathy in COVID-19. Understanding the mechanisms underlying the link between obesity and disease severity as a result of SARS-CoV-2 infection is crucial for the development of new therapeutic interventions and preventive measures in this high-risk group. We propose that multiple features of obesity contribute to the prevalence of severe COVID-19 and complications. First, viral entry can be facilitated by the upregulation of viral entry receptors, like angiotensin-converting enzyme 2 (ACE2), among others. Second, obesity-induced chronic inflammation and disruptions of insulin and leptin signaling can result in impaired viral clearance and a disproportionate or hyper-inflammatory response, which together with elevated ferritin levels can be a direct cause for ARDS and cytokine storm. Third, the negative consequences of obesity on blood coagulation can contribute to the progression of thrombus formation and hemorrhage. In this review we first summarize clinical findings on the relationship between obesity and COVID-19 disease severity and then further discuss potential mechanisms that could explain the risk for major complications in patients suffering from obesity.

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“…C3) [27,89]. The hemoglobin level is often decreased in COVID-19 patients [29,62], but the underlying molecular mechanism of this phenomenon is not yet identi ed [84,90,91]. However, the lower levels seem to correlate with increased levels of the iron-storage protein ferritin.…”

Section: Discussionmentioning

confidence: 99%

Linking COVID-19 and heme-driven pathophysiologies: A combined computational-experimental approach

Hopp

Domingo‐Fernándéz

Gadiya

et al. 2021

Preprint

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The SARS-CoV-2 outbreak has been declared a worldwide pandemic in 2020. Infection triggers the respiratory tract disease COVID-19, which is accompanied by serious changes of clinical biomarkers such as hemoglobin and interleukins. The same parameters are altered during hemolysis, which is characterized by an increase in labile heme. We present two computational-experimental approaches that aim at analyzing a potential link between heme-related and COVID-19 pathophysiologies. Herein, we performed a detailed analysis of the common pathways induced by heme and SARS-CoV-2 by superimposition of knowledge graphs covering heme biology and COVID-19 pathophysiology. Focus was laid on inflammatory pathways and distinct biomarkers as the linking elements. In a second approach, four COVID-19-related proteins, the host cell proteins ACE2 and TMPRSS2 as well as the viral protein 7a and S protein, were computationally analyzed as potential heme-binding proteins with an experimental validation. The results contribute to the understanding of the progression of COVID-19 infections in patients with different clinical backgrounds and might allow for a more individual diagnosis and therapy in the future.

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No evidence of hemoglobin damage by SARS-CoV-2 infection

Cited by 35 publications

References 30 publications

Quantitative plasma proteomics of survivor and non-survivor COVID-19 patients admitted to hospital unravels potential prognostic biomarkers and therapeutic targets

Quantitative plasma proteomics of survivor and non-survivor COVID-19 patients admitted to hospital unravels potential prognostic biomarkers and therapeutic targets

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Linking COVID-19 and heme-driven pathophysiologies: A combined computational-experimental approach

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