Haemoglobin oxygen affinity in patients with severe COVID‐19 infection

Daniel, Yvonne; Hunt, Beverley J.; Retter, Andrew; Henderson, Katherine; Wilson, Sarah M.; Sharpe, Claire C.; Shattock, Michael J.

doi:10.1111/bjh.16888

Cited by 46 publications

(59 citation statements)

References 10 publications

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“…The duration of the disease is generally more prolonged compared to acute respiratory distress syndrome (ARDS) from other aetiologies 1 . As reported by Daniel et al 5 . in this Journal, haemoglobin (Hb) oxygen (O 2 ) affinity in 14 patients with COVID‐19 was not different from 11 control participants, when affinity was measured in vitro with a Hemox analyser, with a standardised pH (7·4) and temperature.…”

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confidence: 54%

A left shift in the oxyhaemoglobin dissociation curve in patients with severe coronavirus disease 2019 (COVID‐19)

et al. 2020

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Critically ill patients with coronavirus disease 2019 (COVID‐19) present with hypoxaemia and are mechanically ventilated to support gas exchange. We performed a retrospective, observational study of blood gas analyses (n = 3518) obtained from patients with COVID‐19 to investigate changes in haemoglobin oxygen (Hb–O2) affinity. Calculated oxygen tension at half‐saturation (p50) was on average (±SD) 3·3 (3·13) mmHg lower than the normal p50 value (23·4 vs. 26·7 mmHg; P < 0·0001). Compared to an unmatched historic control of patients with other causes of severe respiratory failure, patients with COVID‐19 had a significantly higher Hb–O2 affinity (mean [SD] p50 23·4 [3·13] vs. 24·6 [5.4] mmHg; P < 0·0001). We hypothesise that, due to the long disease process, acclimatisation to hypoxaemia could play a role.

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confidence: 54%

A left shift in the oxyhaemoglobin dissociation curve in patients with severe coronavirus disease 2019 (COVID‐19)

et al. 2020

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“…However, this interpretation of the data seems to be confuted by recent reassuring evidence of the lack of alteration of gas exchange and oxygen affinity properties in COVID patients. 31 , 32 On the contrary, damage to the N-term of AE1 may compromise the RBC capacity to inhibit glycolysis and activate the PPP in response to oxidant stress, making the RBCs from COVID patients more susceptible to oxidant stress. Because the damage to AE1 is irreversible, RBCs circulate for up to 120 days without de novo protein synthesis capacity, and this damage may contribute to explaining some of the long-lasting sequelae to COVID-19.…”

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confidence: 99%

Evidence of Structural Protein Damage and Membrane Lipid Remodeling in Red Blood Cells from COVID-19 Patients

et al. 2020

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The SARS-CoV-2 beta coronavirus is the etiological driver of COVID-19 disease, which is primarily characterized by shortness of breath, persistent dry cough, and fever. Because they transport oxygen, red blood cells (RBCs) may play a role in the severity of hypoxemia in COVID-19 patients. The present study combines state-of-the-art metabolomics, proteomics, and lipidomics approaches to investigate the impact of COVID-19 on RBCs from 23 healthy subjects and 29 molecularly diagnosed COVID-19 patients. RBCs from COVID-19 patients had increased levels of glycolytic intermediates, accompanied by oxidation and fragmentation of ankyrin, spectrin beta, and the N-terminal cytosolic domain of band 3 (AE1). Significantly altered lipid metabolism was also observed, in particular, short- and medium-chain saturated fatty acids, acyl-carnitines, and sphingolipids. Nonetheless, there were no alterations of clinical hematological parameters, such as RBC count, hematocrit, or mean corpuscular hemoglobin concentration, with only minor increases in mean corpuscular volume. Taken together, these results suggest a significant impact of SARS-CoV-2 infection on RBC structural membrane homeostasis at the protein and lipid levels. Increases in RBC glycolytic metabolites are consistent with a theoretically improved capacity of hemoglobin to off-load oxygen as a function of allosteric modulation by high-energy phosphate compounds, perhaps to counteract COVID-19-induced hypoxia. Conversely, because the N-terminus of AE1 stabilizes deoxyhemoglobin and finely tunes oxygen off-loading and metabolic rewiring toward the hexose monophosphate shunt, RBCs from COVID-19 patients may be less capable of responding to environmental variations in hemoglobin oxygen saturation/oxidant stress when traveling from the lungs to peripheral capillaries and vice versa.

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“…13 Daniel et al highlight the fact that the oxygen-carrying function of haemoglobin in COVID-19 infection patients is not affected in venous or arterial blood. 1 However, this does not rule out the possibility of significant deviation of ODC to the right in the alveolo-capillary bed because of the presence of heterotropic allosteric effectors related to COVID-19. In the scenario where there is an overload of such effectors, the haemoglobin may change its quaternary state R to T (tense), which has a very low hyperbolic-type ODC with a Hill coefficient less than or equal to 1.…”

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confidence: 95%

“…Daniel et al investigated haemoglobin's affinity to oxygen in patients with severe COVID-19 infection. 1 The authors discuss an important problem. Currently, there are insufficient data on the early pathophysiological changes preceding the development of pneumonia with significant hypoxaemia and full-range acute respiratory distress syndrome (ARDS) in patients infected with COVID-19.…”

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confidence: 99%