Abstract
Objective In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. The aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Methods A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T0) and 24 hours after canakinumab administration (T1). Results At T0, 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07–0.25). In the 13 patients undergoing canakinumab administration, at T1, Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T0: median 0.24, IQR 0.09–0.31 mmol/L; T1: median −0.01, IQR −0.08–0.04 mmol/L; p=0.002). Conclusion A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.
Highlights
Erefore, we performed the present study with the following aims: to describe the Delta a-cv lactate in a population of patients affected by severe COVID-19 pneumonia and to evaluate if the reduction/normalization of the Delta a-cv lactate was positively affected by canakinumab administration
All adult patients consecutively admitted to the intensive care unit (ICU) with severe COVID-19 pneumonia who required sedation and invasive mechanical ventilation were considered for inclusion
23 patients suffering from COVID19-related pneumonia were admitted to the ICU
Summary
Arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. E aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Erefore, we performed the present study with the following aims: to describe the Delta a-cv lactate in a population of patients affected by severe COVID-19 pneumonia (early warning tool) and to evaluate if the reduction/normalization of the Delta a-cv lactate was positively affected by canakinumab administration (early response tool)
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