The Agreed Experts’ Position of the Eurasian Association of Therapists on Some new Mechanisms of COVID-19 Pathways: Focus on Hemostasis, Hemotransfusion Issues and Blood gas Exchange

Arutyunov, G. P.; Козиолова, Н. А.; Tarlovskaya, E. I.; Arutyunov, A G; Grigorjeva, N Yu; Джунусбекова, Г А; Malchikova, S. V.; Mitkovskaya, N. P.; Orlova, Yа A; Петрова, М. М.; Ребров, А. П.; Sisakyan, A S; Skibitsky, V. V.; Sugraliyev, Akhmetzhan; Фомин, И. В.; Чесникова, А. И.; Шапошник, И. И.

doi:10.18087/cardio.2020.5.n1132

Cited by 23 publications

(6 citation statements)

References 40 publications

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“…The process of SARS-CoV-2 reproduction involves Spike-protein (S-protein) glycosylation infecting target cells [3,4]. It is assumed that SARS-CoV-2 infects erythrocytes and captures the porphyrin to inhibit heme metabolism [3,5], resulting in elevated HbA1c in the acute stage of the disease.…”

Section: Introductionmentioning

confidence: 99%

Glycated hemoglobin level dynamics in COVID-19 survivors: 12 months follow-up study after discharge from hospital

et al. 2022

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Introduction One of the stages of reproduction of SARS-CoV-2 is the S-protein glycosylation to facilitate penetration into target cells. It has been suggested that SARS-CoV-2 is able to enter erythrocytes, interact with heme and porphyrin, which could influence HbA1c levels. Assessment of HbA1c levels in individuals with acute COVID-19 and after recovery may show clinical relevance of this hypothesis. Aim To assess HbA1c levels in patients with COVID-19 in the acute phase and in early (6–8 weeks) and late (52±2 weeks) periods after recovery. Materials and methods We conducted a multicenter prospective study, which included patients hospitalized in Endocrinology Research Centre and the City Clinical Hospital № 52" diagnosed with COVID-19, virus identified/ not identified. Patients were divided into three groups according to baseline HbA1c level and the presence or absence of previous history of diabetes previous history of diabetes mellitus (DM): HbA1c ≤ 6.0%, HbA1c > 6.0% and patients with DM. Patients were examined during the acute COVID-19 phase and in early (6–8 weeks) and late (52±2 weeks) periods after recovery. Oral glucose tolerance test was performed in the group with initial HbA1c > 6.0% to clarify the diagnosis. Results We included 194 patients in the study. During the follow-up, 52 patients were examined in 6–8 week period: 7 with HbA1c ≤ 6.0%, 34 with HbA1c > 6.0%, 11—with previously diagnosed DM. Carbohydrate metabolism assessment in the later stages (52±2 weeks) after recovery was performed in 78 patients: 33 patients with HbA1c ≤ 6.0%, 36 patients with HbA1c > 6.0% and 9 patients with previously established diabetes. HbA1c median in patients with HbA1c ≤ 6.0% was 5.7% [5.3;5.8], with HbA1c>6.0% -6.4% [6.2; 6.6], with previously diagnosed DM—7.7% [7.2; 8.9]. Statistically significant decrease in HbA1c over time 6–8 weeks after extracts were obtained in both groups of individuals without a history of DM (Wilcoxon test, p<0.05). After 52±2 weeks we observed HbA1c decrease in all three groups (Fridman test, p<0.05): in patients with HbA1c ≤ 6.0% median HbA1c was 5.5[5.3;5.7], with HbA1c>6.0% - 6.1[6.15;6.54], with previously diagnosed DM—7.8 [5.83; 8.08]. Development of DM after 52±2 weeks was recorded in 7.24% of all examined patients without a history of DM, which is 16.6% of the total number of patients examined in dynamics with HbA1c > 6.0%. Conclusion HbA1c elevation during the acute phase of COVID-19 may be false due to the effect of SARS-CoV-2 on hemoglobin kinetics and/or detection on the surface of the SARS-CoV-2 virion highly glycosylated S-proteins by high performance liquid chromatography determinations. Upon detection HbA1c > 6.0% in patients with COVID-19 in the active phase of the disease without concomitant hyperglycemia re-determine the level of HbA1c after recovery is recommended.

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Section: Introductionmentioning

confidence: 99%

Glycated hemoglobin level dynamics in COVID-19 survivors: 12 months follow-up study after discharge from hospital

et al. 2022

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“…It degrades heme to bilirubin, free iron, and carbon monoxide and plays an important role in the antioxidant and antiapoptotic activity of the cells [192]. The high-affinity binding of the SARS-CoV-2 spike protein to porphyrin [193] upregulates the formation of reactive oxygen species (ROS) and free heme and decreases the level of HO-1 [192,194,195]. Therefore, the SARS-CoV-2-porphyrin complex may cause impairment of HO-1 signaling by downregulating HO-1 gene expression, which results in severe oxidative stress induced by free heme and iron [192,194,196].…”

Section: Heme Oxygenasementioning

confidence: 99%

Human gene polymorphisms and their possible impact on the clinical outcome of SARS-CoV-2 infection

et al. 2021

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The SARS-CoV-2 pandemic has become one of the most serious health concerns globally. Although multiple vaccines have recently been approved for the prevention of coronavirus disease 2019 (COVID-19), an effective treatment is still lacking. Our knowledge of the pathogenicity of this virus is still incomplete. Studies have revealed that viral factors such as the viral load, duration of exposure to the virus, and viral mutations are important variables in COVID-19 outcome. Furthermore, host factors, including age, health condition, co-morbidities, and genetic background, might also be involved in clinical manifestations and infection outcome. This review focuses on the importance of variations in the host genetic background and pathogenesis of SARS-CoV-2. We will discuss the significance of polymorphisms in the ACE-2, TMPRSS2, vitamin D receptor, vitamin D binding protein, CD147, glucose‐regulated protein 78 kDa, dipeptidyl peptidase-4 (DPP4), neuropilin-1, heme oxygenase, apolipoprotein L1, vitamin K epoxide reductase complex 1 (VKORC1), and immune system genes for the clinical outcome of COVID-19.

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“…The consequence of COVID-19 binding the porphyrin molecules results in decreased functional hemoprotein, which has clinical manifestations [ 4 ]. A hemoprotein is a protein linked to iron (Fe).…”

Section: Consequences Of Hemoprotein Malfunction/deficiencymentioning

confidence: 99%

“…The early presenting signs and symptoms of the coronavirus are very non-specific [ 3 ]. SARS-CoV-2, the virus that causes COVID-19, has a tremendous ability to bind porphyrins with even stronger affinity than ACE-2 receptors, resulting in the upregulation of free heme, an oxidant, and severe reactive oxygen species (ROS) formation, and decreased levels of heme oxygenase-1 enzymes (HO-1) [ 4 ]. Some have found these assertions controversial [ 5 ] but these findings may provide insight into the pathophysiologic process occurring with COVID-19 infection and possible treatment options.…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms Complicate COVID-19 Therapy: Pivotal Role of HO-1 in Cytokine Storm

et al. 2020

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Coronaviruses are very large RNA viruses that originate in animal reservoirs and include severe acute respiratory distress syndrome (SARS) and Middle East respiratory syndrome (MERS) and other inconsequential coronaviruses from human reservoirs like the common cold. SARS-CoV-2, the virus that causes COVID-19 and is believed to originate from bat, quickly spread into a global pandemic. This RNA virus has a special affinity for porphyrins. It invades the cell at the angiotensin converting enzyme-2 (ACE-2) receptor and binds to hemoproteins, resulting in a severe systemic inflammatory response, particularly in high ACE-2 organs like the lungs, heart, and kidney, resulting in systemic disease. The inflammatory response manifested by increased cytokine levels and reactive oxygen species results in inhibition of heme oxygenase (HO-1), with a subsequent loss of cytoprotection. This has been seen in other viral illness like human immunodeficiency virus (HIV), Ebola, and SARS/MERS. There are a number of medications that have been tried with some showing early clinical promise. This illness disproportionately affects patients with obesity, a chronic inflammatory disease with a baseline excess of cytokines. The majority of the medications used in the treatment of COVID-19 are metabolized by cytochrome P450 (CYP) enzymes, primarily CYP2D6. This is further complicated by genetic polymorphisms of CYP2D6, HO-1, ACE, and ACE-2. There is a potential role for HO-1 upregulation to treat/prevent cytokine storm. Current therapy must focus on antivirals and heme oxygenase upregulation. Vaccine development will be the only magic bullet.

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The Agreed Experts’ Position of the Eurasian Association of Therapists on Some new Mechanisms of COVID-19 Pathways: Focus on Hemostasis, Hemotransfusion Issues and Blood gas Exchange

Cited by 23 publications

References 40 publications

Glycated hemoglobin level dynamics in COVID-19 survivors: 12 months follow-up study after discharge from hospital

Glycated hemoglobin level dynamics in COVID-19 survivors: 12 months follow-up study after discharge from hospital

Human gene polymorphisms and their possible impact on the clinical outcome of SARS-CoV-2 infection

Genetic Polymorphisms Complicate COVID-19 Therapy: Pivotal Role of HO-1 in Cytokine Storm

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