Effect of ABO blood groups on length of hospital stay according to age in Covid-19 patients

Gürsoy, Vildan; Avcı, Sinan

doi:10.1016/j.htct.2021.08.013

“…In the Turkish population, studies examining this risk were conducted [15][16][17]. The joint results found in these studies; people with group A are more likely to be infected, but the blood group does not have a significant effect on the course of the diseaseexcept for the study of Sertbas et al, which showed that the risk of intubation increased in the AB group [16].…”

Section: Discussionmentioning

confidence: 99%

Exploring the distribution and prognostic effect of the ABO blood types of COVID-19 patients during delta and omicron waves: A case control study

Göker

¹

,

Çınar

²

,

Ismayilov

³

et al. 2023

Acta Medica

0

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Objective: We aimed to delineate the effects of the ABO groups and the main clinical outcomes with the current SARS-CoV-2 variants, i.e., delta and omicron. Materials and Methods: In this retrospective case-control study, the total 360 adult COVID-19 patients who were followed in the pandemic waves of delta and omicron variants and had ABO blood group analysis were included and divided into two groups according to the waves of variant. Demographic characteristics, comorbidities, length of hospitalization and intensive care needs, survival and ABO groups of cases were recorded. These groups were then compared with the ABO group distribution of population-reflecting 1881 healthy individuals and 186 historical alpha variant cases. Results: The demographic characteristics of the case groups and control group were similar. ABO distributions of the delta and omicron wave groups compared to the control group did not show a statistically significant difference. While advanced age (p<0.001) and presence of comorbidity (p=0.006) showed statistically significant differences in terms of overall survival, ABO blood group was not found to be a risk factor for mortality (p=0.114 in delta, and 0.526 in omicron), hospitalization time (p=0.148 in delta, p=0.224 in omicron), and intensive care unit admission (p=0.096 in delta, p=0.229 in omicron). Conclusion: The risk of infection among ABO blood groups, which has been shown in previous studies for the alpha variant against group A and in favor of group O, does not appear to be valid for delta and omicron period patients. Therefore, the anti-infective measures, especially vaccination, should not differ for individuals according to ABO blood group.

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“…Some contrasting literature data were reported on the specific subjects' different susceptibility to the viral attack, based on determined genetic mutations, blood groups/diseases, specific receptors expression. 73,193,311,[353][354][355][356][357][358][359][360] Beyond a specific possible TMPRSS2-related predisposition on a genetic or epigenetic (e.g. diabetic and obese patients) basis, 361 the majority of these speculations refer both to the variability of the membrane expression of certain receptors (namely SA and CD147), and to the consequent cation dysmetabolism.…”

Section: Discussionmentioning

confidence: 99%

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

Cavezzi

¹

,

Menicagli

²

,

Troiani³

et al. 2022

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Background: iron and calcium dysmetabolism, with hyperferritinemia, hypoferremia, hypocalcemia and anemia have been documented in the majority of COVID-19 patients at later/worse stages. Furthermore, complementary to ACE2, both sialic acid (SA) molecules and CD147 proved relevant host receptors for SARS-CoV-2 entry, which explains the viral attack to multiple types of cells, including erythrocytes, endothelium and neural tissue. Several authors advocated that cell ferroptosis may be the core and final cell degenerative mechanism. Methods: a literature research was performed in several scientific search engines, such as PubMed Central, Cochrane Library, Chemical Abstract Service. More than 500 articles were retrieved until mid-December 2021, to highlight the available evidence about the investigated issues. Results: based on COVID-19 literature data, we have highlighted a few pathophysiological mechanisms, associated with virus-based cation dysmetabolism, multi-organ attack, mitochondria degeneration and ferroptosis. Our suggested elucidated pathological sequence is: a) spike protein subunit S1 docking with sialylated membrane glycoproteins/receptors (ACE2, CD147), and S2 subunit fusion with the lipid layer; b) cell membrane morpho-functional changes due to the consequent electro-chemical variations and viroporin action, which induce an altered ion channel function and intracellular cation accumulation; c) additional intracellular iron concentration due to a deregulated hepcidin-ferroportin axis, with higher hepcidin levels. Viral invasion may also affect erythrocytes/erythroid precursors, endothelial cells and macrophages, through SA and CD147 receptors, with relative hemoglobin and iron/calcium dysmetabolism. AB0 blood group, hemochromatosis, or environmental elements may represent possible factors which affect individual susceptibility to COVID-19. Conclusions: our literature analysis confirms the combined role of SA molecules, ACE2, CD147, viroporins and hepcidin in determining the cation dysmetabolism and final ferroptosis in the cells infected by SARS-CoV-2. The altered ion channels and electrochemical gradients of the cell membrane have a pivotal role in the virus entry and cell dysmetabolism, with subsequent multi-organ immune-inflammatory degeneration and erythrocyte/hemoglobin alterations.

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“…Some contrasting literature data were reported on the specific subjects' different susceptibility to the viral attack, based on determined genetic mutations, blood groups/diseases, specific receptors expression. 71,191,309,[348][349][350][351][352][353][354][355] Beyond a specific possible TMPRSS2-related predisposition on a genetic or epigenetic (e.g. diabetic and obese patients) basis, 356 the majority of these speculations refer both to the variability of the membrane expression of certain receptors (namely SA and CD147), and to the consequent cation dysmetabolism.…”

Section: Discussionmentioning

confidence: 99%

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

Cavezzi

¹

,

Menicagli

²

,

Troiani

³

et al. 2022

F1000Res

5

0

View full text Add to dashboard Cite

Background: iron and calcium dysmetabolism, with hyperferritinemia, hypoferremia, hypocalcemia and anemia have been documented in the majority of COVID-19 patients at later/worse stages. Furthermore, complementary to ACE2, both sialic acid (SA) molecules and CD147 proved relevant host receptors for SARS-CoV-2 entry, which explains the viral attack to multiple types of cells, including erythrocytes, endothelium and neural tissue. Several authors advocated that cell ferroptosis may be the core and final cell degenerative mechanism. Methods: a literature research was performed in several scientific search engines, such as PubMed Central, Cochrane Library, Chemical Abstract Service. More than 500 articles were retrieved until mid-December 2021, to highlight the available evidence about the investigated issues. Results: based on COVID-19 literature data, we have highlighted a few pathophysiological mechanisms, associated with virus-based cation dysmetabolism, multi-organ attack, mitochondria degeneration and ferroptosis. Our suggested elucidated pathological sequence is: a) spike protein subunit S1 docking with sialylated membrane glycoproteins/receptors (ACE2, CD147), and S2 subunit fusion with the lipid layer; b) cell membrane morpho-functional changes due to the consequent electro-chemical variations and viroporin action, which induce an altered ion channel function and intracellular cation accumulation; c) additional intracellular iron concentration due to a deregulated hepcidin-ferroportin axis, with higher hepcidin levels. Viral invasion may also affect erythrocytes/erythroid precursors, endothelial cells and macrophages, through SA and CD147 receptors, with relative hemoglobin and iron/calcium dysmetabolism. AB0 blood group, hemochromatosis, or environmental elements may represent possible factors which affect individual susceptibility to COVID-19. Conclusions: our literature analysis confirms the combined role of SA molecules, ACE2, CD147, viroporins and hepcidin in determining the cation dysmetabolism and final ferroptosis in the cells infected by SARS-CoV-2. The altered ion channels and electrochemical gradients of the cell membrane have a pivotal role in the virus entry and cell dysmetabolism, with subsequent multi-organ immune-inflammatory degeneration and erythrocyte/hemoglobin alterations.

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Effect of ABO blood groups on length of hospital stay according to age in Covid-19 patients

Cited by 6 publications

References 30 publications

Exploring the distribution and prognostic effect of the ABO blood types of COVID-19 patients during delta and omicron waves: A case control study

Exploring the distribution and prognostic effect of the ABO blood types of COVID-19 patients during delta and omicron waves: A case control study

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

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