Serum levels of α1-antitrypsin, interleukin-1β and interleukin-6 in Iraqi COVID-19 patients: A cross-sectional study

Abstract

Background: More than half of the individuals diagnosed with coronavirus disease 2019 (COVID-19) have been found to have high levels of interleukin (IL)-6. A recent report showed that more elevated serum IL-6 level predicts COVID-19 disease severity and patients’ clinical outcomes. Therefore, this study aimed to compare the serum levels of α1-antitrypsin (AAT), IL-1β, and IL-6 between COVID-19 patients and healthy individuals. Methods: During the data collection phase, 90 individuals were enrolled, 45 healthy controls, and 45 patients confirmed with COVID-19 using reverse transcription-quantitative PCR (RT-qPCR) at a specialized isolation hospital in Baghdad between November 2021 and March 2022. In this cross-sectional research, venous blood samples were taken, and serum was isolated and stored for quantitative ELISA measurements of AAT, IL-1β, and IL-6 (ELISA). IBM SPSS version 24 was used to analyze the data. Results: This study revealed a significant increase in the serum levels of AAT, IL-1β, and IL-6 in the COVID-19 patients' group compared to the healthy control group with p-values < 0.001 for each of these markers. Conclusions: AAT concentrations were higher during COVID-19; this elevation is essential during infection. IL-1β and IL-6 levels were also elevated during the infection period; however, dysregulated high levels may lead to cytokine release syndrome. Therefore, these three biomarkers can be regarded as diagnostically crucial parameters.

Serum angiopoietin 1 level in patients with severe COVID-19: An observational study

“…Disruption of the endothelial thromboprotective role might lead to hypercoagulation, as primarily described in these patients. 14,15 In a prospective study, Smadja et al, showed that SARS-CoV-2 infection is accompanied by elevated levels of the soluble endothelial activation markers, namely, soluble E-selectin and angiopoietin-2, in critically ill hospitalized COVID-19 patients. 31 Angiopoietin-2, a context-dependent competitive antagonist of angiopoietin-1, is an essential regulator of endothelial homeostasis, angiogenesis, and proliferation through the angiopoietin/Tie-2 pathway.…”

“…13 COVID-19 patients display a state of increased coagulability and thrombotic tendency. 14,15 Antithrombotic prophylaxis represents an essential part of the treatment plan to prevent the development of pulmonary embolism and deep vein thrombosis that develop in severe cases or cases with increased d-dimer. [16][17][18] However, despite antithrombotic prophylaxis, approximately 30% of patients with severe COVID-19 admitted to the intensive care unit have developed arterial and venous thrombotic events, increasing the mortality risk in these patients by 5.4 times.…”

The Inhibition of Serine Proteases by Serpins Is Augmented by Negatively Charged Heparin: A Concise Review of Some Clinically Relevant Interactions

“…Furthermore, the evidence implicates AAT deficiency itself-and not its pulmonary sequelae of emphysema or bronchiectasis-as a major risk factor for the SARS-CoV-2 infection [78]. Even without an AAT deficiency, the AAT response may be insufficient in critically ill COVID-19 patients [87,88], perhaps due to the AAT heterozygosity (e.g., the protease inhibitor (Pi)MZ) that results in a suboptimal increase in AAT levels [6] or to the oxidation of normal AAT in highly oxidative states such as severe COVID-19, causing loss of its serpin activity [89] or inducing its polymerization [9,90]. Interestingly, the IL-6 receptor antagonists (e.g., tocilizumab) that are used as an adjunctive anti-inflammatory treatment for patients with severe COVID-19 recalcitrant to glucocorticoids may reduce AAT expression (since IL-6 induces AAT) [91].…”

Alpha-1-antitrypsin antagonizes COVID-19: a review of the epidemiology, molecular mechanisms, and clinical evidence

“…children), COPD has yet to be detected in them, or have undiagnosed AAT deficiency-associated liver disease. Even in the absence of frank AAT deficiency, the AAT response to a systemic infection may be inadequate as has been shown for hospitalized COVID-19 patients [ 44 , 45 ] and among millions with certain heterozygous AAT mutations (PiMZ) [ 39 ]. Furthermore, oxidation of methionine 351 and/or 358 of even normal AAT may cause loss of its serpin activity [ 46 ].…”