Abstract
COVID-19 patients suffer from hypercoagulation and activated immune-inflammatory pathways. The current study examined the relationship between specific complements and coagulation abnormalities associated with chest CT scan anomalies (CCTAs) and peripheral oxygen saturation (SpO2) in COVID-19 patients. Serum levels of complement C3 and C4, and thromboxane A2 (TxA2) and prostacyclin (PGI2) were measured using an ELISA and albumin, calcium, and magnesium by using the spectrophotometric method in 60 COVID-19 patients and 30 controls. C3 and C4 were significantly decreased (p < 0.001), and TxA2 and PGI2 significantly increased (p < 0.001) in the COVID-19 patients compared with the controls with the highest levels in the CCTA patients’ group. Neural networks showed that a combination of C3, albumin, and TxA2 yielded a predictive accuracy of 100% in detecting COVID-19 patients. SpO2 was significantly decreased in the COVID-19 patients and was inversely associated with TxA2 and PGI2, and positively with C3, C4, albumin, and calcium. Patients with positive IgG results show significantly higher SpO2, TxA2, PGI2, and C4 levels than IgG-negative patients. CCTAs were accompanied by lower SpO2 and albumin and increased PGI2 and TxA2 levels, suggesting that interactions between immune-inflammatory pathways and platelet hyperactivity participate in the pathophysiology of COVID-19 and, consequently, may play a role in an enhanced risk of hypercoagulability and venous thromboembolism. These mechanisms are aggravated by lowered calcium and magnesium levels.
Highlights
The positive IgG group showed a nificant increase in SpO2, thromboxane A2 (TxA2), PGI2, and C4 compared with the patients with negative significant increase in SpO2, TxA2, PGI2, and C4 compared with the patients with negative
In agreement with Al-Hakeim et al (2020) and other studies reviewed in the latter paper [31], this study found that serum albumin, calcium, and magnesium were significantly lowered in COVID-19
COVID-19 is characterized by significantly decreased SpO2, C3, and C4 and significantly increased TxA2 and PGI2
Summary
The COVID-19 virus enters the lung cells after binding viral Spike proteins-S with the ACE2 receptors [5] and, the virus may cause histopathological lesions in the lungs, which appear to be similar to those observed in other forms of ARDS [6]. Complement activation may result in immune-mediated lung damage [8] and is central to the pathophysiology of lung disorders, including asthma, ARDS [9], and severe COVID-19 disease, which often resembles complementopathies [7]. Ghazavi et al (2020) detected increased C3 and C4 complement levels in non-severe COVID-19 but lower levels in severe COVID-19 patients, which could be explained by increased consumption by forming immune complexes [12]. Low serum C3 levels are detected in critically ill COVID-19 patients and are associated with a poor prognosis [13]
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