Abstract
Analysis of liver biopsy specimens showed that SARS-CoV-2 might have led to liver damage. This study aimed to evaluate the role of selected hepatokines and myokines in the development and progression of COVID-19. Seventy patients with laboratory-confirmed COVID-19 and 20 healthy volunteers were enrolled in the study. Irisin, pentraxin 3, fetuin-A, and FGF-21 serum concentrations and biochemical parameters were assessed using an immunoenzymatic method with commercially available enzyme immunoassay (EIA) or enzyme-linked immunosorbent assay (ELISA) kits. Serum fetuin-A concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers. The serum concentration of FGF-21 was significantly increased in obese COVID-19 patients compared to overweight ones. Moreover, the FGF-21 level was higher in COVID-19 patients diagnosed with metabolic syndrome than in patients without metabolic syndrome. PTX3 concentration was higher in COVID-19 patients with higher HOMA-IR values than those with lower HOMA-IR values. COVID-19 patients with HOMA-IR ≤ 3 and >3 had significantly lower fetuin-A levels than the control group. Irisin concentration was significantly decreased in the HOMA-IR ≤ 3 COVID-19 subgroup when comparing with the control group. Lower levels of fetuin-A observed in COVID-19 patients despite higher HOMA-IR, CRP, and ferritin levels, pneumonia, patients requiring ICU care suggests that fetuin-A deficiency predisposes to more severe COVID-19 course. Upregulated pentraxin 3 may be used as a potential predictor of COVID-19 severity.
Highlights
Coronavirus (CoV) is a highly diverse family of single-stranded RNA viruses causing human and animal diseases [1]
Baseline Characteristics and Biochemical Parameters Analyzed in the Serum of COVID-19
Elevated levels of IL-6 are a good marker of poor outcomes in patients with severe COVID-19 with pneumonia and acute respiratory distress syndrome (ARDS) [5]
Summary
Coronavirus (CoV) is a highly diverse family of single-stranded RNA viruses causing human and animal diseases [1]. Some human coronaviruses, such as HCoV-229E and HCoVOC43 or HCoV-NL63 and HCoV-HKU1, cause seasonal respiratory infections usually associated with mild symptoms known as the ‘common cold’. Other human coronaviruses such as severe acute respiratory syndrome coronavirus (SARSCoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) cause infections of bronchial epithelial cells, pneumocytes, and upper respiratory tract cells leading to severe, life-threatening respiratory pathologies and lung injuries. Whereas SARS-CoV-2 infection induces activation of adaptive and innate immune responses, resulting in massive inflammation, the metabolic diseases cause low-grade inflammation with chronically elevated lower levels of inflammatory mediators that is impossible to resolve spontaneously. Low-grade inflammation induces (through the release of inflammatory cytokines) inhibition of insulin signaling, which, when associated with SARS-CoV-2 infection and the accompanying ‘cytokine storm’, starts a vicious cycle [4,5]
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