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?:abstract
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Background Liver injury is commonly seen in coronavirus disease 2019 (COVID-19). However, the mechanism behind liver injury, particularly in severe and critical COVID-19 patients, remains unclear and the clinical course is poorly described. Methods We conducted a single-center, retrospective cohort study of consecutive hospitalized severe and critically ill COVID-19 patients with or without liver injury who underwent immunologic testing (IL-6, IL-8, TNF-α, and IL-1ß). Liver injury was defined as peak aminotransferases ≥3x ULN (40 U/L) or ≥120 U/L. Patients with liver injury were compared to those who had normal aminotransferases throughout the hospital course. Results 176 patients were studied; 109 with liver injury and 67 controls. Patients with liver injury were more likely to be male (71.6% vs 37.3%; p < 0.001). Peak inflammatory markers and IL-6 were higher in the liver injury group: CRP: 247 vs 168 mg/L, p < 0.001; LDH: 706 vs 421 U/L, ferritin: 2,973 vs 751 ng/mL, p < 0.001, IL-6: 121.0 vs 71.8, p < 0.001. There was no difference in the levels of IL-8, TNF-α, and IL-1ß. The liver injury group had a longer length of stay and more severe COVID-19 despite having less diabetes and chronic kidney disease. Discussion An exaggerated hyper inflammatory response (cytokine storm) characterized by significantly elevated CRP, LDH, ferritin, and IL-6 levels and increasing severity of COVID-19 appears to be associated with the occurrence of liver injury in patients with severe/ critical COVID-19.
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