Severe COVID-19 Associated With Liver Injury in Patients Without Preexisting Liver Disease

Objective: Coronavirus disease 2019 (COVID-19) is known to disturb liver function tests (LFTs). Not much literature is available regarding the effect of COVID-19 on LFTs in patients without preexisting liver disease. The study aimed to find the effect of COVID-19 in these patients. Methods: This was a single-center, observational study with 142 patients who were admitted with COVID-19 during three months. Seven patients were excluded due to the presence of chronic liver disease. Results: A total of 135 patients were included in the study aged between 18 and 95 years (mean 57.7 ± 15.6); among them, 93 were males (68.9%). Hypertension was present in 74 patients (54.8%), and diabetes was present in 48 patients (35.6%). Fever was the chief complaint in 112 patients (83%), followed by dyspnea in 93 patients (68.9%) and cough in 79 patients (58.5%). Elevated aspartate aminotransferase (AST) was seen in 35 patients (26%), gamma-glutamyl transferase (GGT) in 43 patients (32%), alanine transaminase (ALT) in 18 patients (24%), alkaline phosphatase in 19 patients (14%), bilirubin in six patients (4%), and low albumin in 27 patients (20%). Severe COVID-19, when compared with mild to moderate disease, was associated with elevated AST > two-time upper limit normal (2ULN) (p = 0.002), GGT > 2ULN (0.026), and lower albumin (p = 0.020), higher systemic inflammatory response syndrome (SIRS) (0.045), raised procalcitonin (p = 0.045), higher ferritin (p = 0.005), lower pO2 (p = 0.044), and higher Sequential Organ Failure Assessment score (SOFA) (p = 0.002) pointing to the inflammatory response as cause of liver injury. Factors predicting mortality with COVID-19 were assessed, which showed that direct bilirubin (p = 0.001), low albumin (p = 0.013), tachypnea (0.002), and leukocytosis (<0.001) were independently associated with increased COVID-19-related mortality. Conclusion: Patients suffering from COVID-19 have evidence of liver injury, which appears to be secondary to an inflammatory response that correlates with the severity of COVID-19.