Liver Injury During New Epidemic Occurrence of COVID-19.

Background: SARS-CoV-2, though primarily a respiratory pathogen, exhibits multi-organ tropism, with the liver among the commonly affected organs. Elevations in liver enzymes are frequent in hospitalized COVID-19 patients, yet acute and pronounced hepatocellular injury in young, clinically stable individuals is uncommon. The underlying mechanisms may include direct viral cytopathic effects mediated by ACE2 receptors, immune-mediated injury, systemic inflammation, and metabolic stress. Notably, hepatic involvement can develop independently of respiratory compromise. Objective: The aim of this case report was to describe three adult patients with serologically confirmed SARS-CoV-2 infection and mild respiratory symptoms who presented with acute liver injury in the absence of other identifiable causes. Case report: During a confirmed COVID-19 wave in Bosnia and Herzegovina, a targeted outpatient study was performed in a family medicine setting. Routine liver testing was conducted for all suspected COVID-19 cases. Laboratory evaluation included liver enzymes, hepatitis serology, autoimmune markers, and inflammatory parameters, with imaging (ultrasound or MRI) to exclude structural pathology. Three previously healthy male patients (aged 25-45) developed acute liver injury during mild febrile illness, all with serologically confirmed SARS-CoV-2 infection (positive IgM and IgG). Retrospective assessment revealed unrecognized metabolic dysfunction-associated steatotic liver disease (MASLD) in all cases. Initial symptoms were fatigue and myalgia without respiratory distress. Laboratory findings demonstrated marked elevations of AST and ALT (>1000 U/L), GGT (>900 U/L), and raised ferritin and D-dimer, while bilirubin remained normal. This biochemical profile - disproportionately elevated transaminases and GGT with preserved bilirubin - was consistent across cases, suggesting SARS-CoV-2-related hepatocellular injury. All patients recovered rapidly with supportive outpatient care, without progression to liver failure. Conclusion: Clinically stable COVID-19 patients may experience acute hepatocellular injury, particularly those with underlying metabolic dysfunction such as MASLD. The recurring biochemical pattern of significantly elevated AST, ALT, GGT, and ferritin with normal bilirubin suggests a distinctive SARS-CoV-2-associated liver injury phenotype. Recognition of this presentation is essential for appropriate evaluation and management. Routine liver function monitoring should be considered in COVID-19 patients, regardless of respiratory symptom severity, especially in those with metabolic risk factors.