Intriguing findings of liver fibrosis following COVID-19

Background: Studies on a new coronavirus disease (COVID-19) show the elevation of liver enzymes and liver fibrosis index (FIB-4) independently on pre-existing liver diseases. It points to increased liver fibrogenesis during acute COVID-19 with possible long-term consequences. This study aimed to assess liver fibrosis in COVID-19 patients by serum hyaluronic acid (HA) and FIB-4. Methods: The study included the acute COVID-19 group (66 patients, 50% females, mean age 58.3 +/- 14.6), the post-COVID group (58 patients in 3-6 months after the recovery, 47% females, mean age 41.2 +/- 13.4), and a control group (17 people, 47% females, mean age 42.8 +/- 11.0). Ultrasound elastography was performed in the post-COVID and control groups. Results: Sixty-five percent of the acute COVID-19 group had increased FIB-4 (> 1.45), and 38% of patients had FIB-4 >= 3.25. After matching by demographics, 52% of acute COVID-19 and 5% of the post-COVID group had FIB-4 > 1.45, and 29% and 2% of patients had FIB-4 >= 3.25, respectively. Increased serum HA (>= 75 ng/ml) was observed in 54% of the acute COVID-19 and 15% of the post-COVID group. In the acute COVID-19 group, HA positively correlated with FIB-4, AST, ALT, LDH, IL-6, and ferritin and negatively with blood oxygen saturation. In the post-COVID group, HA did not correlate with FIB-4, but it was positively associated with higher liver stiffness and ALT. Conclusion: More than half of acute COVID-19 patients had increased serum HA and FIB-4 related to liver function tests, inflammatory markers, and blood oxygen saturation. It provides evidence for the induction of liver fibrosis by multiple factors during acute COVID-19. Findings also indicate possible liver fibrosis in about 5% of the post-COVID group.

Automated summary

The study found that more than half of acute COVID-19 patients had increased serum HA and FIB-4, which were related to liver function tests, inflammatory markers, and blood oxygen saturation, highlighting evidence for the induction of liver fibrosis by multiple factors during acute COVID-19.