Intriguing findings of liver fibrosis following COVID-19

Abstract

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.

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis

“…Pulmonary fibrosis and liver fibrosis are among critical complications in severe COVID-19 patients [34] , [35] , [36] . Therefore, it is imperative to understand the underlying pathomechanisms of tissue fibrosis observed in COVID-19.…”

Gene Network Analysis of the Transcriptome Impact of SARS-CoV-2 Interacting MicroRNAs in COVID-19 Disease

“…PI3K–Akt signaling is also involved in the development of fibrotic processes [ 98 , 99 ] in the lungs [ 100 , 101 ] and liver; of note, COVID-19-related liver fibrosis can develop independently of pre-existing chronic liver disease [ 102 ]. The link between liver fibrogenesis, microRNA, and the PI3K signaling pathway was investigated; in an experimental liver fibrosis model, Lei et al reported that miR-101 has a strong antifibrotic effect through downregulation of the PI3K-Akt signaling pathway [ 103 ].…”

Hepatic dysfunctions in COVID-19 patients infected by the omicron variant of SARS-CoV-2

“…Thereby, the liver injury in COVID-19 patients is acute but transient and mild, and commonly with minimal inflammation, albeit the fatal liver damages have also been sparsely reported in the previously heathy COVID-19 patients (42,43). Insofar, health outcomes following 6, 12, and 24 months after disease onset have not specified the expansive liver-related consequence in long COVID cases (44); however, increased liver fibrogenesis was notified in patients 3-6 months post COVID (45).…”