Published online Dec 27, 2023. doi: 10.4254/wjh.v15.i12.1315
Peer-review started: September 20, 2023
First decision: October 25, 2023
Revised: November 3, 2023
Accepted: November 21, 2023
Article in press: November 21, 2023
Published online: December 27, 2023
Processing time: 95 Days and 20 Hours
Hepatitis C virus (HCV) infection can cause severe liver damage. Chronic HCV infection can be cured with direct acting antiviral therapy, which also decreases insulin resistance. Omentin-1 is regarded a beneficial adipokine and improves insulin resistance. Serum omentin-1 levels are increased in HCV infection. The effect of viral cure on serum omentin-1 levels has not been analysed as far as we know. Moreover, data regarding associations of omentin-1 with liver injury are discordant.
From a pathophysiological standpoint, it can be important to evaluate associations of serum omentin-1 levels with HCV infection and liver disease severity.
The objective of this study was to assess the effect of HCV clearance on serum omentin-1 levels, and to evaluate associations of serum omentin-1 levels with clinical markers of inflammation, liver steatosis, diabetes and liver dysfunction.
This observational study included 84 patients with chronic HCV, and collected serum before therapy, at 4 wk after therapy start, at therapy end and at sustained viological response 12 (SVR12). Serum omentin-1 was measured by enzyme-linked immunosorbent assay. Serum omentin-1 levels of 14 controls were also determined.
The study found evidence of increased serum omentin-1 levels in patients with liver cirrhosis. HCV elimination did not change serum omentin-1 levels, suggesting that viral infection has no effect on serum omentin-1.
Effective elimination of HCV is associated with favourable metabolic outcomes. This study indicates that omentin-1 has no role herein. Serum omentin-1 of HCV patients with liver cirrhosis is increased at baseline and SVR12, and may have a role in liver cirrhosis pathogenesis.
Evaluation whether increased serum omentin-1 is just a marker of impaired liver function or contributes to liver damage.