Differences between the metabolic profiles of decompensated and compensated cirrhosis patients with Hepatitis B virus infections under high-performance liquid chromatography-mass spectrometry

Abstract

To improve the grading and staging of liver cirrhosis among patients with HBV infection noninvasively, a high-performance liquid chromatography with mass spectrometry metabolomics method was used to investigate the potential metabolic biomarkers in the serum of patients with different degrees of hepatic cirrhosis. The results demonstrate that lysophosphatidyl choline (LPC) from positive electrospray ionization (ESI) mode, and fatty acids and bile acids from negative ESI mode play important roles in distinguishing decompensated from compensated cirrhosis. A total of 21 differential metabolites were found from the two groups of patients. LPCs, fatty acids, and taurocholic acid (TCA) 3-sulfate decreased in patients with decompensated cirrhosis, whereas other bile acids increased significantly. The levels of TCA 3-sulfate, LPC 16:0, and LPC 18:0 were significantly correlated with the stages of the decompensated cirrhosis, and they may serve as potential biomarkers for the stage assessment of liver cirrhosis in patients with HBV infections.

Proteomic and metabonomic biomarkers for hepatocellular carcinoma: a comprehensive review

“…The conflicting reports on the serum concentrations may be a result of heterogenic patient groups, in terms of different diets, gender, comorbidities (such as cardiovascular diseases), and of course the extent of liver damage, that is the hepatic compensation/decompensation status. As was the case for bile acids and LPCs, FFA levels seem to be also influenced by background liver disease ( Chen et al , 2012 ). The association of FFA 16 : 0 and FFA 18 : 0 with hepatitis B and cirrhosis has been described by Chen et al , 2011b , who investigated HCC patients with and without LC and hepatitis separately.…”

“…Interestingly, higher bile acid serum levels (glycochenodeoxycholic acid, glycocholic acid, CA, and deoxycholic acid (DCA)) have been found in HCC patients with cirrhosis, than without ( Chen et al , 2011b ), which may indicate that the bile acid concentration is primarily associated with cirrhosis or overall hepatic performance. Evidence for this is given by Chen et al , 2012 , who found serum bile acids increased in patients with hepatic decompensation, when compared to compensated patients. A closer look at the HCC cohorts' characteristics of the matched studies reveals that only a few assessed and included the extent of liver disease in the background of HCC or the hepatic compensation/decompensation status in their analyses ( Table 2 ).…”

“…This upregulation of LPCAT1 could account for the depletion of LPC C16 : 0. However, some LPC species, including 16 : 0, LPC 18 : 0, LPC 20 : 4, and LPC 20 : 5 have also been described as differentially expressed between hepatic decompensated and compensated patients ( Chen et al , 2012 ). As mentioned before, many studies did not control for the background liver disease, that is, hepatic performance, which could have biased the described findings.…”