Serum lipid alterations identified in chronic hepatitis B, hepatitis B virus-associated cirrhosis and carcinoma patients

Abstract

The incidences of chronic hepatitis B (CHB), Hepatitis B virus (HBV)-associated cirrhosis and HBV-associated carcinoma are high and increasing. This study was designed to evaluate serum lipid metabolite changes that are associated with the progression from CHB to HBV-associated cirrhosis and ultimately to HBV-associated HCC. A targeted metabolomic assay was performed in fasting sera from 136 CHB patients, 104 HBV-associated cirrhosis, and 95 HBV-associated HCC using ultra-performance liquid chromatography triple quadrupole mass spectrometry. A total of 140 metabolites were identified. Clear separations between each two groups were obtained using the partial least squares discriminate analysis of 9 lipid metabolites. Progressively lower levels of long-chain lysophosphatidylcholines (lysoPC a C18:2, lysoPC a C20:3, lysoPC a C20:4) were observed from CHB to cirrhosis to carcinoma; lower levels of lysoPC a C20:4 were found in patients with higher model for end-stage liver disease in the same disease group; and lysoPC a C20:3 levels were lower in Child-Pugh Class C than in Class A and Class B in HBV-associated cirrhosis and HBV-associated HCC groups. The octadecadienyl carnitine level was higher in HBV-associated cirrhosis group than in other two groups. Serum levels of selected long-chain lysoPCs are promising markers for the progression of HBV-associated liver diseases.

A retrospective cohort study of preoperative lipid indices and their impact on new‐onset diabetes after liver transplantation

“…In this large sample of Chinese LTRs, the incidence of NODAT in the first postoperative year increased to 30.3%, which is consistent with the findings of previous reports . The preoperative lipid profile of our study population was characterized by prevalent hypocholesterolemia and hypotriglyceridemia, and similar findings were reported by studies of patients with HBV‐associated cirrhosis or carcinoma, which are the two leading causes of liver transplantation . In the present study, discordant associations between preoperative lipid indices and incident NODAT were observed.…”

Analysis of plasma metabolic profile, characteristics and enzymes in the progression from chronic hepatitis B to hepatocellular carcinoma

“…The sensitivity and specificity of AFP, a tumor marker widely used in the clinic, are not notably high [ 23 ], and most patients are already in an advanced stage. Researchers have been looking for new blood markers of HCC, such as AFP-L3, DCP and SCCA [ 24 ], and have evaluated serum metabolism during the progression from CHB to HCC [ 10 , 11 ], but they have not been widely used. In this study, we found that the panel of L-serine, creatine and glycine distinguished LC from CHB, and L-serine, cystathionine, creatine and linoleic acid distinguished HCC from LC and NC, indicating that the panels of multiple DMs may be beneficial to distinguish CHB, LC, and HCC.…”

“…Previous studies have identified the serum metabolic profiles in the progression of HBV infection to HCC using a non-targeted gas chromatography-time of flight-mass spectrometry (GC-TOFMS), and 15 metabolites were determined to be intimately associated with the process [ 10 ]. Wu T et al evaluated the dynamic change in serum lipid metabolism during the progression from CHB to HCC by targeted metabolomics analysis and concluded that the serum levels of long-chain lysophosphatidylcholines (lysoPCs) were promising markers of HBV-associated carcinoma [ 11 ]. In addition, most of the related studies on HCC metabolism have focused on glucose metabolism [ 12 , 13 ] and fatty acids metabolism [ 14 ], and relatively little is known about other metabolic pathways.…”

Patterns and prevalence of dyslipidemia in patients with different etiologies of chronic liver disease

“…The HCV-RNA circulates in large spherical particles, which bind in a competitive way with LDL and VLDL [20] and inhibition of microsomal triglyceride transfer protein by HCV infection leads to reduced VLDL secretion by hepatocytes, ultimately leading to decreased serum concentrations of VLDL and LDL [21]. In HBV, on the other hand, serum lipid levels are not affected [22], leading to higher absolute serum cholesterol levels than in HCV. Based on the findings in this large patient cohort, further research on the association between dyslipidemia, steatosis and CLD of different etiologies is warranted.…”