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The Application Value of Lipoprotein Particle Numbers in the Diagnosis of HBV-Related Hepatocellular Carcinoma with BCLC Stage 0-A.

ABSTRACT: Early diagnosis is essential for improving the prognosis and survival of patients with hepatocellular carcinoma (HCC). This study aims to explore the clinical value of lipoprotein subfractions in the diagnosis of hepatitis B virus (HBV)-related HCC. Lipoprotein subfractions were detected by ¹H-NMR spectroscopy, and the pattern-recognition method and binary logistic regression were performed to classify distinct serum profiles and construct prediction models for HCC diagnosis. Differentially expressed proteins associated with lipid metabolism were detected by LC-MS/MS, and the potential prognostic significance of the mRNA expression was evaluated by Kaplan-Meier survival analysis. The diagnostic panel constructed from the serum particle number of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL-1~LDL-6) achieved higher accuracy for the diagnosis of HBV-related HCC and HBV-related benign liver disease (LD) than that constructed from serum alpha-fetoprotein (AFP) alone in the training set (AUC: 0.850 vs. AUC: 0.831) and validation set (AUC: 0.926 vs. AUC: 0.833). Furthermore, the panel achieved good diagnostic performance in distinguishing AFP-negative HCC from AFP-negative LD (AUC: 0.773). We also found that lipoprotein lipase (LPL) transcript levels showed a significant increase in cancerous tissue and that high expression was significantly positively correlated with the poor prognosis of patients. Our research provides new insight for the development of diagnostic biomarkers for HCC, and abnormal lipid metabolism and LPL-mediated abnormal serum lipoprotein metabolism may be important factors in promoting HCC development.

SUBMITTER: Zuo D

PROVIDER: S-EPMC8617679 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background and Aims: Although previous studies suggested that female patients who underwent curative resection in early-stage hepatocellular carcinoma (HCC) had better survival rates than male patients, it is unclear whether females in different HCC stages actually have survival advantage. This study aimed to investigate whether gender differences in the Barcelona Clinic Liver Cancer (BCLC) classification system contributed to different survival outcomes in hepatitis B virus (HBV)-related HCC. Methods: A retrospective analysis was performed of 1,753 patients diagnosed with HBV-related HCC between January 2008 and June 2017 at the Beijing Ditan hospital. The BCLC stages were classified into BCLC stage 0-B and BCLC stage C-D groups. Factors determining overall survival (OS) and progression-free survival (PFS) were analyzed via univariate and multivariate analysis using the Kaplan-Meier method and Cox proportional-hazards regression models. Results: The cohort consisted of 1,202 BCLC stage 0-B and 551 BCLC stage C-D HBV-related HCC patients. Gender was identified to be an independent risk factor for OS (HR = 0.617; 95% CI, 0.426-0.895; p = 0.011) and PFS (HR = 0.728; 95% CI, 0.558-0.950; p = 0.019) in BCLC stage 0-B HBV-related HCC patients. With respect to OS and PFS, there were significant differences between female and male patients only in BCLC stage 0-B, but not in BCLC stage C-D. The OS and PFS in BCLC stage 0-B for female patients was significantly greater than that for male patients (p = 0.0103, p = 0.0112). Tumor multiplicity and size were independent risk factors for female patients in BCLC stage 0-B, whereas tumor multiplicity, tumor size, HBV-DNA, hemoglobin, total bilirubin, and alpha-fetoprotein levels were independent risk factors for male patients in BCLC stage 0-B. Conclusions: Different outcomes in OS or PFS with respect to gender only exist in BCLC stage 0-B HBV-related HCC patients. Female patients have a better outcome than male patients in BCLC stage 0-B.

Project description:BACKGROUND:It is unclear how high-protein (HP) and high-monounsaturated fat (HMF) meals affect postprandial blood lipids and lipoprotein particle numbers (LPN). PURPOSE:To compare a HP versus a HMF meal on postprandial lipid and LPN responses. METHODS:Twenty-four participants (age: 36.3±15.0 years; body mass index: 23.6±2.0 kg/m2; 45.8% female) were fed a HP (31.9% energy from protein) and a HMF (35.2% fat and 20.7% monounsaturated fat) meal in a randomized cross-over trial design. Energy and carbohydrate content were the same across meals. Blood samples were drawn in the fasting state and 3 hour postprandial state, and assessed for lipids and LPN. RESULTS:Repeated measures analysis showed a significant (p<0.05) treatment by time interaction effect for triglycerides (TG), the primary variable, total high-density lipoprotein particles (T-HDLP) and T-HDLP minus large-buoyant high-density lipoprotein 2b (T-HDLP-LB-HDL2b). HP versus HMF condition led to significantly lower TG at 120 (geometric mean: 90.1 (95% confidence interval (CI): 76.4-106.3) vs. 146.5 (124.2-172.9) mg/dL) and 180 (101.4 (83.1-123.8) vs. 148.7 (121.9-181.4) mg/dL) min and higher T-HDLP at 120 (mean difference: 297.3 (95% CI: 48.6-545.9) nmol/L) and 180 (291.6 (15.8-567.5) nmol/L) min. The difference in T-HDLP by condition was due to the significantly higher small-dense HDLP (T-HDLP-LB-HDL2b) during HP versus HMF condition at 120 (mean difference: 452.6 (95% CI: 177.4-727.9) nmol/L) and 180 (496.8 (263.1-730.6) nmol/L) min. Area under the curve analysis showed that HP versus HMF condition led to significantly lower TG, non-HDLP, and very-low-density lipoprotein particles (VLDLP) responses but significantly less favorable responses in LB-HDL2b particles, T-HDLP-LB-HDL2b, and LB-HDL2b/T-HDLP ratio. CONCLUSION:The HP meal led to lower TG, non-HDLP, and VLDLP but less favorable LB-HDL2b, small-dense HDLP, and LB-HDL2b/T-HDLP ratio responses versus a HMF meal. Further studies are needed to confirm these findings over multiple meals.

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The Application Value of Lipoprotein Particle Numbers in the Diagnosis of HBV-Related Hepatocellular Carcinoma with BCLC Stage 0-A.

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