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Serum Lipid Metabolic Derangement is Associated with Disease Progression During Chronic HBV Infection
Insights
Serum lipid levels, including HDL cholesterol and APOA, are lower in chronic hepatitis B virus (HBV) infection. As HBV disease progresses to cirrhosis, lipid levels significantly decrease, indicating metabolic derangement.
Area of Science:
- Hepatology
- Virology
- Clinical Biochemistry
Background:
- Chronic hepatitis B virus (HBV) infection is a global health concern.
- Understanding the interplay between HBV infection and host lipid metabolism is crucial for disease management.
Purpose of the Study:
- To investigate the relationship between serum lipid profiles and the progression of chronic hepatitis B virus (HBV) infection.
- To assess how lipid levels change across different stages of HBV infection, from carrier state to chronic hepatitis and liver cirrhosis.
Main Methods:
- A cohort study involving 163 patients with chronic HBV infection and 73 healthy controls.
- Patients were categorized into HBV carrier, chronic hepatitis B, and liver cirrhosis groups.
- Statistical analyses included t-tests, Mann-Whitney U tests, one-way ANOVA, and Kruskal-Wallis tests to compare demographic, clinical, and biochemical parameters.
Main Results:
- Serum high-density lipoprotein (HDL) cholesterol and Apolipoprotein A (APOA) concentrations were significantly lower in patients with HBV infection compared to healthy controls.
- As HBV disease advanced to liver cirrhosis, total cholesterol (TC), HDL cholesterol, low-density lipoprotein (LDL) cholesterol, and Apolipoprotein B (APOB) levels were significantly reduced.
- A positive correlation was observed between serum HBV DNA levels and HDL cholesterol in the carrier and chronic hepatitis B groups, but not in the cirrhosis group.
Conclusions:
- Serum lipid metabolic derangement is significantly associated with the progression of chronic HBV infection.
- Patients with hepatitis B-related cirrhosis exhibit significantly lower liver function and blood lipid levels, highlighting the impact of advanced disease on host metabolism.
Background:
To investigate the relationship between serum lipid levels and disease progression during chronic hepatitis B virus infection.
Methods:
We selected 73 healthy controls and 163 patients with chronic HBV infection as the study subjects. The chronic HBV infection patients were divided into the HBV carrier group (74 patients), chronic hepatitis B group (71 patients), and liver cirrhosis group (21 patients). The age, gender, body mass index, blood lipid index, liver function index, and HBV DNA levels of all participants were tested and recorded. A t-test or the Mann-Whitney U test was used to compare the data between two groups; data from multiple groups were compared using one-way ANOVA or the Kruskal-Wallis Test.
Results:
We observed that the serum HDL cholesterol (1.00 ± 0.30 mmol/L in the HBV-infected group, 1.29 ± 0.23 mmol/L in the control group) and APOA (1.29 ± 0.35 mmol/L, 1.36 ± 0.21 mmol/L, respectively) concentrations were significantly lower in the HBV-infected group than in the control group (p < 0.05). As the disease progressed, the blood lipid and lipoprotein values were significantly lower in the cirrhosis group TC (3.26 ± 1.00 mmol/L), HDL cholesterol (0.77 ± 0.33 mmol/L), LDL cholesterol (2.09 ± 0.62 mmol/L), and APOB (0.57 ± 0.18 mmol/L) compared with the control group, the carrier group, and the chronic hepatitis B group (p < 0.05). The serum HBV DNA level was significantly, positively correlated with the blood HDL concentration (carrier group R = 0.340, p = 0.02; chronic hepatitis B group R = 0.329, p = 0.014). There was no correlation between the HBV DNA and lipid levels in patients with cirrhosis.
Conclusions:
Serum lipid metabolic derangement was associated with disease progression during chronic HBV infection. Liver function and blood lipid levels were significantly lower in patients with hepatitis B-related cirrhosis.
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