OBJECTIVE: Our main aim was to investigate the serum lipid levels in a series of patients with liver cirrhosis of viral origin. SUBJECTS AND METHODS: The study comprised 90 patients, 60 with viral liver cirrhosis, equally divided between hepatitis virus C (HCV) and B (HBV) etiologies, and 30 control patients with no known liver pathology. Patients were investigated during a 5-year period in the 1st Medical Clinic of the Emergency County Hospital of Craiova, Romania. The following series of serum lipid parameters were recorded: lipemia, total cholesterol and cholesteryl ester, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglyceride (TG) values. Statistical analysis of these parameters was performed using the ANOVA test followed by Tukey multiple comparison tests to compare replicate means; p < 0.05 was considered statistically significant. RESULTS: We observed significantly lower values for serum lipids (543.5 and 549.37 mg/dl in the HBV and HCV cirrhosis subgroups, compared with 649.9 mg/dl in controls), total cholesterol (143.6 and 147.9 vs. 198.0 mg/dl, respectively), cholesteryl esters (83.6 and 80, compared to 147.9 mg/dl, respectively), LDL cholesterol (91.6 and 88.5 vs. 132.4 mg/dl) in both cirrhosis groups when compared with controls (p < 0.001), as well as HDL cholesterol (32.1 and 36.9 vs. 47.3 mg/dl, p < 0.05). However, TG and VLDL cholesterol values of controls and cirrhosis groups were similar (p > 0.05). We did not register any differences between the two cirrhosis groups (p > 0.05). CONCLUSION: Our data showed that both HCV and HBV cirrhosis severely impaired liver lipid metabolism. Late stages of the disease resulted in a pseudonormalization of VLDL cholesterol and TG values.
OBJECTIVE: Our main aim was to investigate the serum lipid levels in a series of patients with liver cirrhosis of viral origin. SUBJECTS AND METHODS: The study comprised 90 patients, 60 with viral liver cirrhosis, equally divided between hepatitis virus C (HCV) and B (HBV) etiologies, and 30 control patients with no known liver pathology. Patients were investigated during a 5-year period in the 1st Medical Clinic of the Emergency County Hospital of Craiova, Romania. The following series of serum lipid parameters were recorded: lipemia, total cholesterol and cholesteryl ester, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglyceride (TG) values. Statistical analysis of these parameters was performed using the ANOVA test followed by Tukey multiple comparison tests to compare replicate means; p < 0.05 was considered statistically significant. RESULTS: We observed significantly lower values for serum lipids (543.5 and 549.37 mg/dl in the HBV and HCV cirrhosis subgroups, compared with 649.9 mg/dl in controls), total cholesterol (143.6 and 147.9 vs. 198.0 mg/dl, respectively), cholesteryl esters (83.6 and 80, compared to 147.9 mg/dl, respectively), LDL cholesterol (91.6 and 88.5 vs. 132.4 mg/dl) in both cirrhosis groups when compared with controls (p < 0.001), as well as HDL cholesterol (32.1 and 36.9 vs. 47.3 mg/dl, p < 0.05). However, TG and VLDL cholesterol values of controls and cirrhosis groups were similar (p > 0.05). We did not register any differences between the two cirrhosis groups (p > 0.05). CONCLUSION: Our data showed that both HCV and HBV cirrhosis severely impaired liver lipid metabolism. Late stages of the disease resulted in a pseudonormalization of VLDL cholesterol and TG values.