Peter Jarčuška1, Martin Janičko2, Peter Kružliak3, Miroslav Novák4, Eduard Veselíny5, Ján Fedačko6, Gabriela Senajová7, Sylvia Dražilová8, Andrea Madarasová-Gecková9, Mária Mareková10, Daniel Pella11, Leonard Siegfried12, Pavol Kristián13, Eva Kolesárová14. 1. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: petjarc@yahoo.com. 2. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: martin.janicko@gmail.com. 3. Department of Cardiovascular Diseases, International Clinical Research Center, St. Anne's University Hospital, Masaryk University, Pekarska 53, 656 91 Brno, Czech Republic; Division of Cardiovascular Diseases, Mayo Clinic and Mayo College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: kruzliakpeter@gmail.com. 4. Department of Cardiovascular Diseases, International Clinical Research Center, St. Anne's University Hospital, Masaryk University, Pekarska 53, 656 91 Brno, Czech Republic; Division of Cardiovascular Diseases, Mayo Clinic and Mayo College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: miroslav.novak@FNUSA.cz. 5. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: veseliny@yahoo.com. 6. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: janfedacko@hotmail.com. 7. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: gabrielasenajova@gmail.com. 8. Internal Department, Poprad Hospital, Banícka 803/28, 05845 Poprad, Slovakia. Electronic address: drazilova.s@nemocnicapp.sk. 9. Department of Public Health, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: geckova.andrea.madarasova@upjs.sk. 10. Department of Medical Biochemistry, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: maria.marekova@upjs.sk. 11. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: daniel.pella@upjs.sk. 12. Department of Medical Microbiology, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: leonard.siegfried@upjs.sk. 13. Department of Infectious Diseases, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: kristian@unlp.sk. 14. 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia.
Abstract
BACKGROUND: The presence of hepatitis B infection (HBI) and metabolic syndrome (MS) at the same time constitutes a high risk for liver cirrhosis and potentially hepatocellular carcinoma. AIM: In this study we aim to explore the relationship between MS and HBI. METHODS: We used data from the cross-sectional HepaMeta study conducted in 2011 in Slovakia. Patients were tested for presence of MS, while lipid levels (total cholesterol, HDL, LDL, TG, apolipoprotein B100 and HBI (HBsAg and antiHBcIgG)) were also monitored. Viral load was measured in HBsAg positive patients. RESULTS: Altogether 855 patients were screened, MS was diagnosed in 25.1% of patients and 7.9% of patients presented with HBI. AntiHBcIgG antibodies were present in 34.6% patients. HBI patients had lower levels of total and LDL cholesterol along with a decreased apolipoprotein B100 (4.54 ± 0.84 vs. 5.0 ± 0.99 mmol/l, P=0.001; 2.29 ± 0.58 vs. 2.6 ± 0.68 mmol/l, P=0.001 and 0.71 ± 0.21 vs. 0.77 ± 0.23 mmol/l, P=0.013 respectively). Patients diagnosed with MS had higher HBV DNA load than patients without MS - 1300.2 (95% CI 506.06-3440.41) vs. 7661.3 (95% CI 2008.17-29,228.06) IU/ml; P=0.011. HBI patients with TC and apolipoprotein B100 in the reference range had lower HBV DNA load than patients with high or low values of TC or apolipoprotein B100. CONCLUSION: Hepatitis B patients had lower levels of total and LDL cholesterol along with a decreased apolipoprotein B100. Viral load of chronic hepatitis B patients with MS was higher than that in patients without MS.
BACKGROUND: The presence of hepatitis B infection (HBI) and metabolic syndrome (MS) at the same time constitutes a high risk for liver cirrhosis and potentially hepatocellular carcinoma. AIM: In this study we aim to explore the relationship between MS and HBI. METHODS: We used data from the cross-sectional HepaMeta study conducted in 2011 in Slovakia. Patients were tested for presence of MS, while lipid levels (total cholesterol, HDL, LDL, TG, apolipoprotein B100 and HBI (HBsAg and antiHBcIgG)) were also monitored. Viral load was measured in HBsAg positive patients. RESULTS: Altogether 855 patients were screened, MS was diagnosed in 25.1% of patients and 7.9% of patients presented with HBI. AntiHBcIgG antibodies were present in 34.6% patients. HBI patients had lower levels of total and LDL cholesterol along with a decreased apolipoprotein B100 (4.54 ± 0.84 vs. 5.0 ± 0.99 mmol/l, P=0.001; 2.29 ± 0.58 vs. 2.6 ± 0.68 mmol/l, P=0.001 and 0.71 ± 0.21 vs. 0.77 ± 0.23 mmol/l, P=0.013 respectively). Patients diagnosed with MS had higher HBV DNA load than patients without MS - 1300.2 (95% CI 506.06-3440.41) vs. 7661.3 (95% CI 2008.17-29,228.06) IU/ml; P=0.011. HBI patients with TC and apolipoprotein B100 in the reference range had lower HBV DNA load than patients with high or low values of TC or apolipoprotein B100. CONCLUSION:Hepatitis Bpatients had lower levels of total and LDL cholesterol along with a decreased apolipoprotein B100. Viral load of chronic hepatitis Bpatients with MS was higher than that in patients without MS.
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