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Hepatitis B virus infection in patients with metabolic syndrome: a complicated relationship. Results of a population based study
P. Jarčuška, M. Janičko, P. Kružliak, M. Novák, E. Veselíny, J. Fedačko, G. Senajová, S. Dražilová, A. Madarasová-Gecková, M. Mareková, D. Pella, L. Siegfried, P. Kristián, E. Kolesárová, . ,
Language English Country Netherlands
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Hepatitis B, Chronic complications virology MeSH
- Adult MeSH
- Humans MeSH
- Metabolic Syndrome complications epidemiology virology MeSH
- Cross-Sectional Studies MeSH
- Viral Load MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
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- $a Jarčuška, Peter $u 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: petjarc@yahoo.com.
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- $a 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.
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- $a Kružliak, Peter $u 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.
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- $a Novák, Miroslav $u 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.
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- $a Madarasová-Gecková, Andrea $u Department of Public Health, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: geckova.andrea.madarasova@upjs.sk.
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- $a Mareková, Mária $u Department of Medical Biochemistry, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: maria.marekova@upjs.sk.
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- $a Siegfried, Leonard $u Department of Medical Microbiology, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 04001 Košice, Slovakia. Electronic address: leonard.siegfried@upjs.sk.
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