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Liver fat content might be an appropriate measure for estimation of cardiovascular disease risk in non-alcoholic steatohepatitis patients
Background: Non-alcoholic steatohepatitis (NASH) is increasing worldwide due to the metabolic syndrome epidemy. According to the current evidence, a higher cardiovascular disease risk (CVDR) is observed in NASH individuals than the general population. Objective: The relationship between liver fat co...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Iran University of Medical Sciences
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787026/ https://www.ncbi.nlm.nih.gov/pubmed/33437731 http://dx.doi.org/10.34171/mjiri.34.135 |
Sumario: | Background: Non-alcoholic steatohepatitis (NASH) is increasing worldwide due to the metabolic syndrome epidemy. According to the current evidence, a higher cardiovascular disease risk (CVDR) is observed in NASH individuals than the general population. Objective: The relationship between liver fat content (LFC) and CVDR in a cohort of NASH patients was evaluated in this research. Methods: Consecutively selected patients with increased aminotransferase levels and fatty change in liver ultrasonography were enrolled in the study. Those with known causes of viral hepatitis, any hepatotoxic medications or alcohol consumption, autoimmune hepatitis, cigarette smoking, and ischemic heart disease were excluded from the project. The remaining was presumed to have NASH. The Framingham risk score (FRS) and LFC were calculated by means of an online calculator and a valid formula, respectively. The correlation between LFC and independent variables was measured using the Pearson correlation test. The P-value of less than 0.05 was considered significant. The statistical analysis was performed using SPSS program version 18. Results: Finally, two hundred NASH patients were included in the study. Considering diabetes mellitus as a confounder, there was a fair relationship between LFC and FRS (R=0.26 and 0.23, respectively, p<0.05) in the second and third visits. Even after adjustment for known cardiovascular risk factors, LFC was associated with increased CVDR (OR=9.181; 95% CI: 2.00-42.14, p=0.01). The cut-off value of 9.1% for LFC had a sensitivity of 92% and a specificity of 87% for discrimination of the FRS >20% and <20%. Conclusion: LFC might independently be correlated with CVDR in NASH patients. If further research confirmed this relationship, the inclusion of LFC into the FRS formula would provide an appropriate CVDR estimation tool in NASH. |
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