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Non-invasive quantification of liver fibrosis regression following successful treatment of chronic hepatitis C with direct acting antivirals

Abstract

Introduction. The past years have revolutionized the treatment of hepatitis C virus (HCV) infection, with high rates of sustained virologic response (SVR). Furthermore, liver fibrosis has recently been redefined as a dynamic, reversible process. Methods. We performed a prospective cohort study to assess the role of laboratory evaluations and non-invasive measurement of liver stiffness in establishing the right time for starting treatment and in assessing the regression of liver fibrosis in Romanian patients treated with direct acting antivirals (DAA) for genotype 1b chronic hepatitis C. Results. We present the results for 102 patients, with a mean age of 58.5 years, and a rate of SVR of 100%. Our study has ruled out older age (p=0.628), IL28B non-CC genotype (p=0.693), baseline viral load above the cutoff of 600,000 IU/mL (p=0.353), and the presence of diabetes mellitus (p=0.272) or baseline steatosis (p=0.706) as factors potentially influencing the regression of liver fibrosis following DAA treatment of HCV infection with the 3D regimen. The quantitative regression of liver stiffness was inversely correlated with the duration of HCV infection (p=0.017), suggesting that timely treatment might associate better outcomes in terms of liver fibrosis. Conclusion. Our study’s results point towards the need to start DAA treatment earlier in patients with HCV infection.

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Thirty years in hemostasis research in Cluj Napoca

References 1. Brudaşcă I, Cucuianu M. Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for metabolic syndrome, hepatic steatosis and steatohepatitis. Rom J Intern Med. 2007;45(2):149-57. 2. Cucuianu M, Brudaşcă I. Coagulation factor XIII, impaired fibrinolysis and cardiovascular disease. Rev Romana Med Lab. 2011;19(2):119-27. 3. Brudaşcă I, Cucuianu M. Anticoagulant mechanisms are modulated by vascular endothelial cells. Rev Romana Med Lab. 2010;18(3):7-14. 4

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Abnormal lipid metabolism in metabolic syndrome: an epigenetic perspective

epigenome and later health consequences. Food Science and Human Wellness. 2013;2(1):1-11. DOI: 10.1016/j.fshw.2013.03.002. 4. Ginsberg HN, Stalenhoef AFH. The metabolic syndrome: targeting dyslipidaemia to reduce coronary risk. J Cardiovasc Risk. 2003; 10(2):121-8. DOI: 10.1177/174182670301000207 DOI: 10.1097/00043798-200304000-00007. 5. Brudaşcă I, Cucuianu M. Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for the metabolic syndrome, hepatic steatosis and steatohepatitis. Rom J Int Med. 2007

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