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Epidemiology and Natural History of Nafld/Epidemiologija I Prirodna Istorija Nealkoholne Masne Jetre

adults: A systematic review. J Hepatol 2011; 56: 255-66. 7. Socha P, Horvath A, Vajro P, Dziechciarz P, Dhawan A, Szajewska H. Pharmacological interventions for nonalcoholic fatty liver disease in adults and in children: a systematic review. J Pediatr Gastroenterol Nutr 2009; 48: 587-96. 8. Bellentani S, Scaglioni F, Marino M, Bedogni G. Epide - miology of Fatty Liver Disease. Dig Dis 2010; 28: 155-61. 9. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, et al. Prevalence of hepatic steatosis in

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Predictive values of serum uric acid and Alanine-aminotransferase for fatty liver index in Montenegrin population

established as the gold standard for diagnosis of hepatic steatosis ( 4 ). However, due to its invasive diagnostic nature it is not suitable procedure in routine everyday praxis. Therefore, it has been replaced with abdominal ultrasonography, as the commonest technique for NAFLD assessment in clinical trials. In line with this, Bedogni et al. ( 5 ) derived fatty liver index (FLI), an algorithm based on body mass index (BMI), waist circumference (WC), triglycerides (TG) and gamma-glutamyl transferase (GGT), as a simple and accurate predictor of NAFLD. An FLI score ≥60 has

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The Association of Obesity and Liver Enzyme Activities in a Student Population at Increased Risk for Cardiovascular Disease / Veza Između Gojaznosti I Aktivnosti Jetrenih Enzima U Studentskoj Populaciji Sa Povećanim Rizikom Za Nastanak Kardiovaskularnih Bolesti

. 10. Chan DF, Li AM, Chu WC, Chan MH, Wong EM, Liu EK, et al. Hepatic steatosis in obese Chinese children. Int J Obes Relat Metab Disord 2004; 28: 1257-63. 11. Roberts EA. Non-alcoholic fatty liver disease (NAFLD) in children. Front Biosci 2005; 10: 2306-18. 12. Franzese A, Vajro P Argenziano A, Puzziello A, Iannucci MP Saviano MC, et al. Liver involvement in obese children. Ultrasonography and liver enzyme levels at diagnosis and during follow-up in an Italian population. Dig Dis Sci 1997; 42: 1428-32. 13. Oliveira AC

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Pediatric Non-Alcoholic Fatty Liver Disease/Oboljenje Ne-Alkoholne Masne Jetre U Pedijatriji

, Li AM, Chu WC, et al. Hepatic steatosis in obese Chinese children. Int J Obes Relat Metab Disord 2004; 28: 1257-63. 22. Tazawa Y, Noguchi H, Nishinomiya F, Takada G. Serum alanine aminotransferase activity in obese children. Acta Pediatr 1997; 86: 238-41. 23. Monteiro PA, Mota J, Silveria LS, Cayre SU, de Moura M Antunes B, Araujo Fernandes R, Freitas jr IF. Morpho - logical and metabolic determinants of non-alcoholic fatty liver disease in obese youth: A pilot study. BMC res Notes 2013; 6: 89-84. 24. Utzschneider KM

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Women with Polycystic Ovary Syndrome and Risk of Cardiovascular Disease

Hepatology 2007; 47: 412–7. 9. Xiang S, Hua F, Chen L, Tang Y, Jiang X, Liu Z. Lipid Accumulation Product is Related to Metabolic Syndrome in Women with Polycystic Ovary Syndrome. Exp Clin End Diab 2013; 121: 115–8. 10. Sert A, Pirgon O, Aypar E, Yilmaz H, Dündar B. Relationship between aspartate aminotransferase-to-platelet ratio index and carotid intima-media thickness in obese adolescents with non-alcoholic fatty liver disease. J Clin Res Ped End 2013; 5: 182–8. 11. Lee JH, Kim D, Kim HJ, Lee CH, Yang JI, Kim W, et al. Hepatic steatosis index: A simple

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Are Vaspin and Omentin-1 Related to Insulin Resistance, Blood Pressure and Inflammation in NAFLD Patients?

. Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance. Journal of Endocrinology 2013; 218(3): R25–R36. 18. Al Rifai M, Silverman MG, Nasir K, Budoff MJ, Blankstein R, Szklo M, et al. The association of nonalcoholic fatty liver disease, obesity, and metabolic syndrome, with systemic inflammation and subclinical atherosclerosis: the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2015; 239(2): 629–33. 19. Ramadan RA. Serum vaspin and insulin resistance: predictors of steatosis and fibrosis in Egyptian

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Nitric oxide products are not associated with metabolic syndrome

without MetS (n=58) and a group with MetS (n=51). Exclusion criteria for all potential participants were: hsCRP >10 mg/L, acute inflammatory disease, diabetes mellitus, liver diseases other than steatosis, kidney diseases, malignant diseases, gout, ethanol consumption >20 g/day, pregnancy, as well as unwillingness to participate in the study. The Ethical Committee of the Primary Health Care Center in Podgorica, Montenegro approved the study protocol. All the volunteers provided signed informed consent, and the research was carried out in compliance with the

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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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