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The Relationship between Hepatic Steatosis, inflammation and insulin Resistance in type 2 Diabetes with Metabolic Imbalance

, Nascimbeni F, Pais R, et al. Performance And Limitations Of Steatosis Biomarkers In Patients With Nonalcoholic Fatty Liver Disease. Alimentary Pharmacology & Therapeutics, 2014; 40(10):1209-1222. DOI:10.1111/apt.12963. 5. Lonardo A, Nascimbeni F, Maurantonio M, et al. Nonalcoholic Fatty Liver Disease: Evolving Paradigms. World Journal Of Gastroenterology, 2017; 23(36):6571-6592. DOI:10.3748/wjg.v23.i36.6571. 6. Kitade H, Chen G, Ni Y and Ota T. Nonalcoholic Fatty Liver Disease And Insulin Resistance: New Insights And Potential New Treatments. Nutrients, 2017; 9

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Noninvasive Markers of Improvement of Liver Steatosis Achieved by Weight Reduction in Patients with Nonalcoholic Fatty Liver Disease

of steatohepatitis in mice. J Inflamm (Lond). 2011; 8:8. 9. PARK SH, KIM BI, KIM SH, KIM HJ, PARK DI, CHO YK, SUNG IK, SOHN CI, KIM H, KEUM DK, KIM HD, PARK JH, KANG JH, JEON WK. Body fat distribution and insulin resistance: beyond obesity in nonalcoholic fatty liver disease among overweight men. J Am Coll Nutr 2007; 26:321-326. 10. PARK BJ, KIM YJ, KIM DH, KIM W, JUNG YJ, YOON JH, KIM CY, CHO YM, KIM SH, LEE KB, JANG JJ, LEE HS. Visceral adipose tissue area is an independent risk factor for hepatic steatosis. J Gastroenterol Hepatol

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Insulin Resistance in Liver Diseases

;82(6):2606-12. Negro F, Sanyal AJ. Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data. Liver Int. 2009; Suppl 2:26-37. Koike K. Steatosis, liver injury, and hepatocarcinogenesis in hepatitis C viral infection. J Gastroenterol. 2009;44(Suppl 19):82-8. Del Campo JA, Romero-Gómez M. Steatosis and insulin resistance in hepatitis C: a way out for the virus? World J Gastroenterol. 2009;15(40):5014-9. Miquilena-Colina ME, Cabello EL, Sanchez-Campos S, et al. Hepatic fatty acid

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Hepatic fibrosis, measured by fibroscan in a group of patients with obesity

Abstract

Introduction.Hepatic steatosis is a reversible condition caused by accumulation of triglycerides in liver cells. Non-alcoholic fatty liver disease (NAFLD) can progress to advanced liver disease: fibrosis, cirrhosis, liver failure, cancer, and finally can lead to death; therefore NAFLD contributes significantly to morbidity and mortality of hepatic cause. Materials and methods: The study was conducted on a group of 88 patients with Body Mass Index (BMI) ≥ 30kg/m², they were excluded patients with known diabetes. Results, Discussion: The statistical analysis showed that in more than half of subjects elastometry values were higher than those considered normal, obesity is a risk factor for NAFLD that progresses in hepatic fibrosis. Conclusions: Liver fibrosis is present in high percentage in patients with obesity (52% of subjects) and it was positively correlated with age, arterial stiffness and fasting glucose.

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The Severity of Non-Alcoholic Fatty Liver in Type II Diabetes

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that affects up to one third of the adult population of industrialized countries. The pathophysiological spectrum includes the following entities that are clinically and histologically distinct: hepatic steatosis and steatohepatitis; their subsequent evolution can lead to cirrhosis and hepatocellular carcinoma.The increase of the prevalence of NAFLD during the last decade is caused by the epidemiological and pathophysiological association with type II diabetes and obesity, NAFLD being present in about 70-80% of patients with type II diabetes mellitus. It has long been thought that the relationship between type II diabetes mellitus and NAFLD is unidirectional, fatty liver being secondary to insulin resistance and type II diabetes mellitus, but recent studies show that hepatic steatosis may precede insulin resistance and diabetes mellitus, thus demonstrating abidirectional causal relationship between these two disorders. Weight loss through diet andexercise is effective in preventing and treating NAFLD in diabetic patients; also, drugs that causeweight loss need to be evaluated. Both anti-diabetic medication and statins play an important vrole in the prevention and treatment of NAFLD.

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Polyphenols treatment in patients with nonalcoholic fatty liver disease

Introduction In the last few decades, the term nonalcoholic fatty liver disease (NAFLD) has been evoked increasingly in research frameworks and in clinical practice. It defines the presence of significant fat accumulation in the liver (> 5% of hepatocytes), in the absence of alcohol abuse and any other cause of liver diseases.[ 1 ] The term NAFLD includes different clinical entities, and in particular, the fat accumulation in liver, also known as simple fatty liver and nonalcoholic steatohepatitis (NASH); it is characterized by steatosis along with

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The Prevalence of Coronary Heart Disease, Stroke and Selected Co-Morbidities in Patients with Newly Diagnosed Type 2 Diabetes Population - Based on Cohort Study of Outpatients

Abstract

The prospective study analyses prevalence of coronary heart disease, stroke, elevated serum levels of ALT and GGT and prevalence of cancer diseases in patients with newly diagnosed type 2 diabetes mellitus, and usage of this epidemiological data in everyday clinical practice. Outpatients with newly diagnosed type 2 diabetes mellitus were monitoring during the period of August 2007 - August 2011. The patients with previously treated type 2 diabetes mellitus were eliminated from the monitoring. The population consists of 117 males and 83 females aged 30 to 92 years sent by GPs and various specialists.

The relatively low prevalence of known coronary artery disease was recorded in men (34%) and in women (19%). Prevalence of stroke history was confirmed in 12% of men and 7% of women. The elevated serum ALT levels > 0.55 μkat/l was recorded in 45% of men and 45% of women and elevated serum GGT levels > 0.45 μkat/l was recorded in 81% of men and 68% of women. Prevalence of cancer diseases was recorded 5% in women and 5.26% of men. In the studied group of patients there was recorded the occurrence of colon cancer in men over 64 years old and the occurrence of breast cancer, endometrial cancer and colon cancer in women over 62 years old.

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Effect of weight reduction on histological activity and fibrosis of lean nonalcoholic steatohepatitis patient

Introduction Non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disorder worldwide, is a clinico-histopathological entity ranging from simple fat accumulation (steatosis) to non-alcoholic steatohepatitis (NASH). [ 1 , 2 ] NASH is diagnosed by the joint presence of steatosis and inflammation along with hepatocyte injury (evident as hepatocyte ballooning). [ 3 ] It is estimated that NASH occurs in 20% of patients with NAFLD, whereas in Bangladesh, it shows a higher proportion (42.4%). [ 4 , 5 ] Due to its progressive nature

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Effect of pentoxifylline on histological activity and fibrosis of nonalcoholic steatohepatitis patients: A one year randomized control trial

Introduction Non-alcoholic fatty liver disease (NAFLD) is a condition pathologically linked to the metabolic syndrome by the intervention of insulin resistance (IR), characterized by hepatic steatosis in the absence of significant alcohol use, hepatotoxic medications or other known liver diseases.[ 1 ] Globally, the prevalence of NAFLD is 25.24%.[ 2 ] In the Asia-Pacific region, the prevalence of NAFLD has increased remarkably over the years affecting up to 30% of the general population.[ 3 ] In case of NAFLD, Bangladeshi ethnicity is an independent risk

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The pathogenesis of non-alcoholic fatty liver disease is closely related to the metabolic syndrome components

, atherosclerosis, and aspects of insulin action. Diabetes Care 28: 2312-2319, 2005. 18. Targher G, Bertolini L, Scala L et al . Nonalcoholic hepatic steatosis and its relation to increased plasma biomarkers of inflammation and endothelial dysfunction in nondiabetic men. Role of visceral adipose tissue. Diabet Med 22: 1354-1358, 2005. 19. Savage DB, Petersen KF, Shulman GI . Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol Rev 87: 507-520, 2007. 20. Cnop M, Landchild MJ, Vidal J et al. The

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