Person: BAŞARANOĞLU, METİN
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Publication Open Access Rate and Predictors of Endoscopic Mucosal Healing in Biologic Naive Patients with Inflammatory Bowel Disease by Azathioprine Treatment: A Real World, 10 Years- Experience from a Single Centre in Turkey.(2016-08-01T00:00:00Z) Basaranoglu, METİN; Ertan, A; Mathew, S; Senturk, H; Ala, A; Demirbag, AE; BAŞARANOĞLU, METİN; ŞENTÜRK, HAKANBackground: There is increasing evidence that endoscopic mucosal healing (EMH) is a key target in inflammatory bowel disease (IBD) therapy. However, there is limited evidence of EMH rates with conventional IBD therapy outside of Western population groups. Ai̇m: To evaluate the role of azathioprine (AZA) in inducing EMH in IBD patients. Methods: Patients with inflammatory bowel disease were evaluated in terms of endoscopic mucosal healing and the incidence of surgical interventions during the azathioprine treatment between 1995 to 2014. Results: A total of 120 inflammatory bowel disease patients were enrolled. Endoscopic mucosal healing was found in 37% patients with inflammatory bowel disease (42% in chronic ulcerative colitis and 33% in Crohn's disease). Male gender had a negative impact on the efficacy of azathioprine (P<0.05). Responder inflammatory bowel disease patients were older (age at the IBD diagnose) than the nonresponder (P<0.05). Azathioprine therapy reduced the number of the surgical interventions (P<0.05). Conclusi̇on: We showed that azathioprine therapy significantly induced endoscopic mucosal healing in biologic naïve patients with active inflammatory bowel disease as well as decreasing the surgical interventions, with negative predictive factors identified by a younger age at IBD presentation and male gender.Publication Open Access From fatty liver to fibrosis: A tale of -second hit-(2013-02-28) Basaranoglu, METİN; Basaranoglu, GÖKÇEN; Senturk, HAKAN; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN; ŞENTÜRK, HAKANAlthough much is known about how fat accumulates in the liver, much remains unknown about how this causes sustained hepatocellular injury. The consequences of injury are recognized as nonalcoholic steatohepatitis (NASH) and progressive fibrosis. The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired. An additional stressor is sometimes referred to as a “second hit” in a paradigm that identifies the accumulation of fat as the “first hit”. Possible candidates for the second hit include increased oxidative stress, lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal, decreased antioxidants, adipocytokines, transforming growth factor (TGF)-β, Fas ligand, mitochondrial dysfunction, fatty acid oxidation by CYPs (CYP 2E1, 4A10 and 4A14), and peroxisomes, excess iron, small intestinal bacterial overgrowth, and the generation of gut-derived toxins such as lipopolysaccharide and ethanol. Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury. Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products, with reduced hepatic and plasma levels of antioxidants. There is also some indirect evidence of the benefit of antioxidants such as vitamin E, S-adenosylmethionine, betaine, phlebotomy to remove iron, and N-acetylcysteine in NASH. However, a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far. A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor (TNF)-α, iron overload, overburdened and dysfunctional mitochondria, CYPs, and peroxisomes. Briefly, the pathogenesis of NASH is multifactorial and excess intracellular fatty acids, oxidant stress, ATP depletion, and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver.Publication Open Access Significant cohort of non-alcoholic fatty liver disease with portal vein thrombosis in transplant waiting list.(2016-03-08T00:00:00Z) Senturk, H; Basaranoglu, METİN; Najjar, SM; Demirbag, AE; BAŞARANOĞLU, METİN; ŞENTÜRK, HAKANAim: To characterize non-alcoholic fatty liver disease (NAFLD) presentation with esophageal varices. Methods: We carried out a retrospective cohort study on 258 patients with esophageal varices at a single tertiary referral center. These patients underwent diagnosis of several liver diseases, including: NAFLD-associated cirrhosis, hepatitis B, hepatitis C, Wilson disease, autoimune liver diseases, and others. Results: Of the 258 patients, 39% of patients exhibited esophageal varices due to NAFLD-associated cirrhosis. Of the 38 (14.7%) patients developed hepatocellular carcinoma during follow-up, 52% were due to hepatitis B, 26% due to hepatitis C and 13.2% due to NAFLD. Of the 258 patients, 50.0% with NAFLD, 33.3% with hepatitis B, 26.3% with hepatitis C, and 58.3% with other diseases were alive at the end of the 5-year period with a significant difference according to the Kaplan-Meier log Rank test (P = 0.040). Portal vein thrombosis was detected in 47.5% of patients with NAFLD, in 29% of patients with hepatitis B, in 17% of patients with hepatitis C, and in 62% of patients with other related diseases (P < 0.0001). Conclusion: Our study showed a proportionally greater elevation in liver transplant candidacy in patients with NAFLD and portal vein thrombosis. Older patients were more prone to developing cirrhosis, hepatocellular carcinoma and a high mortality rate. However, younger patients exhibited more portal vein thrombosis and gastric varices.Publication Open Access Fructose as a key player in the development of fatty liver disease(2013-02-01T00:00:00Z) BAŞARANOĞLU, METİN; BAŞARANOĞLU, Gökçen; SABUNCU, TEVFİK; ŞENTÜRK, HAKAN; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN; ŞENTÜRK, HAKANWe aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver. The prevalence of nonalcoholic steatohepatitis (NASH) is 3% and 20% in nonobese and obese subjects, respectively. Obesity is a low-grade chronic inflammatory condition and obesity-related cytokines such as interleukin-6, adiponectin, leptin, and tumor necrosis factor-a may play important roles in the development of nonalcoholic fatty liver disease (NAFLD). Additionally, the prevalence of NASH associated with both cirrhosis and hepatocellular carcinoma was reported to be high among patients with type 2 diabetes with or without obesity. Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in mice, the American Lifestyle-Induced Obesity Syndrome model, which included consumption of a high-fructose corn syrup in amounts relevant to that consumed by some Americans. The observation reinforces the concerns about the role of fructose in the obesity epidemic. Increased availability of fructose (e. g., high-fructose corn syrup) increases not only abnormal glucose flux but also fructose metabolism in the hepatocyte. Thus, the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and amino acids. Fructose was previously accepted as a beneficial dietary component because it does not stimulate insulin secretion. However, since insulin signaling plays an important role in central mechanisms of NAFLD, this property of fructose may be undesirable. Fructose has a selective hepatic metabolism, and provokes a hepatic stress response involving activation of c-Jun N-terminal kinases and subsequent reduced hepatic insulin signaling. As high fat diet alone produces obesity, insulin resistance, and some degree of fatty liver with minimal inflammation and no fibrosis, the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis, inflammation, endoplasmic reticulum stress and lipoapoptosis. Hepatic de novo lipogenesis (fatty acid and triglyceride synthesis) is increased in patients with NAFLD. Stable-isotope studies showed that increased de novo lipogenesis (DNL) in patients with NAFLD contributed to fat accumulation in the liver and the development of NAFLD. Specifically, DNL was responsible for 26% of accumulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD compared to an estimated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinemia. In conclusion, understanding the underlying causes of NAFLD forms the basis for rational preventive and treatment strategies of this major form of chronic liver disease. (C) 2013 Baishideng. All rights reserved.