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    Concentrations of connective tissue growth factor in patients with nonalcoholic fatty liver disease: Association with liver fibrosis
    (Hindawi Ltd, 2012) Colak, Yasar; Senates, Ebubekir; Coskunpinar, Ender; Oltulu, Yasemin Musteri; Zemheri, Ebru; Ozturk, Oguzhan; Doganay, Levent
    Aim: In this study, we aimed to investigate the relationship between the histological fibrosis stage of nonalcoholic fatty liver disease (NAFLD) and serum connective tissue growth factor (CTGF) to determine the usefulness of this relationship in clinical practice. Methods: Serum samples were collected from 51 patients with biopsy-proven NAFLD and 28 healthy controls, and serum levels of CTGF were assayed by ELISA. Results: Levels of CTGF were significantly higher in patients with NAFLD compared with controls (P = 0.001). The serum CTGF levels were significantly increased, that correlated with histological fibrosis stage, in patients with NAFLD [in patients with no fibrosis (stage 0) 308.2 +/- 142.9, with mild fibrosis (stage 1-2) 519.9 +/- 375.2 and with advanced fibrosis (stage 3-4) 1353.2 +/- 610 ng/l, P < 0.001]. Also serum level of CTGF was found as an independent predictor of histological fibrosis stage in patients with NAFLD (beta = 0.662, t = 5.6, P < 0.001). The area under the ROC curve was estimated 0.931 to separate patients with severe fibrosis from patients with other fibrotic stages. Conclusion: Serum levels of CTGF may be a clinical utility for distinguishing NAFLD patients with and without advanced fibrosis.
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    Evaluation of gallbladder kinetics in patients with nonalcoholic fatty liver disease
    (Wiley-Blackwell, 2013) Colak, Yasar; Bozbey, Gulcin; Senates, Ebubekir; Doganay, Levent; Coskunpinar, Ender; Ozturk, Oguzhan; Mesci, Banu
    [Abstract Not Available]
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    The Evaluation of Mean Platelet Volume in Hepatitis C Infection
    (Galenos Yayincilik, 2014) Demircan, Fatih; Kilinc, Faruk; Gozel, Nevzat; Erkalma Senates, Banu; Senates, Ebubekir
    Objective: Mean platelet volume (MPV) is a simple test that can be detected by routine blood counts and is considered a risk factor for atherothrombosis. In our study, we aimed to compare platelet count and mean platelet volume of patients with diagnosis of hepatitis C with healthy patients groups. Materials and Methods: In this study, blood test results, age and gender of 107 HCV patients and 100 healthy individuals who admitted to our internal medicine polyclinic between January 2010 and August 2013 were evaluated retrospectively. Patient information was obtained from hospital records. Serum platelet counts, MPV, total cholesterol, triglycerides, LDL cholesterol, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), and alkaline phosphatase (ALP) levels were recorded. Results: Of the 107 patients diagnosed with HCV, 55 (51.4%) were males and 52 (48.6%) were females and the mean age was 45.0 +/- 11.0 years (range 23-66). In the control group, 51 patients were males and 49 were females, the mean age was 43.9 +/- 12.0 years (range 17-67). The mean ALT and AST levels of the patients with HCV were 58.8 +/- 76.0 IU/L (12-401) and 79.7 +/- 124.6 IU/L (14-670), respectively; in the control group it was 31.6 +/- 12 IU/L (15-82) and 33.1 +/- 10 IU/L (15-78), respectively and the difference between the groups was significant (p<0.001). The mean triglyceride level was significantly higher in the HCV group (205.5 +/- 53.3 mg/dL) than that in the control group (185.5 +/- 34.4 mg/dL) (p<0.001). The mean platelet count was 152.2 +/- 53.8 x 10(3)/mm(3) in patients with HCV infection and it was 190.7 +/- 66.8 x 10(3)/mm(3) in the control group; the difference between the groups was significant (p<0.001). The mean MPV was 9.1 +/- 1.7 fL in HCV group and 7.4 +/- 1.0 fL in the healthy group, and the difference was statistically significant (p<0.001). Conclusion: In conclusion, according to our study; significant elevation in MPV level in patients with HCV infection may be responsible for the effect of the virus that leads to platelet dysfunction. This condition supports the relationship between the existence of HCV infection and the risk of atherothrombosis.
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    Gallstone Disease Does Not Predict Liver Histology in Nonalcoholic Fatty Liver Disease
    (Editorial Office Gut & Liver, 2014) Yilmaz, Yusuf; Ayyildiz, Talat; Akin, Hakan; Colak, Yasar; Ozturk, Oguzhan; Senates, Ebubekir; Tuncer, Ilyas
    Background/Aims: We sought to examine whether the presence of gallstone disease (GD) in patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) is associated with liver fibrosis and histological nonalcoholic steatohepatitis (NASH) score. Methods: We included 441 Turkish patients with biopsy-proven NAFLD. GD was diagnosed in the presence of sonographic evidence of gallstones, echogenic material within the gallbladder with constant shadowing and little or no visualization of the gallbladder or absence of gallbladder at ultrasonography, coupled with a history of cholecystectomy. Results: Fifty-four patients (12.2%) had GD (GD+ subjects). Compared with the GD- subjects, GD+ patients were older, had a higher body mass index and were more likely to be female and have metabolic syndrome. However, GD+ patients did not have a higher risk of advanced fibrosis or definite NASH on histology. After adjustment for potential confounding variables, the prevalence of GD in NAFLD patients was not associated with significant fibrosis (>= 2) (odds ratio [OR], 1.06; 95% confidence interval [Cl], 0.53 to 2.21; p=0.68) or definite NASH (OR, 1.03; 95% Cl, 0.495 to 2.12; p=0.84). Conclusions: The presence of GD is not independently associated with advanced fibrosis and definite NASH in adult Turkish patients with biopsy-proven NAFLD.
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    Hepatic expression and serum levels of syndecan 1 (CD 138) in patients with nonalcoholic fatty liver disease
    (Informa Healthcare, 2012) Yilmaz, Yusuf; Eren, Fatih; Colak, Yasar; Senates, Ebubekir; Celikel, Cigdem Ataizi; Imeryuz, Nese
    Background and aims. Syndecan-1 (CD 138) is a transmembrane heparan sulfate proteoglycan expressed in the liver which may exert metabolic effects by mediating the hepatic clearance of triglyceride-rich lipoproteins. In the present study, we assayed serum levels and the hepatic expression of syndecan-1 and examined their association with clinical, biochemical, and histologic phenotypes in patients with histology-proven nonalcoholic fatty liver disease (NAFLD). Methods. A total of 59 patients with biopsy-proven NAFLD and 54 matched controls were enrolled. The analysis of syndecan-1 expression in liver biopsies was performed by immunohistochemistry on formalin-fixed, paraffin-embedded samples. Serum syndecan-1 levels were measured by ELISA. Results. NAFLD patients had significantly higher serum syndecan-1 levels [median: 61 ng/mL (interquartile range: 36-97 ng/mL)] than controls [median: 37 ng/mL (interquartile range: 25-59 ng/mL, Mann Whitney U test, p < 0.001]. However, we did not find any significant association between serum syndecan-1 and the mean syndecan-1 immunohistochemical score (n = 59, r = 0.064, p = 0.63). Interestingly, the syndecan-1 immunohistochemical score was an independent predictor of HDL cholesterol in NAFLD patients (beta = 0.27; t = 1.99, p < 0.05). Conclusions. Our data suggest that serum syndecan-1 levels are raised in patients with NAFLD. Moreover, the syndecan-1 immunohistochemical score in the liver is independently associated with HDL cholesterol in this group of patients. These pilot results support further investigation of this molecule in metabolic liver diseases.
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    HLA DQB1 alleles are related with nonalcoholic fatty liver disease
    (Springer, 2014) Doganay, Levent; Katrinli, Seyma; Colak, Yasar; Senates, Ebubekir; Zemheri, Ebru; Ozturk, Oguzhan; Enc, Feruze Yilmaz
    Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease. NAFLD is a complex disease and inflammation is a crucial component in the disease pathogenesis. Recent genome wide association studies in hepatology area highlighted significant relations with human leukocyte antigen (HLA) DQ region and certain liver diseases. The previous animal models also emphasized the involvement of adaptive immune system in the liver damage pathways. To investigate possible polymorphisms in the HLA region that can contribute to the immune response affecting the NAFLD, we enrolled 93 consecutive biopsy proven NAFLD patients and a control group consisted of 101 healthy people and genotyped HLA DQB1 alleles at high resolution by sequence specific primers-polymerase chain reaction. The mean NAFLD activity score (NAS) was 5.2 +/- 1.2, fibrosis score was 0.9 +/- 0.9, ALT was 77 +/- 47.4 U/L, AST was 49.4 26.3 U/L. Among 13 HLA DQB1 alleles analyzed in this study, DQB1*06:04 was observed significantly at a more frequent rate among the NAFLD patients compared to that of healthy controls (12.9 vs. 2 % chi(2) = 8.6, P = 0.003, P-c = 0.039, OR: 7.3 95 % CI 1.6-33.7). In addition, the frequency of DQB1*03:02 was significantly higher in the healthy control group than the NAFLD patients (24.8 vs. 7.5 %, chi(2) = 10.4, P = 0.001, P-c = 0.013, OR: 0.2, 95 % CI 0.1-0.6). NAFLD patients were grouped according to their fibrosis score and NAS. The distribution of DQB1 alleles over stratified NAFLD patients did not reveal any statistically significant relation. Taken together, immune repertoire of individuals may have an effect on NAFLD pathogenesis and therefore, in NA-FLD, adaptive immunity pathways should be investigated.
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    Linking nonalcoholic fatty liver disease to hepatocellular carcinoma: from bedside to bench and back
    (Sage Publications Ltd, 2013) Yilmaz, Yusuf; Colak, Yasar; Kurt, Ramazan; Senates, Ebubekir; Eren, Fatih
    Aims and background. Nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) are two major causes of liver disease worldwide. Epidemiological and clinical data have clearly demonstrated that NAFLD and its associated metabolic abnormalities are a risk factor for HCC. Traditionally, the mechanisms whereby NAFLD acts as a risk for HCC are believed to include replicative senescence of steatotic hepatocytes and compensatory hyperplasia of progenitor cells as a reaction to chronic hepatic injury. Recent years have witnessed significant advances in our understanding of the mechanisms underlying the link between NAFLD and HCC. Methods. In the present review, we provide an update on the pathophysiological pathways linking NAFLD and its associated metabolic derangements to malignant hepatic transformation, with a special focus on insulin resistance, adipokines, inflammation, and angiogenesis. We will also discuss the potential therapeutic implications that such molecular links carry. Results. Although treating NAFLD could reduce the risk of malignant hepatic transformation, no long-term studies focusing on this issue have been conducted thus far. Insulin resistance, inflammation as well as derangements in adipokines and angiogenic factors associated with NAFLD are closely intertwined with the risk of developing HCC. Conclusions. Traditional therapeutic approaches in NAFLD including metformin and statins may theoretically reduce the risk of HCC by acting on common pathophysiological pathways shared by NAFLD and HCC.
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    Not only type 2 diabetes but also prediabetes is associated with portal inflammation and fibrosis in patients with non-alcoholic fatty liver disease
    (Elsevier Science Inc, 2014) Yilmaz, Yusuf; Senates, Ebubekir; Yesil, Atakan; Ergelen, Rabia; Colak, Yasar
    Aims: Growing evidence suggests that not only type 2 diabetes (T2D) but also prediabetes (PD) is common in patients with non-alcoholic fatty liver disease (NAFLD). However, few data exist on how PD impacts the histological characteristics of NAFLD patients. In this exploratory study, we sought to investigate the associations of PD and T2D with the severity of the histological features in patients with NAFLD. Methods: The population consisted of 280 patients with biopsy-proven NAFLD. The associations of PD and T2D with the severity of histological features of NAFLD were analyzed using multiple logistic (or ordinal logistic) regression models after adjustment for confounding factors. Results: PD and T2D was noted in 102 (36.4%) and 92 (32.8%) of patients, respectively. Of the 92 patients with T2D, ten (10.9%) were diagnosed de novo after the OGTT. PD and T2D were significantly associated with more severe portal inflammation (P < 0.01); the adjusted odds ratios (ORs) of PD and T2D for having a higher grade of portal inflammation were 1.8 [95% CI, 1.1, 3.2] and 2.6 [95% CI, 1.3, 5.8]), respectively. A similar relationship was observed for liver fibrosis (P < 0.001); specifically, the adjusted ORs of PD and T2D for having a higher grade of hepatic fibrosis were 2.4[95% CI, 1.3, 3.7] and 3.8 [95% CI, 1.9, 6.1]), respectively. Conclusion: Not only T2D but also PD is independently associated with portal inflammation and fibrosis in NAFLD patients. PD may be useful as a clinical indicator of patients who are likely to have already more severe histological findings. (C) 2014 Elsevier Inc. All rights reserved.
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    Re-Evalluation of Cases with Gastroenteropancreatic Neuroendocrine Tumors between 2004 and 2012 according to 2010 Criteria
    (H G E Update Medical Publishing S A, 2013) Ozkara, Selvinaz; Aker, Fugen; Yesil, Atakan; Senates, Ebubekir; Canbey, Ceren; Yitik, Ali; Gonen, Can
    Background/Aims: We re-evaluated the clinical, histopathological and immunohistochemical features of neuroendocrine tumors (NETs) diagnosed in our pathology laboratory between 2004 and 2012 and re-classified them according to the WHO-2000 and WHO-2010 criteria. Methodology: The study included NET samples of 106 patients having gastroenteropancreatic and hepatobiliary tumors. The histopathological findings were re-assessed. The cases were re-appraised based on the WHO-2000 and WHO-2010 criteria. The association between survival and Ki-67 index was analysed. Results: The most frequent localization was the stomach, The average tumor size was 3.0 +/- 4.1 cm. Differentiation was poor in 17 cases (16.0%). Lymphovascular invasion was detected in 16.1% (n=17) and necrosis was identified in 15.1% (n=16). The average number of Ki-67 was 9.1 +/- 19.9. Ki-67 measurements were significantly higher in patients who died compared to those who survived (p <0.01). In ROC analysis, the cut-off point for Ki-67 was 5. Conclusions: Our study is a single-center study comprising patients from Turkey for a period of 8 years. We found that the most frequent localization is the stomach. This ratio is associated with common use of endoscopy in our center. The specimens were re-evaluated according to the WHO-2000 and WHO-2010 classification systems the data and terminology have been updated.
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    Relationship Between Neutrophil Gelatinase-Associated Lipocalin (NGAL) Levels and Inflammatory Bowel Disease Type and Activity
    (Springer, 2013) Yesil, Atakan; Gonen, Can; Senates, Ebubekir; Paker, Nurcan; Gokden, Yasemin; Kochan, Koray; Erdem, Emrullah Duzgun
    Background and Aim Neutrophil gelatinase associated lipocalin (NGAL) is a recently identified molecule, which is bacteriostatic, has tissue destructive effects and is proinflammatory with chemoattractant molecule binding properties. Our aim was to investigate the relationship between serum NGAL levels and the type and level of disease activity of IBD. Methods A total of 92 patients [43 with Crohn's disease (CD) and 49 with ulcerative colitis (UC)], and 30 age-and sex-matched healthy controls (HC) were included in this study. Serum NGAL levels were measured using ELISA. Results Serum NGAL levels were elevated in the IBD group [median 171, range (57-312) ng/mL] compared to the HC group [107 (45-234) ng/mL] (p < 0.0001) and were elevated in UC patients [188 (74-312) ng/mL] compared to CD patients [168 (57-279) ng/mL] (p = 0.006). When NGAL levels were further analysed based on localization of the CD and UC, the levels in ulcerative pancolitis [233 (144-312) ng/mL] were significantly higher (p = 0.004) than the left-sided colitis [156 (103-309) ng/mL]. Similarly, NGAL levels were significantly higher in colonic CD [207 (125-249) ng/mL] than ileal CD [114 (78-210) ng/mL], and also in ileocolonic CD [198 (57-279) ng/mL] than ileal CD (p = 0.033). When CD and UC groups were further categorized as active and inactive according to clinical and endoscopic activity indices, serum NGAL concentrations did not differ between inquiescent versus active stages. When a cut-off level of 129 ng/mL was used to distinguish IBD from HC, a sensitivity of 76.1 % and a specificity of 60.9 % was reached. Conclusions The serum NGAL levels in the IBD group was significantly higher than the HC group. Serum NGAL levels were higher in more extensive colonic involvement.
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    Serum osteopontin levels as a predictor of portal inflammation in patients with nonalcoholic fatty liver disease
    (Elsevier Science Inc, 2013) Yilmaz, Yusuf; Ozturk, Oguzhan; Alandab, Yesim Ozen; Senates, Ebubekir; Colak, Yasar; Doganay, Hamdi Levent; Coskunpinar, Ender
    Background: Osteopontin is a secreted phosphorylated glycoprotein that is expressed by a variety of cell types and that mediates numerous and diverse biological functions. Osteopontin knockout mice are protected from obesity-induced hepatic steatosis. In the present study, we sought to investigate whether serum osteopontin concentrations are associated with liver histology in patients with nonalcoholic fatty liver disease. Methods: Serum levels of osteopontin were measured by enzyme-linked immunosorbent assay in 179 Well-characterized patients with nonalcoholic fatty liver referred for liver histology and 123 control subjects. Results: Serum osteopontin levels were markedly higher in patients with nonalcoholic fatty liver disease than in controls (p < 0.001). Multivariable analysis showed that osteopontin levels were strongly and independently associated with both portal inflammation (beta = 0.294, p < 0.01) and serum aminotransferase levels (aspartate aminotransferase: beta = 0.295, p < 0.01; alanine aminotransferase; beta = 0.285, p < 0.01). Conclusion: In summary, these data demonstrate that serum levels of osteopontin are elevated in nonalcoholic fatty liver disease and are a significant independent predictor of portal inflammation in this clinical entity. (C) 2012 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
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    THE STATUS OF OXIDATIVE STRESS AND ANTIOXIDANT DEFENSE IN PATIENTS WITH CHRONIC HEPATITIS D
    (Carbone Editore, 2016) Ucmak, Feyzullah; Solmaz, Ihsan; Ekin, Nazim; Kaplan, Ibrahim; Tuncel, Elif Tugba; Senates, Ebubekir; Yalcin, Kendal
    Introduction: Oxidative stress is increasingly recognized as an important factor in the progression of chronic liver disease of varying etiologies and antioxidants are utilized in the treatment of some of them. Chronic viral hepatitis D continues to be a significant health problem in certain regions of the world. Rates of response to currently proposed treatments are rather low. The aim of this study was to investigate oxidative stress in patients with chronic viral hepatitis D. Materials and methods: A total of 91 patients with chronic hepatitis D virus infection were included in this study (mean age: 42.2 +/- 11.7). In addition, 40 healthy volunteers were included in the study to form the control group. Patients were divided into two main sub-groups as cirrhotic (n=30) and non-cirrhotic (n=61) groups. Blood samples were taken from both patients and control subjects and compared for total oxidant status (TOS), total anti-oxidant status (TAS) and oxidative stress index (OSI). Results: TOS levels were significantly higher in the patients compared to the control sub-jects (p<0.001). Moreover, TOS levels were higher in the cirrhotic patients compared to the non-cirrhotic patients (p=0.006). TAS levels were significantly lower in the patients compared to the control subjects (p=0.003). OSI levels were significantly higher in the patients compared to the control subjects (p<0.001). Moreover, OSI levels were higher in the cirrhotic patients compared to the non-cirrhotic patients (p<0.05). Conclusion: These results are supportive of the role of oxidative stress in the pathogenesis of chronic viral hepatitis D. Antioxidant therapies might be considered in patients with chronic viral hepatitis D considering the presence of oxidative stress in these patients.
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    SYMPTOMATIC HYPOCALCAEMIA FOLLOWING INTRAVENOUS ADMINISTRATION OF ZOLEDRONIC ACID IN A FEMALE PATIENT WITH OSTEOPOROSIS
    (Carbone Editore, 2015) Senates, Banu Erkalma; Dogan, Abdullah; Senates, Ebubekir
    Bisphosphonates (BPs) are widely used in the treatment of postmenopausal osteoporosis. Zoledronic acid has the highest affinity with the bone as well as alters mineral surface properties, allowing greater adsorption. A 58-year-old woman presented with osteoporosis, was treated with a once-a-year IV of 5 mg of Zoledronic Acid. Before this once-a-year treatment, her serum calcium levels were normal although after the treatment, she was hospitalized with nausea, perioral and acral paresthesias and tingling. Biochemical analysis recorded Calcium levels as 5.94 mg/dl and low levels of vitamin D Serum. The Hypocalcaemia was initially treated with IV Calcium Gluconate solution followed by oral calcium and vitamin D supplements.
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    SYNBIOTIC THERAPY INCREASES ERADICATION RATE IN HELICOBACTER PYLORI ERADICATION
    (Carbone Editore, 2013) Sahin, Onder; Yesil, Atakan; Senates, Ebubekir; Akdogan, Mehmet Fatih; Konur, Sevki; Erdem, Emrullah; Dal, Mehmet Sinan
    Background: Probiotics are used in combinations of H. pylori eradication regimens with variable results. Many strains tested had shown positive effects on side effect profiles. However, a clear effect on eradication rate is studied thoroughly. We aimed to investigate the beneficial effect of a synbiotic combination in clarithromycin-based triple eradication therapy. Methods: Ninety-two patients who were infected with H. pylori (confirmed via endoscopic biopsy) were randomized into two groups: those undergoing standard triple treatment (control group (rabeprozol plus amoksisilin plus clarithromycin bid) n=49) and those receiving symbiotic (triple plus symbiotic bid group n=43). The symbiotic product contained lactobacillus, bifidobacterium and enterococcus. The 13C-breath test was performed at least 6 weeks after completing both therapy regimens. Results: In the synbiotic group, 3 of the patients complained of metallic taste (7.0%). 1 complained of diarrhea (23%), 3 had nausea (7.0%), 2 had gas (4.7%), 3 experienced vomiting (7.0%) and 1 had constipation (23%). In the control group, 3 of the patients experienced a metallic taste (63%), 7 had diarrhea (14.6%), 5 had nausea (10.4%), 3 had intestinal bloating (63%), 3 experienced vomiting (63%) and I had constipation (2.1%). There was no significant difference between the two groups. However, side effect intensity and eradication rates were significant different between the groups (p<0.05). The eradication rate in the synbiotic group was 88.4%, while it was 68.8% in the control group (p<0.05). Conclusion: The addition of synbiotic to triple therapy decreases the rate of antibiotic-related side effects. It also increases H. pylori eradication rates in clarithromycin-based triple therapy.