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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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    Öğe
    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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    Öğe
    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.