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    HFE mutations analysis of Turkish patients with nonalcoholic steatohepatitis
    (Springer, 2006) Şimşek, Halis; Balaban, Hatice Yasemin; Sümer, Hale; Yılmaz, Engin; Tatar, Gonca
    Chronic liver disease is a well-known cause of secondary iron overloading. Iron overloading of liver is associated with severity of fibrosis and increased risk for hepatocellular carcinoma as well as resistance to antiviral treatment. Iron content of liver in nonalcoholic steatohepatitis (NASH) patients is important because NASH causes chronic hepatitis, and there is also a debate on the role of iron for the pathogenesis of NASH.
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    Metabolic syndrome, non-alcoholic steatohepatitis (NASH), and hepatocyte growth factor (HGF)
    (Fundacion Clinica Medica Sur, 2006) Balaban, Hatice Yasemin; Sumer, Hale; Şimsek, Halis; Us, Durdal; Tatar, Gonca
    Background: Hepatocyte growth factor (HGF) is not only an antiapoptotic and antifibrotic factor of liver, but it is also an adipokine. Serum HGF levels are strongly associated with liver diseases, obesity, insulin resistance (IR), and metabolic syndrome (MS). Non-alcoholic steatohepatitis (NASH) is the hepatic component of MS. To the best of our knowledge, serum HGF levels in patients with NASH have not been previously studied. Our aim was to elucidate the correlation of HGF with the clinical and histopathological parameters of NASH. Methods: The study group consisted of 26 patients (13 men) who had clinical diagnoses of NASH and underwent liver biopsies. Controls were 13 volunteers (3 men) with negative viral autoimmune markers, and with normal levels of serum lipids and liver enzymes. Results: Among the NASH patients, 14 (54%) were overweight and 10 (39%) had grade I-II obesity. All the patients had class 3-4 non-alcoholic fatty liver disease (NAFLD) except for 2 who had class 2 disease. All of the patients had Child's class A liver disease, and MS was present in 5 (19%) patients and 8 (31%) patients had Homeostasis Model Assessment of Insulin Resistance (HOMA) > 3. Serum HGF levels were similar in NASH patients (1.24 ± 1.09 pg/mL) and controls (0.86 ± 0.22 pg/mL) (p = 0.21). The levels of serum HGF did not differ between the patients with or without MS (1.65 ± 1.48 pg/mL and 1.04 ± 0.80 pg/mL, respectively, p=0.65). HGF was not correlated with the laboratory or histopathological parameters. Conclusions: Serum HGF levels were higher in NASH patients than in the controls, although it was statistically insignificant and a correlation with MS could not be detected in this study.