[14, 15] By assessing the graft steatosis in living donor liver transplantation,

Iwasaki et al. performed a study comparing L/S ratio on CT with histological findings for the diagnosis of steatosis.[16] However, reports comparing L/S ratio with histological findings in Japanese patients with NAFLD are scarce. In this study, we evaluated the grades of liver steatosis by comparing the L/S ratio on CT with the fat area of liver samples that was calculated by using the image analysis software. SIXTY-SEVEN BIOPSY-PROVEN NAFLD patients that included the patients with repeat biopsy for the evaluation of the clinical course of previously diagnosed NASH were enrolled. L/S ratio on CT was calculated.[14] Informed consent was obtained from each patient, and the study check details was conducted in conformity with the ethical guidelines of the 7th revision of the Declaration selleck chemicals llc of Helsinki (in October 2008),[17] and was approved by the ethics and research committees of our hospital. In patients, current and past daily alcohol

intake was less than 20 g per week or less than 140 g per week, respectively; details regarding alcohol consumption were obtained independently by at least two physicians and confirmed by close family members. None of the patients had received any medication that could cause NASH. Among these patients, those with the following disorders were excluded: secondary cause of steatohepatitis and drug-induced liver disease, alcohol liver disease, viral hepatitis, autoimmune hepatitis, primary biliary cirrhosis, α1-antitrypsin deficiency, hemochromatosis, Wilson’s disease

and biliary obstruction.[18] A complete physical examination was performed on each patient within 1 month prior Carnitine palmitoyltransferase II to the liver biopsy. The body mass index (BMI) was calculated as the weight (kg) divided by height squared (m2). Venous blood samples were taken in the morning following overnight fasting for 12 h. The laboratory evaluation in all patients included a blood cell count, platelet count (Plt) and measurement of the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyltransferase (GGT), total bilirubin, direct bilirubin, albumin, total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, fasting plasma glucose (FPG), fasting insulin, hemoglobin A1c (HbA1c), ferritin, uric acid, free fatty acid (FFA), and hyaluronic acids, type IV collagen 7 S, C-reactive protein, were measured using the standard techniques of clinical chemistry laboratories periodically during the treatment. Insulin resistance was calculated by the Homeostasis Model of Assessment – Insulin Resistance (HOMA-IR) using the following formula: HOMA-IR = fasting insulin (μU/mL) × plasma glucose (mg/dL) / 405.[19] Patients enrolled in this study underwent percutaneous liver biopsy under ultrasonic guidance after obtaining informed consent.