Abstract: | UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is a clinicopathological condition which ranges from simple steatosis and steatohepatitis to cryptogenetic cirrhosis. As insulinresistance plays a central pathogenetic role, NAFLD is regarded as the hepatic feature of the metabolic syndrome. Type 2 diabetes mellitus and obesity are the conditions most frequently associated with NAFLD. Subclinical inflammation has been suggested as a possible connective mechanism between glycoregulation disorders and NAFLD. The purpose of our study was to evaluate the prevalence and severity of glycoregulation disorders (impaired glucose tolerance and type 2 diabetes mellitus) in patients with ultrasonographical certified NAFLD, and to determine medium levels ofC reactive protein in these individuals. MATERIAL AND METHODS: The study was conducted on 104 patients with ultrasonographical certified steatosis, divided into two subgroups: simple steatosis and steatohepatitis, based on the elevation of hepatic enzymes. A control group of 100 subjects without ultrasonographical proof of hepatic steatosis had been used. Fasting glucose, oral glucose tolerance test and C reactive protein levels were performed for each patient. Statistical analysis was based on student t-test and Hi-square test. RESULTS: The prevalence of glycoregulation disorders was significantly higher in patients with NAFLD than in controls (p < 0.05). Patients with steatohepatitis had a significantly higher prevalence of type 2 diabetes mellitus than those with simple steatosis. Medium levels of C reactive protein were significantly higher in patients with NAFLD than in controls, respectively in subjects with steatohepatitis than in those with simple steatosis. CONCLUSIONS: NAFLD is at risk for developing glycoregulation disorders compared with controls; the severity of liver damage is correlated with an augmentation in the severity of glycoregulation disorders. Patients with NAFLD have higher levels of C reactive protein compared with controls, the medium levels C reactive protein increasing with an increase in hepatic damage. |