[Relation of non-alcoholic hepatic steatosis to early carotid atherosclerosis in diet-controlled impaired glucose tolerance subjects]. / Relazione della steatoepatite non alcolica all'aterosclerosi carotidea precoce in pazienti con Intolleranza ai carboidrati.

AIMS: To compare carotid artery intima-media thickness values, as a reliable marker of early atherosclerosis, in individuals with and without nonalcoholic hepatic steatosis, and to evaluate whether such differences are mediate by metabolic syndrome variables. MATERIALS AND METHODS: Carotid intima-media thickness (by ultrasonography), hepatic steatosis (by ultrasonography), insulin resistance (by Homeostasis Model Assessment-HOMA), steatohepatitis (by histologic specimen) were measured in 54 non-alcoholic steatohepatitis, and 54 IGT, compared with 54 healthy subjects. RESULTS: Subjects with nonalcoholic steatohepatitis had markedly greater carotid intima-media thickness measurements (1.38±0.12 vs 1.12±0.10 mm; p<0.001) than controls. The marked differences in carotid intima-media thickness that were observed between the groups were little affected by adjustment for age, sex, body mass index, waist/hip ratio, diabetes duration, blood pressure, lipids. CONCLUSIONS: These results suggest that in IGT non smoking subjects, the significant increase of carotid intima-media thickness in presence of nonalcoholic steatohepatitis cannot be mediated by HOMA-estimated insulin resistance; thus the NAFDL and NASH can be independent features of metabolic syndrome and other unknown factors can be responsible to progression of steatosis to NAFLD and NASH.

Carotid intima-media thickness and liver histology in hemodialysis patients with nonalcoholic Fatty liver disease.

The prevalence of atherosclerotic cardiovascular disease in chronic hemodialysis (HD) patients has been demonstrated to be higher than in healthy people. Severe liver fibrosis is strongly associated with early carotid atherosclerosis and it might reduce the survival of patients who undergo both renal replacement therapy and transplantation. We wanted to assess whether nonalcoholic fatty liver disease (NAFLD) was associated with altered intima-media thickness (IMT) in HD patients as an independent marker of subclinical atherosclerosis. We enrolled 42 patients undergoing HD and 48 patients with normal renal function, all of them with high levels of aminotransferases and an ultrasonographic diagnosis of liver steatosis. The control group consisted of 60 healthy subjects. Laboratory tests for inflammatory and oxidative markers, ultrasonographic liver evaluation, carotid IMT measurement, and liver biopsy were performed. Different degrees of fibrosis were detected in our study cohort. Worse liver histopathological scores and higher plasmatic levels of C-reactive protein, reactive oxygen species, and vascular cell adhesion molecule-1 were found in HD patients. Carotid IMT was significantly higher (p < 0.005) in patients with histological steatosis. HD patients may develop active and progressive chronic hepatitis faster than patients with normal renal function and the thickness of their carotid intima-media might be markedly increased. These two conditions seem to be independent on classical risk factors and on metabolic syndrome. They might be related to the high levels of oxidants and to the inflammatory state, which are typical of patients undergoing HD. Independently related with the traditional risk factors for cardiovascular disease, nonspecific inflammation and oxide-reductive imbalance may play an important role in the progression of NAFLD and atherosclerotic disease in HD patients.