Salta al contenuto principale
Passa alla visualizzazione normale.


Effects of Steatosis on Hepatic Hemodynamics in Patients with Metabolic Syndrome

  • Autori: Soresi, M.; Giannitrapani, L.; Noto, D.; Terranova, A.; Campagna, M.; Cefalù, A.; Giammanco, A.; Montalto, G.
  • Anno di pubblicazione: 2015
  • Tipologia: Articolo in rivista (Articolo in rivista)
  • Parole Chiave: Doppler ultrasonography; Metabolic syndrome; Non-alcoholic fatty liver; Radiology, Nuclear Medicine and Imaging; Radiological and Ultrasound Technology; Biophysics
  • OA Link:


The aim of our study was to assess the hemodynamic changes in hepatic and splenic circulation using B-mode ultrasonography and color Doppler ultrasonography, in a population of patients with metabolic syndrome divided with respect to the presence or absence of steatosis diagnosed by ultrasonography. One hundred forty-one patients were included in the study. The severity of non-alcoholic fatty liver disease was classified as mild, moderate or severe. Visceral fat thickness, longitudinal diameter of the spleen, diameter of the portal vein, mean maximum portal vein flow velocity, hepatic artery and splenic artery resistivity indexes and hepatic vein flow phasicity were measured. Non-alcoholic fatty liver disease was detected in 114 of 141 patients, with a prevalence of 80.8%. Patients with steatosis had significantly greater diameters of the portal vein, longitudinal diameters of the spleen, visceral fat thickness and hepatic artery and splenic artery resistivity indexes, whereas their portal vein flow velocities were significantly lower. Non-alcoholic fatty liver disease severity correlated positively with diameter of the portal vein, longitudinal diameter of the spleen and visceral fat thickness and negatively with hepatic artery and splenic artery resistivity indexes and reduced hepatic vein flow phasicity. Our patients with metabolic syndrome and non-alcoholic fatty liver disease had a flattened hepatic vein flow phasicity, greater portal vein diameter, reduction in portal vein flow velocity and intrahepatic arterial vasodilation. The vasodilation of the intrahepatic arterial system was likely activated both by the effect of insulin resistance and as a physiologic adaptation to restore hepatic flow. The increase in spleen volume might be related to the organomegaly typical of obese patients.