Alterations in liver hemodynamics have been described in non-alcoholic fatty liver disease (NAFLD), the most common liver disease. Aim of the study was to evaluate by Doppler sonography alterations in liver and spleen hemodynamics of NAFLD, which may have both diagnostic and pathophysiological implications.
Patients and Methods. Two-hundred and fifty subjects were studied: 40 control subjects (age 52±12yr), 210 patients with >5% steatosis (110 with hepatitis-C (age 47±12yr), 100 with non-obese metabolic syndrome (age 56±7yr)), evaluated by sonography. For diagnosis of >5% steatosis, liver-to-kidney ratio (L/K) of grey intensity of 50mm2 regions of interest, 5cm deep, was digitally measured in all patients (100% sensitivity and specificity for diagnosis of >5% steatosis, with a cut-off L/K>1.26). Portal vein diameter (PV) and flow velocity (PVvel), hepatic (PI-L) and splenic (PI-S) arterial pulsatility index, hepatic vein flow pattern and a-wave velociy (HV-a- vel) were evaluated by Doppler sonography.
Results. In patients with steatosis (>5%), PI-L (1.35±0.34) was increased (p<0.01), and hepatic vein a-wave velocity (8.29±9.05) was decreased (p<0.01), compared to controls (PI 1.02±0.18; a-wave: 14.8±3.0 cm/sec). PI-L was also increased in patients with severe steatosis (>50%) compared to patients with <25% steatosis (p<0.05). Portal velocity was decreased only in patients with >50% steatosis compared to controls (PVve: 26±5 vs 35±5 cm/sec), to patients with 5-25% steatosis (33±8cm/sec, p<0.001) and to patients with 25-50% steatosis (33±8cm/sec, p<0.001). 8% of patients without steatosis had a biphasic pattern of the hepatic vein waveform while 27% of patients with steatosis had a biphasic or monophasic waveform. No significant differences in portal vein diameter, splenic arterial PI, were found in any group of patients with steatosis.
In conclusion, in patients with NAFLD signs of portal hypertension (reduced portal velocity) are present only when steatosis is severe, while increased hepatic arterial resistance is present already in the early phase, possibly due also to oxidative stress and/or inflammation. Alterations in hepatic vein flow profile are not peculiar of steatosis.
