HEPATIC-ARTERY RESISTANCE IN ALCOHOLIC LIVER-DISEASE

Citation
A. Colli et al., HEPATIC-ARTERY RESISTANCE IN ALCOHOLIC LIVER-DISEASE, Hepatology, 28(5), 1998, pp. 1182-1186
Citations number
21
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
28
Issue
5
Year of publication
1998
Pages
1182 - 1186
Database
ISI
SICI code
0270-9139(1998)28:5<1182:HRIAL>2.0.ZU;2-Y
Abstract
Patency and direction of flow in portal veins and their branches are g enerally assessed by duplex Doppler ultrasonography (DDUS), whereas fe w data are available on hepatic arterial hemodynamics. In this study, resistive (RI) and pulsatility indexes (PI) were calculated at DDUS in 21 controls, 22 chronic alcoholic patients without evidence of liver damage, 19 patients with acute alcoholic hepatitis (AAH), 30 patients with chronic viral hepatitis (CVH), 23 patients with alcoholic cirrhos is, and 22 patients with viral-related cirrhosis. Diagnosis was based on clinical and histological findings. Mean +/- SD RI was similar in c ontrols and CVH patients (0.64 +/- 0.02 and 0.66 +/- 0.04, respectivel y), significantly decreased in alcoholic patients without liver damage and AAH patients (0.61 +/- 0.07 and 0.60 +/- 0.07) (P <.05), and sign ificantly increased in patients with alcoholic (0.72 +/- 0.04) and vir al-related cirrhosis (0.74 +/- 0.04) (P <.05), It was <0.60 in 9 of th e 19 FLAW patients (47%) and 11 of the 22 alcoholic patients without l iver damage (50%), and >0.70 in 39 of the 45 cirrhotic patients (87%) and 12 of the 71 noncirrhotic patients pooled together (17%). A signif icant correlation was observed between RI and PI (r =.83; P <.05). The coefficients of variation for intraobserver variability were 6.3% +/- 5.1% for RI and 10.1% +/- 6.2% for PI, and the corresponding figures for interobserver variability were 5.2% +/- 3.5% and 9.3% +/- 4.6%. Th ese findings support the existence of ethanol-related hepatic arterial vasodilation in AAH and alcoholic patients without liver damage. Prog ression of liver damage from AAI-I to cirrhosis profoundly impairs the hepatic responsiveness as a consequence of fibrosis with vascular dis tortion.