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Hepatic artery resistance in alcoholic liver disease

✍ Scribed by Agostino Colli; Massimo Cocciolo; Nicola Mumoli; Nadia Cattalini; Mirella Fraquelli; Dario Conte


Publisher
John Wiley and Sons
Year
1998
Tongue
English
Weight
456 KB
Volume
28
Category
Article
ISSN
0270-9139

No coin nor oath required. For personal study only.

✦ Synopsis


Patency and direction of flow in portal veins and their branches are generally assessed by duplex Doppler ultrasonography (DDUS), whereas few 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 cirrhosis, and 22 patients with viral-related cirrhosis. Diagnosis was based on clinical and histological findings. Mean +/- SD RI was similar in controls and CVH patients (0.64 +/- 0. 02 and 0.66 +/- 0.04, respectively), significantly decreased in alcoholic patients without liver damage and AAH patients (0.61 +/- 0. 07 and 0.60 +/- 0.07) (P < .05), and significantly increased in patients with alcoholic (0.72 +/- 0.04) and viral-related cirrhosis (0.74 +/- 0.04) (P < .05). It was <0.60 in 9 of the 19 AAH patients (47%) and 11 of the 22 alcoholic patients without liver damage (50%), and >0.70 in 39 of the 45 cirrhotic patients (87%) and 12 of the 71 noncirrhotic patients pooled together (17%). A significant 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%. These findings support the existence of ethanol-related hepatic arterial vasodilation in AAH and alcoholic patients without liver damage. Progression of liver damage from AAH to cirrhosis profoundly impairs the hepatic responsiveness as a consequence of fibrosis with vascular distortion.


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