Autonomic dysfunction and cholelithiasis in patients with cirrhosis

Citation
A. Chawla et al., Autonomic dysfunction and cholelithiasis in patients with cirrhosis, DIG DIS SCI, 46(3), 2001, pp. 495-498
Citations number
22
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTIVE DISEASES AND SCIENCES
ISSN journal
01632116 → ACNP
Volume
46
Issue
3
Year of publication
2001
Pages
495 - 498
Database
ISI
SICI code
0163-2116(200103)46:3<495:ADACIP>2.0.ZU;2-V
Abstract
Gallstones are seen in 33-46% of patients with cirrhosis, and their prevale nce is known to increase with the duration and severity of liver disease. W e hypothesized that autonomic neuropathy may contribute to the formation of gallstones or gallbladder disease, as in diabetics with autonomic neuropat hy, due to impaired gallbladder emptying. The objective of our study was to determine the prevalence of gallstones or gallbladder disease in cirrhotic patients with and without autonomic neuropathy. We determined autonomic fu nction tests, gallstones, and other gallbladder disease in 123 (male 71) wi th varying severity of liver disease (Child classes: A, 40; B, 45; C, 35). In all, 54 patients had gallstones and an additional 22 patients had other gallbladder disease (cholecystitis, common bile duct stones, or debris). Au tonomic neuropathy was seen in 97 patients (one abnormal test in 48 and two or more in 49). The prevalence of gallstones was similar in Child A (57%), Child B (64%), and Child C (63%) cirrhosis. The gallstones or gallbladder disease was not increased in women, blacks, diabetics, or alcoholic cirrhot ics. The prevalence of gallbladder disease was increased in patients with a utonomic neuropathy (51% vs 35%, P = 0.08); in patients with Child C cirrho sis, gallstones (P = 0.018) and gallbladder disease (P = 0.03) were seen mo re commonly in patients with autonomic neuropathy. Our findings suggest tha t autonomic neuropathy may contribute to the formation of gallstones in pat ients with advanced cirrhosis, perhaps by impairing gallbladder and sphinct er of Oddi dysmotility.