Gall-bladder wall thickening in patients with liver cirrhosis

Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58±8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Fortyone (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (>4mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6±0.6 vs 2.9±0.7 gm/dL, respectively; P< 0.05), a longer prothrombin time (13±6 vs 16±6s, respectively; P<0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P<0.05) and more patients with ascites (8 vs 50%, respectively; P<0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9±4.5 vs 17.1±4.1 mmHg, respectively; P<0.01) and a lower systemic vascular resistance (SVR; 1144±332 vs 1010±318 dyn.s/cm⁵, respectively; P< 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm⁵, were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.