Gallstones and gallbladder wall thickening in patients with cirrhosis: Prevalence and clinical impact

Table 1 Baseline demographics and clinical characteristics of the study population, n (%)

Variable	Value
Age (years), mean ± SD	64 ± 12
Sex, male	94 (73.4)
Cirrhosis status
Compensated	28 (21.9)
Decompensated	100 (78.1)
Etiology of cirrhosis
Alcohol-associated liver disease	61 (47.7)
Metabolic dysfunction-associated steatohepatitis
Hepatitis B	21 (16.4)
Hepatitis C	21 (16.4)
Other	19 (14.8)
Child-Pugh classification
A	19 (14.8)
B	68 (53.1)
C	41 (32.0)
Cholelithiasis	51 (39.8)
Compensated	6 (21.4)
Decompensated	45 (45)
Asymptomatic gallbladder wall thickening	42 (32.8)
Compensated	3 (10.7)
Decompensated	39 (39)

Table 2 Proposed pathophysiologic mechanisms behind increased prevalence of cholelithiasis and asymptomatic gallbladder wall thickening in patients with cirrhosis

Patients with cirrhosis	Pathophysiologic mechanisms
Altered bile composition	Impaired bile acid synthesis and secretion; supersaturation of bile with cholesterol; hypersplenism/chronic hemolysis
Gallbladder hypomotility/bile stasis	Autonomic dysfunction-impaired gallbladder emptying
Portal hypertension	Impaired venous outflow; bacterial translocation; ascites
Hypoalbuminemia	Reduced oncotic pressure
Cause of cirrhosis	HCV; MASLD

HCV: Hepatitis C; MASLD: Metabolic dysfunction-associated steatotic liver disease.