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. 2021 Sep 16;12(2):551–559. doi: 10.1016/j.jceh.2021.09.011

Gallstone Disease in Cirrhosis—Pathogenesis and Management

Bipadabhanjan Mallick 1,∗, Anil C Anand 1
PMCID: PMC9077239  PMID: 35535063

Abstract

Gallstones are more common in patients with cirrhosis of the liver, and the incidence increases with severity of liver disease. Pigment stones are the most frequent type of gallstones (GSs) in cirrhotics, and majority remain asymptomatic. Hepatitis C virus infection and nonalcoholic fatty liver disease are the underlying etiologies of liver diseases that most often associated with GSs. Multiple altered mechanisms in cirrhosis such as chronic hemolysis due to hypersplenism, reduced bile acid synthesis and transport, decreased cholesterol secretion, decreased apolipoprotein A-I and A-II secretion, gallbladder hypo-motility, autonomic dysfunction, and portal hypertension collectively lead to increased risk of lithogenesis. Asymptomatic GSs should be followed up closely and offered laparoscopic cholecystectomy once symptomatic in Child-Pugh class A and B patients. The model for the end-stage liver disease score is the best predictor of the outcome after cholecystectomy. In patients of Child-Pugh class C, conservative or minimally invasive approaches should be used to treat complications of GSs.

Keywords: gallstone, cirrhosis, Child-Pugh class, laparoscopic cholecystectomy

Abbreviations: ACLF, acute-on-chronic liver failure; CBD, common bile duct; CTP, Child-Pugh; EPBD, Endoscopic papillary balloon dilatation; EST, endoscopic sphincterotomy; EUS, endoscopic ultrasound; FXR, farnesoid X receptors; GSs, Gallstones; HBV, hepatitis B virus; HCV, Hepatitis C virus; IR, insulin resistance; LC, laparoscopic cholecystectomy; MELD, Model for end-stage liver disease; NAFLD, non-alcoholic fatty liver disease; NS 5A, non-structural protein 5A

The incidence of gallstones (GSs) is rising globally because of increasing incidence of metabolic diseases, sedentary life styles, and dietary changes in the society. The prevalence of GSs is 10–15% in the United States and Europe and 5–6% in India.1, 2, 3 GSs are essentially of two types: cholesterol stones (80%) and pigment stones (20%). The cholesterol stones are either pure cholesterol stones or mixed stones which contain >50% of their dry weight as cholesterol.4 Pigment GSs, on the other hand, are composed of essentially calcium bilirubinate, and they contain <20% dry weight as cholesterol.4 The prevalence of GSs is higher among women and increases with increasing age and parity. The risk factors for development of GSs are obesity, diabetes mellitus, dyslipidemia, total parenteral nutrition, rapid weight loss, ileal disease or resection, and chronic hemolysis.4 The reported prevalence of GS disease in patients with liver cirrhosis ranges between 25% and 30%, which is higher than that of the general population.5,6 In this review, we discuss the mechanisms responsible for the development of GSs as well as the clinical and therapeutic aspects of GSs formed in patients with cirrhosis of the liver.

Incidence and prevalence

Higher prevalence of GSs in patients with liver cirrhosis has been shown (Table 1) in both postmortem series7,8 and antemortem cross-sectional or longitudinal ultrasonography studies.6,9,10 In a longitudinal study of 618 patients with cirrhosis over a mean follow-up period of about 5 years, 22.8% developed GSs, and in another study of 182 patients with cirrhosis on a median follow-up period of 3.5 years, 11.5% developed GSs with an annual incidence rate of about 3–5%.10,11 The incidence of GSs in patients with cirrhosis is 3–8 times higher than that in the general population.6,9, 10, 11, 12 These studies have reported the incidence and prevalence of asymptomatic GSs. The prevalence of symptomatic GSs in patients with cirrhosis of the liver is largely unknown. In a longitudinal cohort study of 34 patients with asymptomatic GSs and cirrhosis, 6 (18%) patients developed symptoms for GSs over 6 years.13 In another study of 45 patients with a mean follow-up period of about 2.5 years, only 4.4% patients developed either symptoms or complication with an estimated annual rate of less than 2% (Table 2).14 Although these figures are comparable with noncirrhotic patients,15 the number of patients in the studies was small and the duration of follow-up was short, so there is no clear evidence whether asymptomatic GSs behave similarly in cirrhotic and noncirrhotic patients. Most of the GSs in patients with liver cirrhosis are pigment stones although a small proportion of patients harbor cholesterol stones.8,16,17 In a study of 369 transplant recipients with liver cirrhosis and GSs, the reported incidence of pigment stones was in 318 (86.2%) patients and cholesterol stones was in 51 (13.8%) patients.18

Table 1.

Prevalence of Asymptomatic Gallstones in Cirrhosis of the Liver.

Author
 Year
 Type of study
 No. of participants
 Prevalence of gallstones (%)
Cirrhosis Control Cirrhosis Control
Bouchier et al.7 1969 Postmortem 235 4460 29.4 12.8
Iber et al.8 1990 Postmortem 460 316 33 12
Acalovschi et al.5 1988 Ultrasonography 140 140 29.2 13.6
Fornari et al.9 1994 Ultrasonography 410 414 31.9 20.7
Del Olmo et al.20 1997 Ultrasonography 313 357 23.3 16.8
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Table 2.

Incidence of Asymptomatic and Symptomatic Gallstones in Cirrhosis of the Liver.

Characters Author Year No. of patients Follow-up years Incidence of gallstones Annual incidence rate (%)
Asymptomatic gallstones Benvegnu et al.11 1997 182 3.5 11.5% 3%
Conte et al.10 1999 618 5 22.8% 5%
Symptomatic gallstonesa Orozco et al.13 1994 34 6 18% 3%
Maggi et al.14 1997 45 2.5 4.4% <2%
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a

Patients already harboring asymptomatic gallstones.

Risk factors for GSs in cirrhosis

Age and Sex

Similar to the GSs in the general population, the incidence of GSs in patients with cirrhosis has female preponderance.10,19,20 The risk of GSs becoming symptomatic is also significantly higher in women than that in men.21 However, the degree of female predominance may be less in comparison with the general population as few studies have reported equal incidence of GSs in male and female cirrhotics.22, 23, 24 The overall prevalence of GSs in cirrhotics is increased significantly with advancing age.5,10,21

Family History of GSs

Similar to the general population, the incidence of GSs in cirrhotics is significantly higher in patients with family history of GSs.20 The incidence of symptomatic GSs is also higher in patients with positive family history.21 However, the role of genetic variants associated with familial GSs is yet to be proven in cirrhotics.

Metabolic Syndrome

Type 2 diabetes mellitus, hyperlipidemia, and high body mass index are reported to be independent risk factors for GSs in patients with liver cirrhosis.10,25 Increased insulin resistance (IR) associated with these disorders is the main culprit, as clinical studies have shown that IR could play a major role in the lithogenesis by favoring the production of cholesterol supersaturated bile and impaired gallbladder function.26

Severity of Liver Disease

The severity of liver disease is an independent risk factor for development of GSs. Most studies have shown that prevalence of GSs is higher in Child B or C cirrhosis than that in Child A cirrhosis and in decompensated cirrhosis than that in patients with compensated cirrhosis.9, 10, 11,24,25 This high prevalence of GSs in advanced liver disease could be probably due to longer duration of underlying disease.20 However, reduced hepatic synthesis and transport of bile salts with high estrogen levels in patients with decompensated cirrhosis can lead to development of GSs.27,28 A further explanation for increased prevalence of GSs in advanced liver disease can be associated with gallbladder hypo-motility.29,30

GSs in relation to etiology of liver cirrhosis

The etiology of cirrhosis may directly influence GS formation. The evidence for an association is conflicting. Some studies support it,9,11,23 whereas others negate it.5,20,31,32

Chronic Alcoholism

Fornari et al reported that previous alcohol abuse is an independent risk factor for development of GSs on prospective follow-up of patients with cirrhosis, and the risk ratio for GSs in alcoholic cirrhosis is 14 times higher than virus-associated cirrhosis.9 Benvegnu et al observed a higher rate of GS development in cirrhotic patients with prior history of alcohol abuse than in those without history of alcohol abuse (20.9% vs. 8.6%).11 Another study comparing the prevalence of GSs in alcoholic and viral etiology of cirrhosis reported that the frequency of GSs is higher in the alcohol etiology of cirrhosis.23 However, in a study of 313 cirrhotic patients, the etiology of cirrhosis did not seem to be important as a risk factor for GS formation.20 Another study by Sarin et al did not find any significant difference in prevalence of GSs in alcoholic and nonalcoholic cirrhotics.31 Genzini et al also did not find any evidence that the etiology of liver cirrhosis affects the prevalence of GSs in this group of patients.32 Thus, there is no agreement regarding the role of alcohol in directly affecting the risk of GS formation.

Hepatitis B and C

The association of hepatitis B and C infection with development of GSs has been evaluated in several studies.11,24,33,34 Benvegnu et al reported that the prevalence of GSs is higher in hepatitis B surface antigen (HBsAg)–negative cirrhotics than that in HBsAg-positive cirrhotics, and no difference was noted in relation to hepatitis C virus (HCV) infection.11 On follow-up of 182 patients with cirrhosis and without GSs for 40 months, the rate of development of new GSs is significantly lower in HBsAg-positive patients than that in HBsAg-negative patients, and there is no relevant difference in relation to anti-HCV positivity.11 Stroffolini et al observed that patients with HCV-related cirrhosis have higher prevalence of GSs than patients with hepatitis B virus (HBV) and alcohol-related cirrhosis.33 Chang et al observed that the prevalence of GSs in anti–HCV-positive patients, HBsAg-positive patients, and both marker–negative patients to be 11.7%, 5.4%, and 6%, respectively.34 Elzouki et al also reported that HCV-related cirrhosis has an increased risk of developing GSs in comparison with other etiology of cirrhosis.24 Acalovschi et al observed that the prevalence of GSs is higher in all age groups up to 60 years in patients with HCV-related chronic hepatitis without cirrhosis than that in the general population, indicating GSs occur earlier in patients with HCV infection.35 Thus, the evidence for the role of HBV infection in development of GSs is lacking. On the other hand, the association of HCV infection and GSs appears more solid, probably due to associated chronic hepatic inflammation in HCV infection.36

Nonalcoholic Fatty Liver Disease

Most of the epidemiological studies of GSs in cirrhosis were carried out before the concept of nonalcoholic fatty liver disease (NAFLD). The prevalence of both the conditions in the general population is high. One may think that an association between them is likely to be incidental as they share common risk factors. Interestingly, several studies have shown that the prevalence of GSs is higher in patients with NAFLD than that in the general population.37, 38, 39 Fracanzani et al reported that the prevalence of GSs progressively increases with advancing fibrosis stages, 15% in the F0-2 stage to 29% in the F3 stage and 56% in the F4 stage, and the prevalence of GSs increases with severity of necroinflammatory activity without differences in the severity of steatosis.38 Two recent meta-analyses have shown that the prevalence of GSs is higher in patients with NAFLD than that in the general population.40,41 In nutshell, NAFLD is an independent risk factor for GS disease, and the risk increases with advancing fibrosis of the liver.

Pathogenesis: how it is different from noncirrhotic patients

Multiple mechanisms in cirrhosis such as chronic hemolysis due to hypersplenism,5,16 reduced bile acid synthesis and transport,27 reduced cholesterol secretion, decreased apolipoprotein (apo) A-I and A-II secretion,42 gallbladder hypo-motility,29,30 autonomic dysfunction,43 and portal hypertension31 jointly lead to the formation of GSs (Figure 1). All these mechanisms can affect any one of the major steps in the pathogenesis of GSs such as the change in bile composition, enhanced crystal nucleation, and impaired gallbladder emptying.4

Figure 1.

Figure 1

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Overview of pathogenesis and management of gallstones in patients with cirrhosis of the liver. Factors contributing to pathogenesis are summarized in the blue balloons, whereas the approach to management is shown in green balloons below the cartoon.

Change in Bile Composition

Pigment Stones

Pigment stones develop when the bile is supersaturated with calcium bilirubinate, and the super-saturation occurs in the presence of an increased concentration of unconjugated bilirubin or free ionized calcium in the bile.44,45 Increased hemolysis in patients with cirrhosis leads to increased concentration of unconjugated bilirubin and bilirubin monoconjugates in bile which are more easily deconjugated by either nonenzymatic hydrolysis or β-glucuronidase secreted by hepatocytes and biliary epithelial cells.27,46 There is marked reduction of bile acid pools in patients with cirrhosis because of impaired synthesis and reduced secretion of phospholipids, especially cholesterol in bile.47, 48, 49 Combined effect of all these pathophysiological factors will enhance the risk of pigment stone formation in patients with cirrhosis.

Cholesterol Stones

Cholesterol stones occur mainly in patients with HCV and NAFLD-related cirrhosis because of super-saturation of cholesterol in bile as both are associated with IR.50, 51, 52, 53 Hepatic IR has been proved to play a major role in the formation of cholesterol stones by producing cholesterol supersaturated bile and impairing gallbladder function.26,54 IR also decreases the bile acid synthesis by enzyme inhibition and produces resistance to the farnesoid X receptors, leading to increased lithogenesis.55

Enhanced Crystal Nucleation

Both pigment and cholesterol stones develop on a matrix of mucin glycoproteins secreted by biliary epithelial cells. Cirrhosis of the liver is associated with reduced secretion of apo A-I and A-II which enhance the crystal nucleation as they act as antinucleating factors.42,56 HBV infection can modulate the function of apo A-I through HBx protein, resulting in decreased self-association and lipid binding ability.57 Similarly, nonstructural protein 5A of the HCV binds with apo A-I and potentially increases the risk of lithogenesis.58

Impaired Gallbladder Emptying

Impaired gallbladder emptying in cirrhosis has been proved by both ultrasonography and radionuclide hepatobiliary scintigraphy,29,30,59,60 and the degree of impairment is proportional to the severity of liver disease.61 Autonomic neuropathy associated with liver cirrhosis can contribute to the formation of GSs, perhaps by impairing gallbladder and sphincter of Oddi motility.43 Cirrhosis is a state of hyper-estrogenization, and a high serum level of estrogen can lead to development of GSs by impairment of gallbladder emptying, especially in men.22 However, a subsequent study did not find any effect of the plasma estrogen level on gallbladder emptying.30,62

In addition to these abovementioned mechanisms, some people believe that the HCV impairs gallbladder mucosal function and contributes to the development of GSs by directly infecting gallbladder epithelial cells.33,63 Sarin et al reported that the incidence of GSs is two times higher in people with noncirrhotic portal hypertension than that in the general population, and it is similar in comparison with cirrhotic portal hypertension, indicating a role of portal hypertension per se in pathogenesis of GSs.31

Treatment

Asymptomatic GSs

GSs in liver cirrhosis are usually asymptomatic and have more chances to be detected incidentally by ultrasonography at periodical evaluation for liver disease. There is a paucity of data on the natural history of asymptomatic GSs in patients with liver cirrhosis. In a longitudinal follow-up study of 34 patients with asymptomatic GSs and cirrhosis, only 6 (18%) patients developed symptoms for GSs (4 patients of acute cholecystitis and 2 patients of chronic cholecystitis) and 3 (8.8%) patients died because of complications of cholecystitis.13 In another longitudinal follow-up study of 45 patients, only 4.4% patients developed either symptoms or complications.14 The estimated annual rate of development of symptoms or complication is less than 3% in both the studies.13,14 Earlier studies have also reported that the incidence of acute cholecystitis is less in cirrhotic patients with GSs.64, 65, 66 In a case–control study of 140 patients with liver cirrhosis and with GSs, the multivariate analysis showed that only advanced age and family history of GSs are independent risk factors for development of symptoms.21 The lower complication rate despite having higher incidence of GSs in cirrhotic patients could probably be related to a higher percentage of pigment stones. The smaller size and greater friability of pigment stones make them less likely to obstruct the cystic duct.64 Given the high rate of morbidity associated with surgery in patients with cirrhosis, prophylactic cholecystectomy is not recommended in asymptomatic GSs, and they should be followed up closely.67

Symptomatic GSs

Medical Management

Bile acid dissolution therapy is not effective in resolution of symptoms or complications of GSs and is not recommended.68 A higher percentage of pigment stones and associated impaired gallbladder emptying in cirrhosis makes it more unsuitable for treatment of GSs in cirrhotic patients.

Surgical Management

Early elective cholecystectomy is recommended when symptoms supervene, and laparoscopic cholecystectomy (LC) is the treatment of choice for symptomatic GSs.67,68 The first study regarding the outcome of LC for symptomatic GSs in cirrhotic patients was published in 1993.69 Subsequently, multiple meta-analyses have shown that LC has advantage of fewer postoperative and infectious complications and shorter operative time and hospital stay than open cholecystectomy (OC) in patients with cirrhosis.67,70, 71, 72 However, the mortality and postoperative hepatic decompensation rates are similar in both LC and OC groups.70,72 The reported conversion rate from LC to OC is 4–14%.70,73, 74, 75 A population-based study analyzing cholecystectomy in cirrhotic patients showed that patients converted from LC to OC have lower infection rate, need for blood transfusion, and hepatic decompensation rates than the OC group.75 The model for the end-stage liver disease (MELD) score is a better predictor of the outcome after LC than the Child-Pugh (CTP) score.73,76,77 Delis et al observed that patients with a preoperative MELD score above 13 have a higher postoperative complication rate.76 All the abovementioned meta-analyses have included a majority of Child-Pugh class A and B patients and very few number of Child-Pugh class C patients. The risk of mortality and postoperative hepatic decompensation is very high in Child-Pugh class C patients.78, 79, 80 The conservative approach would be preferable for symptomatic GSs in Child-Pugh class C patients (Figure 2).

Figure 2.

Figure 2

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The flowchart for management of gallstones in cirrhosis of the liver. ∗Ascites, variceal bleed, and/or hepatic encephalopathy. ∗∗Severe acute cholecystitis.

Management of Acute Calculus Cholecystitis

Antibiotics and cholecystectomy, including open and laparoscopic, are the standard of care for acute calculus cholecystitis. As mentioned previously, these procedures are quite safe in patients with Child-Pugh class A and B cirrhosis. In patients with Child-Pugh class C, cholecystectomy is associated with a higher rate of postoperative complications and mortality. The conservative approach with antibiotics should be the first line of management in these patients presenting with acute cholecystitis. Minimally invasive gallbladder drainage procedures, that is percutaneous cholecystostomy, trans-papillary or endoscopic ultrasound (EUS)–guided transmural gallbladder drainage, can be considered in case of failure of medical management. Cholecystectomy can be performed in the later stage if liver function improves. Percutaneous gallbladder aspiration has shown to be an effective alternative to LC for acute cholecystitis in Child-Pugh class C patients.79 Percutaneous cholecystostomy can be performed with an accepted complication rate in cirrhotic patients who are at high risk for surgery.81 Endoscopic trans-papillary gallbladder stenting is also an effective option to prevent morbidity and mortality in Child-Pugh class C patients with symptomatic GSs.82,83 Per-oral cholecystoscopy with lithotripsy can be another treatment option with added advantage of stone clearance.84 EUS-guided transmural gallbladder drainage using the self-expandable metal stent or lumen apposing metal stent has shown to be effective in treating acute cholecystitis with lower adverse events in patients who are deemed to be poor candidates for surgery.85,86 It has been already established as a safe and efficacious modality for cholecystitis in patients with Child-Pugh class A and B cirrhosis who are nonoperative candidates, but studies are needed to determine its role in patients with Child-Pugh class C cirrhosis.87

Management of Common Bile Duct Stones

The prevalence of common bile duct (CBD) stones is three times higher in cirrhotic patients than that in noncirrhotics patients.8,88 The reported incidence of acute cholangitis is 19% in cirrhotic patients with CBD stones.89 There is an increased risk of morbidity and mortality with CBD exploration; endoscopic sphincterotomy (EST) is a safer option for management of choledocholithiasis in patients with cirrhosis.89, 90, 91 However, the overall risk of post-EST bleeding and pancreatitis is higher in cirrhotic patients than that in noncirrhotic patients.92 Endoscopic papillary balloon dilatation (EPBD) without sphincterotomy has been shown to be safe and effective treatment of CBD stones in patients with liver cirrhosis.93,94 A population-based study of cirrhotic patients has shown that EPBD is associated with lesser incidence of post-procedure bleeding than EST (1.9% vs. 3.5%).95 The risk of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis, cholangitis, and bleeding is significantly higher in decompensated cirrhotics than that in compensated cirrhotics, and the MELD score can predict the risk of post-ERCP complication.96, 97, 98 The incidence of acute-on-chronic liver failure (ACLF) is higher in patients who develop post-ERCP complications, especially cholangitis.98 Patients with an MELD score ≥15 are three times more likely to develop ACLF after ERCP.98 Thus, a thorough risk and benefit assessment should be performed before ERCP in decompensated cirrhotic patients. ERCP in patients with cirrhosis should be performed at high-volume centers and in expert hands to minimize the post-ERCP complications, which will subsequently reduce the rate of hepatic decompensation after ERCP. When the indication is strong, the benefit of ERCP still outweighs the risk among patients with cirrhosis.

The frequency of GSs is higher in patients with cirrhosis of the liver than that in the general population, and it increases with severity of liver disease. Most of GSs in cirrhotics are pigment stones. Hepatitis C and NAFLD are strongly associated with increased lithogenesis. Asymptomatic GSs should be followed up closely and offered LC once symptomatic in Child-Pugh class A and B patients. In patients of Child-Pugh class C, conservative or minimally invasive procedures should be used to treat complications of GSs.

Credit authorship contribution statement

Bipadabhanjan Mallick: literature search, writing the manuscript and approval to final version. Anil C Anand: Conceptualization, editing the manuscript and approval to final version.

Conflicts of interest

The authors have none to declare.

Funding

None.

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