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- Stones in common bile duct (CBD)
- Several types: cholesterol (majority), calcium bilirubinate or pigment, and mixed stones
- System(s) affected: gastrointestinal; hepatobiliary
- Synonym(s): CBD stones; CBD calculi
- Gallstone disease affects >20 million Americans (14.2 million females, 6.3 million males).
- Choledocholithiasis noted in 7–12% of patients undergoing cholecystectomy for symptomatic gallstones
- Choledocholithiasis noted in 18–33% of patients with acute biliary pancreatitis
- Incidence increases with age (30–50% of patients >60 years with gallstones have concurrent CBD stones):
- Patients with choledocholithiasis are, on average, 10 years older than those with cholelithiasis.
- Internationally, incidence is increased due to parasitic infections (e.g., Ascaris lumbricoides).
- Associated with chronic conditions such as dyslipidemia, obesity, cardiovascular disease, as well as increased risk of mortality
- Symptomatic gallstone disease affects 10% of the U.S. population, leading to ~700,000 cholecystectomies at an annual cost of ~$6.5 billion.
- Twice as common among women
- Increased prevalence among Hispanics, Asians, Native Americans
Etiology and Pathophysiology
- CBD stones may be primary or secondary:
- Primary stones form within the biliary tract with bile stasis or chronic bactibilia.
- Secondary stones (more common) form within the gallbladder and migrate to the biliary tree.
- Stones may migrate to the duodenum or remain in the CBD (due to small diameter of Vater papilla). Not all CBD stones are symptomatic.
- Obstruction leads to jaundice. Biliary stasis can trigger infection (e.g., ascending cholangitis).
- Dysfunction/obstruction of the CBD and/or main pancreatic duct can trigger acute pancreatitis.
- Chronic hemolytic states increase the risk for gallstone formation.
- Formation of de novo pigment stones can result from:
- Dilated, sclerosed, or strictured ducts (e.g., recurrent cholangitis)
- Hepatobiliary parasitism (A. lumbricoides or Clonorchis sinensis)
- MDR3 defects may predispose to biliary sludge, cholelithiasis, cholestasis of pregnancy, and subsequent choledocholithiasis.
- Variants of UGT1A1 responsible for bilirubin conjugation may increase cholesterol and pigment gallstone formation.
- Hepatobiliary cholesterol hemitransporter ABCG8 variant p.D19H doubles the odds of gallstone recurrence after cholecystectomy.
- LITH genes are thought to increase susceptibility to development of gallstones. Studies in mice show this class of genes creates a lithogenic environment by altering various lipid transporters, nuclear hormone receptors, and enzymes.
- Obesity; high caloric diet, low-fiber diet
- Rapid weight loss (>25% of original weight, especially after bariatric surgery) or prolonged fasting
- Gender (females > males)
- Family history
- Crohn disease
- Gallbladder stasis: spinal cord injury, somatostatin
- Drugs (octreotide, thiazide diuretics)
- Chronic estrogen exposure
- Prior cholecystectomy:
- <2 years prior: Consider retained stone.
- >2 years prior: Consider recurrent stone.
- Maintain healthy weight and lifestyle. Avoid rapid weight loss.
- Consider UDCA therapy in LPAC syndrome.
Commonly Associated Conditions
- Cholelithiasis, cholecystitis, cholangitis
- Gallstone pancreatitis
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