SAT-872 - An Uncommon Adverse Effect of Tirzepatide: Biliary Dyskinesia

Biliary dyskinesia is a functional gallbladder disorder characterized by impaired motility without any structural disease. Tirzepatide is a dual GLP-1 and GIP receptor agonist, which slows gastric and gallbladder emptying. It can improve postprandial glucose and triglyceride control but may also increase susceptibility to biliary disease. Current evidence primarily focuses on gallstone-related pathology while not emphasizing gallbladder motility. A meta-analysis done by (Zheng et al., 2024) of 12,351 patients demonstrated that tirzepatide was significantly associated with gallbladder and biliary disease (RR = 1.52) and cholelithiasis (RR = 1.67), without a dose–response relationship. Importantly, these trials did not assess biliary dyskinesia as an outcome.

A 28-year-old female presented to the ED with a complaint of pain over the epigastrium and right upper quadrant. Was also having nausea without any vomiting. She was on Mounjaro and has been taking it for the past 2-years. Liver enzymes and bilirubin were within normal limits with an AST of 15, an ALT of 10, Alkaline Phosphatase of 53, and a Total Bilirubin of 0.70. No significant lab abnormalities were found. The US abdomen showed no evidence of wall thickening, pericholecystic fluid, or calculi. A few gallbladder polyp was found, the largest was 5 mm. The common bile duct was 3 mm in diameter. The HIDA scan was suggestive of biliary dyskinesia with the EF of 7%. MRCP No evidence of intrahepatic or extrahepatic biliary ductal dilatation. No evidence of distal obstructing lesions within the pancreatic head or at the ampulla. She has undergone a laparoscopic cholecystectomy without any complications. Her abdominal pain was better afterwards.

Our case highlights biliary dyskinesia as a potential and often underrecognized consequence of tirzepatide. Unlike cholelithiasis, biliary dyskinesia reflects abnormal motility without obstruction, however it can present with recurrent colicky pain. Further research is needed to clarify the incidence, mechanisms, and clinical relevance in patients receiving GLP-1–based therapies.

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