A 44-year-old woman comes to the office due to indigestion. The patient says she often develops right upper quadrant abdominal discomfort and nausea with fatty meals, which subside spontaneously after several hours. She does not use tobacco, alcohol, or illicit drugs. The patient immigrated to the United States from Nepal 10 years ago. Abdominal ultrasound reveals numerous gallstones, and she undergoes elective laparoscopic cholecystectomy. The stones in her gallbladder have very low cholesterol content and appear small, dark, and spiculated. Which of the following conditions most likely predisposed this patient to gallstone formation?
Show Explanatory Sources
Gallstones are formed by the aggregation of bile constituents and are categorized as cholesterol stones, pigment stones, or mixed stones. Pigment gallstones, which account for only 10%-25% of gallstone cases in the United States, are most common in rural Asian populations. These stones can be brown to black and arise from conditions that increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation. Brown pigment stones are associated with biliary tract infections (microbes producing β-glucuronidases), whereas black stones occur in the setting of chronic hemolysis (eg, sickle cell anemia, β-thalassemia, hereditary spherocytosis) and increased enterohepatic cycling of bilirubin (eg, ileal disease).
Grossly, black pigment stones are usually present in significant numbers and are small, spiculated, and friable. Because these stones contain high amounts of calcium carbonates and phosphates, they are often radiopaque and appear on x-ray.
(Choices B, C, D, and E) Obesity/metabolic syndrome, multiparity, oral contraceptive use, and rapid weight loss are significant risk factors for development of cholesterol gallstones.
Educational objective:
Black pigment stones arise from conditions that increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation. This may occur in the setting of chronic hemolysis (eg, sickle cell anemia, β-thalassemia, hereditary spherocytosis) and increased enterohepatic cycling of bilirubin (eg, ileal disease).