Relationship of bile acid pool size to the formation of lithogenic bile in female Indians of the southwest.

Abstract

Bile acid kinetics and pool size were determined in 18 female American Indians of the Southwest. Eleven patients had a lithogenic bile and 7 patients had a normal bile. Eight of the patients with a lithogenic bile had cholesterol gallstones which were confirmed both at surgery and by analysis of the gallstones; the remaining 3 patients in this group had no radiological evidence of gallstones. The group of 7 patients with a normal bile had no evidence of gallstones by oral cholecystogram. The patients were administered orally 14C-cholic and 14C-chenodeoxycholic acids. The primary and total bile acid pools were found to be significantly smaller in patients with a lithogenic bile than in patients with a normal bile (1.1 g versus 1.6 g). The 3 patients with a lithogenic bile and no gallstones also had greatly diminished bile acid pools (under 1 g). The primary bile acids of patients with a lithogenic bile turned over at a faster rate than in patients with a normal bile. There was no significant difference in the daily production of the primary bile acids between the two groups. The production of primary bile acids in the female Indian averaged 350 mg per day. The data suggest that the diminished bile acid pool in the female Indians with a lithogenic bile resulted from an inability of the liver to synthesize adequate amounts of bile acids to compensate for bile acid excretion. Biliary lipid excretion was estimated from the total bile acid pool size and biliary lipid composition. Although there was a slight decrease in phospholipid and a slight increase in cholesterol excretion in the patients with a lithogenic bile, these differences were not significant. However, these alterations in biliary lipid excretion were of sufficient magnitude when coupled with the reduction in the bile acid pool to tip the bile out of the micellar zone. Based on the findings of this and earlier reports, it is suggested that a diminished bile acid pool could be responsible for the development of a bile supersaturated with cholesterol and subsequent cholesterol gallstone formation.