OBJECTIVE:

Our aim was to establish whether small intestine transit time is defective in subjects with cholesterol gallstones.

METHODS:

We enrolled 10 patients (eight women, two men; mean age, 48.7 yr; mean body mass index [BMI], 22.4 Kg/m 2) with recently diagnosed cholelithiasis, with no liver pathology, who were not taking any drugs, and 11 comparable healthy volunteers (eight women, three men; mean age, 46.2 yr; mean BMI, 22.7 Kg/m 2), who served as controls. All subjects underwent orocecal (by starch breath test technique and serum assays of salazopyrin), oroileal (by serum assays of tauroursodeoxycholic acid), and duodenoileal (by serum assays of taurocholic acid) transit times; cholesterol saturation index; and bile acid composition and gallbladder motility studies (by ultrasound). For serum assays, blood samples were collected over a period of 7 h. Gallbladder motility and orocecal transit time were evaluated simultaneously.

RESULTS:

All four means of assessing transit time gave longer times in cholesterol gallstone patients than in controls: orocecal transit time (salazopyrin)= 366±13 vs 258±16 min, p< 0.0005; orocecal transit time (starch breath test)= 415±139 vs 290±15 min, p< 0.01; duodenoileal transit time: 272±23 vs 205±23 min, p< 0.03; and oroileal transit time: 308±18 vs 230±19 min, p< 0.009. Cholesterol gallstone patients showed an increase in percent molar biliary deoxycholic acid (30%±4.5% vs 16%±1.3%, p< 0.02) and a decrease in percent molar cholic acid 32%±2.2% vs 40%±1.3%, p< 0.03) and chenodeoxycholic acid (34%±3% vs 41%±1.8%, p< 0.03), compared with controls; patients also had greater percent molar biliary cholesterol. A linear relationship (r 2= 0.6324, p= 0.0012) between biliary deoxycholic acid and small bowel transit time was found. Residual gallbladder volumes were larger in cholesterol gallstone patients (11.38±1.27 vs 7.55±0.39 ml, p< 0.04), whereas basal gallbladder volumes, although higher, did not reach statistical significance (24.25±2.41 vs 19.98±1.63 ml; p= ns).

CONCLUSIONS:

This study confirms that patients with cholesterol gallstones have delayed small bowel transit, defective gallbladder motor function, and increased biliary deoxycholic acid. Delayed small bowel transit may contribute to supersaturation of bile with cholesterol by increasing deoxycholic acid production.