摘要
AIM: To simultaneously evaluate the presence of defects in gallbladder and gastric emptying, as well as in intestinal transit in gallstone patients (GS) and the effect of chronic ursodeoxycholic acid (UDCA) administration on these parameters and on serum bile acids and clinical outcome in GS and controls (CTR). METHODS: After a standard liquid test meal, gallbla-dder and gastric emptying (by ultrasound), oroileal transit time (OITT) (by an immunoenzymatic technique) and serum bile acids (by HPLC) were evaluated before and after 3 mo of UDCA (12 mg/kg bw/d) or placebo administration in 10 symptomatic GS and 10 matched healthy CTR. RESULTS: OITT was longer in GS than in CTR (P < 0.0001); UDCA significantly reduced OITT in GS (P < 0.0001), but not in CTR. GS had longer gastric half-emptying time (t1/2) than CTR (P < 0.0044) at baseline; after UDCA, t1/2 significantly decreased (P < 0.006) in GS but not in CTR. Placebo administration had no effect on gastric emptying and intestinal transit in both GS and CTR. CONCLUSION: The gallstone patient has simultaneous multiple impairments of gallbladder and gastric emptying, as well as of intestinal transit. UDCA administration restores these defects in GS, without any effect in CTR. These results confirm the pathogenetic role of gastrointestinal motility in gallstone disease and suggest an additional mechanism of action for UDCA in reducing bile cholesterol supersaturation.
AIM： To simultaneously evaluate the presence of defects in gallbladder and gastric emptying, as well as in intestinal transit in gallstone patients （GS） and the effect of chronic ursodeoxycholic acid （UDCA） administration on these parameters and on serum bile acids and clinical outcome in GS and controls （CTR）. METHODS： After a standard liquid test meal, gallbladder and gastric emptying （by ultrasound）, oroileal transit time （OITT） （by an immunoenzymatic technique） and serum bile acids （by HPLC） were evaluated before and after 3 mo of UDCA （12 mg/kg bw/d） or placebo administration in 10 symptomatic GS and 10 matched healthy CTR. RESULTS： OITT was longer in GS than in CTR （P 〈 0.0001）; UDCA significantly reduced oITT in GS （P 〈 0.0001）, but not in CTR. GS had longer gastric halfemptying time （t1/2） than CTR （P 〈 0.0044） at baseline; after UDCA, t1/2 significantly decreased （P 〈 0.006） in GS but not in CTR. Placebo administration had no effect on gastric emptying and intestinal transit in both GS and CTR. CONCLUSION： The gallstone patient has simultaneous multiple impairments of gallbladder and gastric emptying, as well as of intestinal transit. UDCA administration restores these defects in GS, without any effect in CTR. These results confirm the pathogenetic role of gastrointestinal motility in gallstone disease and suggest an additional mechanism of action for UDCA in reducing bile cholesterol supersaturation.
