Motility and dysmotility of the biliary tract

Muscle fibers in the biliary tree, and therefore the potential for dysmotility, are located in the gallbladder and the sphincter of Oddi. Dysmotility at either site is a potential cause of biliary pain in the absence of stones, although significant controversy persists. Diminished gallbladder emptying measured by biliary scintigraphy is an indication for cholecystectomy, although studies are contradictory regarding clinical benefit. It is likely that careful selection of patients for cholescintigraphic testing, many of whom have had missed stones or sludge, will identify patients who benefit from cholecystectomy. However, given the increased incidence of gallbladder stasis in functional gastrointestinal disorders, wide use of this study in patients with abdominal symptoms leads to a frequent failure to respond to cholecystectomy. Sphincter of Oddi dysfunction (SOD) has been best studied in patients with biliary type pain who have had prior cholecystectomy. Much less understood is the association of SOD with idiopathic recurrent acute pancreatitis and chronic pancreatitis. The least-studied clinical association for SOD is in patients with biliary pain and intact gallbladders. Elevated basal sphincter of Oddi pressure is predictive of clinical response to sphincterotomy in patients with postcholecystectomy pain in two randomized sham-controlled studies. However, patients with suspected SOD have the highest complication rate from endoscopic retrograde cholangiogram and sphincterotomy, and, therefore, careful patient selection is mandatory.     

Intragastric acidification reduces the occurrence of false-negative urea breath test results in patients taking a proton pump inhibitor

OBJECTIVE: The aim of this study was to investigate whether reducing intragastric pH, at the time of urea ingestion, decreases the likelihood of false-negative (FN) urea breath test (UBT) results in patients taking a proton pump inhibitor (PPI). METHODS: Patients with active Helicobacter pylori infection underwent a baseline 14C-UBT (UBT-1) followed by treatment with lansoprazole 30 mg/day for 14 to 16 days. On day 13, patients returned for a repeat standard UBT (UBT-2). Between days 14 to 16, patients underwent a modified UBT (UBT-3), which included consuming 200 ml of 0.1 N citrate solution 30 min before and at the time of 14C-urea administration. Breath samples were collected 10 and 15 min after 14C-urea ingestion. Mean 14CO2 excretion and the number of FN and equivocal UBT results were compared for the three UBTs. RESULTS: A total of 20 patients completed the study. Lansoprazole caused a significant decrease in mean breath 14CO2 excretion (disintegrations per minute) between UBT-1 (2.96 +/- 0.23) and UBT-2 (2.08 +/- 0.52, p < 0.05). Lansoprazole caused six (30%) FN and eight (40%) equivocal UBT-2 results. Mean breath 14CO2 excretion for UBT-3 (677 +/- 514) was greater than for UBT-2 (234 +/- 327, p = 0.001). UBT-3 caused only two (10%) FN and three (15%) equivocal results. The 15-min breath sample caused fewer FN and equivocal results than the 10-min sample for both UBT-2 and UBT-3. CONCLUSIONS: Giving citrate before and at the time of 14C-urea administration increases mean breath 14CO2 excretion and decreases FN and equivocal UBT results in patients taking a PPI. These observations suggest that it may be possible to design a UBT protocol that will remain accurate in the face of PPI therapy.