Acid suppression increases rates of Barrett's esophagus and esophageal injury in the presence of duodenal reflux.

BACKGROUND: The contribution of gastric acid to the toxicity of alkaline duodenal refluxate on the esophageal mucosa is unclear. This study compared the effect of duodenal refluxate when acid was present, decreased by proton pump inhibitors (PPI), or absent. METHODS: We randomized 136 Sprague-Dawley rats into 4 groups: group 1 (n = 33) were controls; group 2 (n = 34) underwent esophagoduodenostomy promoting "combined reflux"; group 3 (n = 34) underwent esophagoduodenostomy and PPI treatment to decrease acid reflux; and group 4, the 'gastrectomy' group (n = 35) underwent esophagoduodenostomy and total gastrectomy to eliminate acid in the refluxate. Esophaguses were examined for inflammatory, Barrett's, and other histologic changes, and expression of proliferative markers Ki-67, proliferating cell nuclear antigen (PCNA), and epidermal growth factor receptor (EGFR). RESULTS: In all reflux groups, the incidence of Barrett's mucosa was greater when acid was suppressed (group C, 62%; group D, 71%) than when not suppressed (group B, 27%; P = 0.004 and P < .001). Erosions were more frequent in the PPI and gastrectomy groups than in the combined reflux group. Edema (wet weight) and ulceration was more frequent in the gastrectomy than in the combined reflux group. Acute inflammatory changes were infrequent in the PPI group (8%) compared with the combined reflux (94%) or gastrectomy (100%) groups, but chronic inflammation persisted in 100% of the PPI group. EGFR levels were greater in the PPI compared with the combined reflux group (P = .04). Ki-67, PCNA, and combined marker scores were greater in the gastrectomy compared with the combined reflux group (P = .006, P = .14, and P < .001). CONCLUSION: Gastric acid suppression in the presence of duodenal refluxate caused increased rates of inflammatory changes, intestinal metaplasia, and molecular proliferative activity. PPIs suppressed acute inflammatory changes only, whereas chronic inflammatory changes persisted.

Cocaine-associated lower limb ischemia.

Cocaine-associated thrombosis has been reported in the literature with reports of vascular injuries to cardiac, pulmonary, intestinal, placental, and musculoskeletal vessels; however, injury of the pedal vessels is rare. We report on a 31-year-old man who presented 2 months following a cocaine binge with limb-threatening ischemia without an otherwise identifiable embolic source. Angiography confirmed extensive occlusive disease of the tibioperoneal vessels. The patient improved following therapy with heparin and a prostacyclin analogue. Cocaine-induced thrombosis should be considered in patients presenting with acute arterial insufficiency in the lower limb without any other identifiable cause.

A prospective study of common bile duct calculi in patients undergoing laparoscopic cholecystectomy: natural history of choledocholithiasis revisited.

OBJECTIVE: To define the incidence of problematic common bile duct calculi in patients undergoing laparoscopic cholecystectomy. SUMMARY BACKGROUND DATA: In patients selected for laparoscopic cholecystectomy, the true incidence of potentially problematic common bile duct calculi and their natural history has not been determined. We evaluated the incidence and early natural history of common bile duct calculi in all patients undergoing laparoscopic cholecystectomy with intraoperative and delayed postoperative cholangiography. METHODS: Operative cholangiography was attempted in all patients. In those patients in whom a filling defect was noted in the bile duct, the fine bore cholangiogram catheter was left securely clipped in the cystic duct for repeated cholangiography at 48 hours and at approximately 6 weeks postoperatively. RESULTS: Operative cholangiography was attempted in 997 consecutive patients and was accomplished in 962 patients (96%). Forty-six patients (4.6%) had at least one filling defect. Twelve of these had a normal cholangiogram at 48 hours (26% possible false-positive operative cholangiogram) and a further 12 at 6 weeks (26% spontaneous passage of calculi). Spontaneous passage was not determined by either the number or size of calculi or by the diameter of the bile duct. Only 22 patients (2.2% of total population) had persistent common bile duct calculi at 6 weeks after laparoscopic cholecystectomy and retrieved by endoscopic retrograde cholangiopancreatography. CONCLUSIONS: Choledocholithiasis occurs in 3.4% of patients undergoing laparoscopic cholecystectomy but more than one third of these pass the calculi spontaneously within 6 weeks of operation and may be spared endoscopic retrograde cholangiopancreatography. Treatment decisions based on assessment by operative cholangiography alone would result in unnecessary interventions in 50% of patients who had either false positive studies or subsequently passed the calculi. These data support a short-term expectant approach in the management of clinically silent choledocholithiasis in patients selected for LC.