Nonanastomotic biliary strictures that involve only the biliary tree of the graft occur after orthotopic liver transplantation in patients with hepatic artery thrombosis, chronic ductopenic rejection and ABO blood group incompatibility. This complication may also occur in the absence of these known risk factors. The major focus of our study was to evaluate the risk factors for nonanastomotic biliary stricturing of unknown cause after orthotopic liver transplantation. Results demonstrate that the development of biliary strictures is strongly associated with the duration of cold ischemic storage of allografts in both Euro-Collins solution and University of Wisconsin solution. Results also demonstrate that strictures are not associated with the type of biliary reconstruction, the primary liver disease, cytomegalovirus infection, allograft rejection or the presence of a positive lymphocytotoxic crossmatch. More recently, we have markedly reduced the occurrence of nonanastomotic biliary stricturing by decreasing the ischemia time of our allografts. Thus nonanastomotic biliary strictures appear to be the result of the ischemia/reperfusion-induced tissue injury associated with the harvest and implantation of allografts.

The clinical significance and outcome of nonanastomotic strictures and dilatations involving only the biliary tree of the graft with a radiological appearance of biliary ischemia is unknown. Therefore we analyzed the grafts of 128 patients to evaluate the biochemical, radiological and histological features that prompted the diagnosis of ischemic-type biliary stricture and the clinical outcome of this complication. Ischemic-type biliary strictures were diagnosed in 25 patients (19%). Initial graft function was similar in all patients, whether or not this complication developed. Most ischemic-type biliary strictures occurred between 1 and 4 mo after orthotopic liver transplantation. However, the appearance of ischemic-type biliary stricture in the month after transplantation was predictive for a poor outcome in all six grafts with early onset of ischemic-type biliary strictures. Eighteen patients (72%) were treated with biliary stents and repeated dilatations. Long-term patency was achieved in 88% of these patients. Repeat transplantation was performed in six patients (24%); five survived. Finally, patients with ischemic-type biliary strictures spent more time in the hospital during the first year after orthotopic liver transplantation than did patients without the complication (62 +/- 27 days vs. 37 +/- 20 days; p < or = 0.001). This was due to repeated hospitalizations and a higher incidence of retransplantation. One-year graft survival was lower in patients with ischemic-type biliary strictures than in patients without ischemic-type biliary strictures (69% vs. 88%; p = 0.006). However, 1-yr patient survival was similar in the two groups (91% vs. 89%). In conclusion, early appearance of ischemic-type biliary stricture features is associated with poor graft prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Routine acquisition of images in the arterial phase is unnecessary for detection of pancreatic adenocarcinoma. Images of the pancreas obtained in the hepatic phase with multi-detector row CT most accurately display vascular invasion.

BE is common in unscreened male and female patients at least 65 yr of age who are referred for colonoscopy. Men were more likely than women to have BE although it occurred in both sexes. Reflux symptoms were fairly common but a poor predictor of BE.

The non‐inherited gastrointestinal polyposis syndromes represent a group of rare disorders characterized by the presence of multiple, non‐adenomatous polyps on the gastrointestinal mucosa occurring in unrelated patients. We present here a review of the clinical and histo‐ pathological aspects of the syndromes to include the Cronkhite–Canada syndrome, hyperplastic polyposis and lipomatous polyposis. While infrequently encoun‐ tered, these diseases can have devastating clinical effects that may be aggravated by delays in diagnosis and treatment. Prompt accurate diagnosis and treatment of these uncommon disorders depend on a sound working knowledge of the distinct clinical and pathological features described herein.

A retrospective analysis was performed of contrast material-enhanced current-generation computed tomographic (CT) examinations in 56 patients with documented chronic pancreatitis. Dilatation of the main pancreatic duct was seen in 68% of cases, parenchymal atrophy in 54%, pancreatic calcifications in 50%, fluid collections in 30%, focal pancreatic enlargement in 30%, biliary ductal dilatation in 29%, and alterations in peripancreatic fat or fascia in 16%. The relatively small proportion of examinations in which no abnormalities were observed, 7%, differs from that in early reports, as does the absence of generalized pancreatic enlargement. Pancreatic ductal dilatation and parenchymal atrophy were notably more prevalent than reported previously. Nine of the 17 patients with focal pancreatic enlargement had calculi within the mass, which suggested benign disease; of the eight other patients, two of whom had coexistent carcinoma, this finding was absent and the masses were considered indeterminate at CT.

As implemented at the authors' institution, use of CT fluoroscopy for the guidance of interventional radiologic procedures markedly decreased patient radiation dose and total procedure time compared with use of conventional CT guidance.

Nonanastomotic hilar bile duct strictures developed in 16 of 152 patients who underwent liver transplantation. The type of pretransplantation liver disease did not significantly affect the likelihood of hilar stricture formation. Possible causes of hilar biliary strictures include hepatic artery occlusion, ductopenic arteriopathic rejection, and cytomegalovirus infection; however, five of the 16 patients had hilar strictures without these complications. Hilar strictures developed within 3 months after transplantation in 11 of the 16 patients. Strictures began as a slight common hepatic duct irregularity and progressed to mucosal cast formation and later to firm strictures. Fifteen of the 16 patients underwent percutaneous stricture dilation. Of 12 patients who no longer have stents, four have had no stricture recurrence for 12-30 months. Eight patients have had to undergo retransplantation or have died. Percutaneous dilations were most likely to result in patient bile ducts if strictures developed within 3 months after transplantation and in the absence of pretransplantation primary sclerosing cholangitis, ductopenic arteriopathic rejection, cytomegalovirus infection, or hepatic artery thrombosis.