[Acute pancreatitis and duodenobiliary fistula--a rare complication of Crohn's disease]. / Akute Pankreatitis und choledochobulbäre Fistel--eine seltene Komplikation bei Morbus Crohn.

HISTORY: A 53-year-old man with long-standing Crohn's disease presented with recurrent abdominal pain and vomiting; lipase levels were elevated. INVESTIGATIONS AND DIAGNOSIS: At admission ultrasound demonstrated a swollen head of the pancreas, dilated pancreatic and intrahepatic bile ducts and peripancreatic fluid. At upper gastrointestinal endoscopy a 10 mm bleeding ulcer was identified, which histologically proved to be epitheloid cell-containing granulomas. A fistula connecting to the hepatocholedochal duct was identified at the floor of the ulcer. Helicobacter pylori was not demonstrated. TREATMENT AND COURSE: After sphincterotomy of the papilla of Vater concrements were extracted and a stent was implanted into the common bile duct. Ultimately a total of five stents were consecutively implanted via the major papilla, closing the fistula. After three years all stents were removed and pancreatitis did not recur. CONCLUSION: The differential diagnosis of abdominal pain in patients with Crohn's disease is often difficult and should include fistulas of the upper gastrointestinal tract which may be treated endoscopically.

Escherichia coli strain Nissle 1917 ameliorates experimental colitis via toll-like receptor 2- and toll-like receptor 4-dependent pathways.

Toll-like receptors (TLRs) are key components of the innate immune system that trigger antimicrobial host defense responses. The aim of the present study was to analyze the effects of probiotic Escherichia coli Nissle strain 1917 in experimental colitis induced in TLR-2 and TLR-4 knockout mice. Colitis was induced in wild-type (wt), TLR-2 knockout, and TLR-4 knockout mice via administration of 5% dextran sodium sulfate (DSS). Mice were treated with either 0.9% NaCl or 10(7) E. coli Nissle 1917 twice daily, followed by the determination of disease activity, mucosal damage, and cytokine secretion. wt and TLR-2 knockout mice exposed to DSS developed acute colitis, whereas TLR-4 knockout mice developed significantly less inflammation. In wt mice, but not TLR-2 or TLR-4 knockout mice, E. coli Nissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coli Nissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coli Nissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coli Nissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-kappaB activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coli Nissle 1917 ameliorates experimental induced colitis in mice via TLR-2- and TLR-4-dependent pathways.