Acute upper gastrointestinal hemorrhage: is a radiological interventional approach an alternative to emergency surgery?

The aim of our study was to discuss the option of endovascular treatment compared to surgery for patients with endoscopically unmanageable nonvariceal hemorrhage of the upper gastrointestinal tract. From 2000 to 2006, 23 patients (male, 15 male; female, 8; mean age, 69 years) who failed endoscopic therapy for upper gastrointestinal hemorrhage were retrospectively evaluated. Twelve patients were operated on (SG), whereas 11 patients had an endovascular intervention (IG). Technical and primary clinical success rates and complications rates were calculated. Clinical parameters and comorbidities were related to outcome. The surgical group suffered less frequently from pre-existing pulmonary diseases (SG, 17%; IG, 55%; p = 0.05) and had a higher incidence of shock requiring catecholamines (p < 0.01) or plasma expander therapy (p < 0.01). There was no significant difference in the incidence of recurrent bleeding episodes (SG, 17%; IG, 27%; p = 0.35) and mortality rates (SG, 17%; IG, 27%, p = 0.35). Deaths in the IG were due to recurrent bleeding. In patients with unsuccessful endoscopic control of nonvariceal bleeding of the upper GI tract, surgery remains a very effective treatment. However, in patients with a high surgical risk due to unknown bleeding sources and/or severe pre-existing diseases/comorbidities, endovascular therapy offers an excellent treatment option. These patients should then be operated on as early as possible to minimize the risk of recurrent bleeding episodes, which are associated with high morbidity and mortality.

Immunological escape mechanisms in pancreatic carcinoma.

Malignancies have developed several strategies to evade immune surveillance. We have investigated pancreatic cancer cell lines and pancreatic cancer surgical specimens to evaluate possibilities of tumor escape in the Fas system, and local immune suppression. Despite Fas expression the majority of cell lines was resistant to Fas-mediated apoptosis. The Fas-associated phosphatase-1 is a strong candidate to confer Fas resistance in pancreatic cancer cells. In addition, all investigated pancreatic cancer cell lines and cancer specimens expressed Fas ligand. Fas ligand was functional in cancer cell lines as shown by coculture assays of pancreatic cancer cell lines with Jurkat cells as targets. Additional local immune suppression was demonstrated by loss of T-cell receptor/CD3-zeta chain of pancreatic cancer infiltrating T-lymphocytes. We conclude that these tumor escape mechanisms may contribute to the poor prognosis of pancreatic cancer but also represent targets for new treatment modalities.