Pancreatic leak related hemorrhage following pancreaticoduodenectomy. A case series.

CONTEXT: Delayed arterial hemorrhage, secondary to pancreaticojejunal leakage, is an infrequent complication (2-4%) of pancreaticoduodenectomy but it carries a high mortality rate with more than half of the patients dying from overwhelming sepsis and/or bleeding. Its ideal management remains unclear. CASE REPORTS: We hereby present our experience with respect to the presentation and management of this severe post-pancreaticoduodenectomy complication which occurred in 3/149 patients (2.1%) operated on between 1996 and 2008 in our department and we review the role of endoscopy, interventional radiology and surgery in its management. CONCLUSIONS: The severity of the underlying sepsis and the prompt identification of the sentinel bleed determine surgical and angiographic intervention and define the outcome in the treatment of a pancreatic leak-related hemorrhage. Endoscopy has no role in this setting.

Molecular aspects of carcinogenesis in pancreatic cancer.

BACKGROUND: Pancreatic cancer (PCa) is one of the most aggressive human solid tumors, with rapid growth and metastatic spread as well as resistance to chemotherapeutic drugs, leading rapidly to virtually incurable disease. Over the last 20 years, however, significant advances have been made in our understanding of the molecular biology of PCa, with a focus on the cytogenetic abnormalities in PCa cell growth and differentiation. DATA SOURCES: A MEDLINE search and manual cross-referencing were utilized to identify published data for PCa molecular biology studies between 1986 and 2008, with emphasis on genetic alterations and developmental oncology. RESULTS: Activation of oncogenes, deregulation of tumor suppressor and genome maintenance genes, upregulation of growth factors/growth factor receptor signaling cascade systems, and alterations in cytokine expression, have been reported to play important roles in the process of pancreatic carcinogenesis. Alterations in the K-ras proto-oncogene and the p16INK4a, p53, FHIT, and DPC4 tumor suppressor genes occur in a high percentage of tumors. Furthermore, a variety of growth factors are expressed at increased levels. In addition, PCa often exhibits alterations in growth inhibitory pathways and evades apoptosis through p53 mutations and aberrant expression of apoptosis-regulating genes, such as members of the Bcl family. Additional pathways in the development of an aggressive phenotype, local infiltration and metastasis are still under ongoing genetic research. The present paper reviews recent studies on the pathogenesis of PCa, and includes a brief reference to alterations reported for other types of pancreatic tumor. CONCLUSIONS: Advances in molecular genetics and biology have improved our perception of the pathogenesis of PCa. However, further studies are needed to better understand the fundamental changes that occur in PCa, thus leading to better diagnostic and therapeutic management.