Has the biology and treatment of pancreatic diseases evolved?

This review will present recent findings and emerging questions on the major diseases of the pancreas: acute and chronic pancreatitis as well as pancreatic carcinoma. It is now clear that acute pancreatitis is initiated inside acinar cells by premature activation of digestive enzymes and disturbances of intracellular calcium. The release of proinflammatory mediators expands the local disturbances to a systemic inflammatory response. The transfer of these findings into clinical management had only limited success so far. Genetic mutations have been identified as pathogenetic factors in hereditary pancreatitis and are increasingly detected in patients with idiopathic chronic pancreatitis. In pancreatic carcinoma and in putative premalignant lesions, different alterations in cancer causing genes have been identified. Pancreatic cancer is at large a signal transduction disease leading to unregulated cell proliferation and migration. All three pancreatic diseases are characterized by profound alterations of extracellular matrix (ECM) formation. Essential data concerning composition and regulation of ECM has emerged after the description of the pancreatic stellate cell.