Acute pancreatitis.

Efforts to unravel the intracellular processes that occur in acute pancreatitis continue. In cerulein pancreatitis, new evidence supports the idea that a very early event is premature trypsinogen activation triggered by lysosomal cathepsin B. Clinicians persist in trying to identify more sensitive and specific prognostic signs of the severity of attacks of pancreatitis; one study suggests that computer-based neural networks may be an alternative to biochemical markers and clinical scoring systems. The systemic severity of episodes of pancreatitis seems to be related to a multitude of proinflammatory cytokines and chemokines acting at sites distant from the pancreas. Selective blockade of some of these peptides (eg, endothelin-1 and platelet-activating factor) has decreased mortality and distant organ damage in animal models and may deserve clinical evaluation. Gene therapy may be more efficient than pharmacologic therapy in increasing anti-inflammatory cytokine (interleukin-10) levels. Clinical studies have further underlined the usefulness of prophylactic antibiotics in severe acute pancreatitis. Radiologic and endoscopic techniques may be alternatives to surgery for certain complications of pancreatitis (eg, infected necrosis and pseudocysts) in particular subsets of patients.