“…1 Recent investigations have established that one of the earliest pathophysiologic events in pancreatitis is the colocalization of acinar cell organelles containing digestive and lysosomal enzymes, resulting in premature intracellular activation of proteases. 2,3 Numerous treatments directed at inhibiting this autodigestive process have been ineffective, 4,5 in part because patients seek medical attention long after these initiating events have occurred. The individual pancreatic cell injury becomes magnified and propagated by inducing (through incompletely defined mediators) impaired microcirculation, leukocyte adhesion, and leukocyte infiltration.…”