“…Indeed, analysis of sequential biopsies of human pancreatic allografts confirmed both clinical and morphological signs of acute pancreatitis, making post-transplant pancreatitis a manifestation of ischemia-reperfusion injury [2, 31. Besides the disturbed integrity of structures within the acinar cells, which can clearly be attributed to the ischemic insult, reperfusion-associated events are thought to account for other distinct cellular and metabolic responses, including autophagocytosis, acceleration of cellular metabolism, and leukocyte activation/reaction. These, in turn, may lead to acinar cell necrosis [2,3]. Accordingly, reperfusion of pancreatic transplants after 6 h, but not after 1 h, of cold storage revealed classical pancreatitis-associated microvascular injury, i. e., the deterioration of nutritive blood supply (no-reflow), lending support to the role of ischemia/reperfusion-associated mechanisms in the manifestation of acute post-transplant pancreatitis.…”