The Morphologic Basis for the Evolution of Acute Pancreatitis into Chronic Pancreatitis

Abstract

The pathogenesis of chronic pancreatitis is still unsettled. The most commonly cited theory postulates that the deposition of protein plugs which later calcify leads to duct obstruction with subsequent fibrotic replacement of the acinar tissue upstream of the occlusion [13]. Alternatively, we have proposed a working hypothesis that relates the pathogenesis of chronic pancreatitis with that of acute pancreatitis [8, 9]. The sequence of events that we believe may connect acute with chronic pancreatitis starts with interstitial fat necrosis and hemorrhage that induces perilobular fibrosis. Perilobular fibrosis, in turn, may also distort the interlobular ducts, creating stenoses and dilatations. The ducts, once altered, hamper the normal flow of pancreatic secretions, thereby enabling the precipitation of proteins (protein plugs) and eventually their calcification (calculi). If duct obstruction becomes more extensive, the acinar cells upstream of such a stenosis disappear, leaving dense intralobular fibrosis.