Pathology of Chronic Pancreatitis

Abstract

The pathology of alcoholic pancreatitis has been studied in great detail. The earliest changes are the deposition of protein plugs within pancreatic ductules.¹ At first, protein plugs are deposited in random fashion within some lobules but not in others, but eventually this process becomes relatively diffuse. Various histologic abnormalities follow the deposition of enzymic protein in the form of plugs and probably occur on the basis of other toxic effects of alcohol as yet not clarified.^1–5 At points of contact with proteinaceous material, ductal epithelium may undergo squamous metaplasia and ulceration. Inspissation of protein plugs causes ductular dilatation followed by acinar atrophy. An inflammatory process may occur in the interstitium. Eventually, a considerable amount of fibrous tissue is deposited in the vicinity of pancreatic ducts, between pancreatic lobules, and within lobules cleaving acinar tissue. As this process becomes more extensive, acinar tissue may disappear leaving dense scar tissue associated with a scant number of inflammatory cells. Pancreatic ducts may be widely dilated as a result of obstruction by protein plugs or intraductal stones (Figure 30). At times, however, pancreatic ducts are widely dilated with no apparent major obstruction.