Netter’s Gastroenterology, 2nd Edition - Print Version Only
نویسنده
چکیده
T he cardinal manifestations of chronic pancreatitis are re current or persistent abdominal pain that lasts for months to years, accompanied by diabetes, steatorrhea, and pancreatic calculi. Morphologically, the disease is characterized by destruction and loss of exocrine parenchyma that may be focal, segmental, or diffuse, as well as by fi brosis of the pancreas (Fig. 194-1). These changes may be associated with strictures and dilatation of segments of the pancreatic duct and with intraductal protein plugs or calculi. The epidemiology of chronic pancreatitis parallels the prevalence of alcohol abuse in the community. In the United States, almost 75% of cases of chronic pancreatitis are associated with chronic alcoholism, which is thus the most important etiologic factor. Although the pathogenesis of pancreatic injury is still speculative, current data indicate that acinar cells are injured fi rst, with subsequent development of secretory changes and mor phologic alterations such as fi brosis, ductular abnormalities, and stone formation. Toxic metabolites, unopposed free-radical injury and genetic mutations that promote premature activation of trypsinogen to trypsin within the acinar cell are associated with the pathogenesis of chronic pancreatitis. Three genes are currently believed to play a major role: cationic trypsinogen gene (PRSS1 7q35), CFTR, and SPINK1.
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