The pathology of chronic pancreatitis

Abstract

We describe the current concepts of the pathology of alcoholic and obstructive chronic pancreatitis (CP). These 2 types of CP possess distinct pathological features. Alcoholic CP is associated with a lobular distribution of the lesions, with both obstruction (from protein plugs) and dilatation of the canalicular and intercalated ducts. In alcoholics, the concentration of protein in the pancreatic juice is increased, making the precipitation of proteinaceous plugs likely. Obstructive CP, on the other hand, is rarely associated with intraductal precipitates; the small ducts are often normal in appearance, but exocrine damage is much more widespread. The complications of CP are varied. Jaundice, while usually transient, may occasionally be permanent. This results from the compression of the distal common bile duct by fibrotic changes in the pancreatic head. Transient or permanent obstruction of the duodenum and/or colon may also occur. Nearby vessels may be involved, leading to thrombosis and/or hemorrhage from veins or arteries. Electron microscopic changes recently described in the pancreatic nerves may play a role in the etiopathogenesis of the severe pain so common in patients with CP.

Histological Loss of Pancreatic Exocrine Cells Correlates With Pancreatic Exocrine Function After Pancreatic Surgery

“…Several investigators reported that obstructive pancreatitis induced fibrosis and atrophy of pancreatic parenchyma. 10,11,28,29 The results of this study were consistent with these reports. In addition, the current study showed that the acinar cell area of the pancreatic stump in patients undergoing PD was significantly lower than that in patients undergoing DP.…”

Expression of Transforming Growth Factor-β₁ in Chronic Pancreatitis

“…Surgical resection of 55% of the rat pancreas is followed by acinar regeneration although this is a relatively slow process when compared with that of the liver or kidney. It is not known whether or not the human pancreas has this proliferative capacity [32], Computerized tomographic studies of patients who have had severe bouts of acute pancreatitis characterized by extensive necrosis have shown that complete resolu tion of the pancreatic structure occurs in the majority of patients [9], The observation that TGF-Pi inhibits the proliferation of mouse acinar cells and cultured human pancreatic adenocarcinoma cells has suggested the possiblity that TGF-Pi may be involved in regulating pancreatic epithelial cell division [25]. In normal pancreatic tissues and in morphologically normal areas of chronic pancreati tis, TGF-P) expression appears to be confined to the centroacinar/distal ductular epithelia.…”

“…Chronic pancreatitis is classified into two major cate gories [8] with definitive pathological features and statis tically linked to different etiological agents: (1 ) The ob structive type may be found in congenital and acquired strictures of the main duct, papillary inflammation and fibrosis, and 'behind' pancreatic parenchymal tumors [9], Upstream of the obstructing lesion, the pancreas shows uniform and diffuse tissue damage, which may follow ductular rupture and escape of pancreatic juice. The con dition is potentially reversible and is predated by the obstructing lesion.…”

Expression of major histocompatibility antigens in human chronic pancreatitis.

“…Ethanol (63 patients), recurrent acute pancreatitis (12), congenital lesions (2), and unknown (16) were suggested to be the causes of the disease. Immunohistochemical staining of formalin fixed and paraffin wax embedded tissue sections used conventional immunohistochemical techniques with specific anti-serum samples.…”