Pathogenesis

With regard to the etiopathogenetic possibilities, Stolte et al. summarized four clinical characteristics of GP: (1) previous diseases of the biliary system, peptic ulcer and gastric resection; (2) mild dilation of the pancreatic duct; (3) higher frequency of narrowing of the duodenal lumen, and (4) cyst formation in the duodenal wall. The etiology of GP, however, so far remains controversial. Currently, two types of research approach have reported on etiopathogenetic possibilities.

Firstly, the disturbance of pancreatic juice outflow in Santorini's duct is highlighted, because stricture of the duct may be caused by inflammation around the duct. This can affect the intrapancreatic common bile duct and lead to fibrosis, inflammatory infiltrates and scarring. Other organic changes such as duodenal wall cysts, pancreatic head cysts, pancreatitis in duodenal pancreatic heterotopia and Brunner's gland hyperplasia may lead to develop stricture and disturbance of secretion of the orifice of the minor papilla. Chronic consumption of alcohol seems to be an important pathogenic factor.

Adsay and Zamboni [3] have proposed a new clinicopathologic entity named paraduodenal pancreatitis, unifying (1) cystic dystrophy of heterotopic pancreas, (2) pancreatic hamartoma of the duodenum, (3) paraduodenal wall cyst, (4) myoadenomatosis and (5) groove pancreatitis, because these lesions have common characteristics. They considered that fibrosis of the duodenum may affect the groove area and produce GP. They provided a new view on the pathogenesis of GP.

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