ABSTRACT
BACKGROUND: A retrospective analysis of de etiologic factors and fisiopathogenic mechanisms underlyng an acute biliar pancreatitis episode put in evidence the complexity of the attempt to acquire a clear understanding of the entity. In this presentation the authors try to re-examine the main factors involved in the triggering of the disease. Beasides the clasic theories and their own approach to the management of an acute pancreatic inflammation episode are discussed. AIMS: The main purpose of this endeavor was to identify and discuss the etiopahogenic machanisms that were prevalent in a series of 148 patients observed and trated in a 10 years period. Besides, another distinctive aim was to analyze their evolution and somehow to try to assess their probable prognosis. PLACE OF APPLICATION: Close comunity. POPULATION: The whole group of patients that were admitted with the diagnosis of acute pancreatitis in the time period comprised between 1987-1997. METHODS: The acute pancreatitis subgroups and their respective number of patient included were the following: BILIARY ACUTE PANCREATITIS 140 CASES POST ERCP 8 CASES CONCLUSIONS: As a result of the present reviewing endeaveur several observations deserve to be pointed out: a. The pancreatic gland undoubtedly is a neuroendocrine organ, that is subjeted to complex neural and hormonal influence. b. Undeniably, the involvement of the autonomic nervous system in the physiopathogenic mechanism of acute pancreatitis has been surprisingly disregarded. c. The biliary acute pancreatitis variant is the most frequent. What we consider a simplification is to accept the Opie's postulation without taking into account the intermediate steps, centered on autonomic reflexes, that ultimately lead to the acute inflammatory lesions. d. Although without an absolute proof, it is undeniable that "stress" is a primary etiologie in some cases of acute pancreatitis. e. We favor the idea that the pancreon's functional status influences on the extension and intensity degree of the acute pancreatic inflammatory lesions.