An Hypothesis for the Pathogenesis and Treatment of Recurrent Peptic Ulcers

1961 Digestion  
The Zollinger-Ellison triad -gastric hypersecretion, recurrent peptic ulcer and non-ß-cellular pancreatic insuloma -is a well known syndrome and a generally accepted clinical entity. More than one hundred cases have been reported in the U.S.A. and elsewhere. Since the first reports on the Zollinger-Ellison syndrome [1], we never omitted a careful examination of the pancreas during any gastric operation, whether for ulcer or not, but not a case of insuloma has been discovered in more than 3000
more » ... nsecutive gastrectomies although several re-resections were performed for recurrent ulcers, often of severe or atypical localization, viz. in cases where an islet-cell adenoma could be suspected. It was on these very occasions that we noticed the existence of pancreatic lesions of nonneoplastic but inflammatory type in those patients whose symptomatology and history were probatory for a Zollinger-Ellison case. Needless to say, we do not refer to pancreatic alterations near a penetrating ulcer and dependent on the ulcer. We always found an enlarged pancreas, of increased consistency, especially in the body and the tail, in multinodular form, rarely with some Editorial 333 swelling of the capsule. Biopsy specimens taken in any case of this type failed to demonstrate the existence of neoplastic lesions, even of an adenomatous type. Clear signs of hypertrophy, hyperplasy and inflammatory changes were, on the contrary, always present. These alterations were found by us at the second or third operation for peptic ulcers, but they were always already present at the first one, at least in those patients of whose operatory findings we were certain. As every research for an islet-cell adenoma had been unsuccessfull, and many inflammatory changes had been observed instead, we thought it possible that not only nesidioblastomata could be responsible for a recurrent ulcer but also cronic and subacute types of pancreatitis. Some cases were reported by one of us in 1959 [2]. Although glucagon could be the intermediate pathogenetic factor, in this case also, as Ellison suggested for nesidioblastomata, many clinical and experimental facts seem to demonstrate for the HGF and inhibitory action on gastric secretion. Moreover, we cannot overlook other substances related to pancreatic function such as vagotonin, pancreozymin, callicrein and trypsin. Our observations which seemed to suggest an inflammatory pancreatic participation in the pathogenesis of recurrent peptic ulcer persuaded us that a therapy with a callicrein-trypsin inhibitor could prove useful and we therefore assayed in these patients the effect of trasylol, a pancreatic purified extract, that Asang and others [3-6] had successfully used in acute pancreatitis treatment. Though our experience is obviously limited, therapeutic results were consistently good.
doi:10.1159/000202601 fatcat:24ogptl53fcpbdvc3o6xxqdcyu