[Physiopathology of the Zollinger-Ellison syndrome. Present aspects].

Recent technics, e.g. radio-immunoassay of gastrin (MacGuigan 1968), cellular immuno-fluroescence (Polak and Pearse 1972) have modified our concepts of the physiopathology of the Zollinger-Ellison syndrome hypergastrinemia of pancreatic origin. 1. Pollak and Pearse, (1972) Ganguli, Pollak and Pearse (1974) have shown that apart from the Zollinger-Ellison syndrome of pancreatic origin (ZE type II) there are cases where the hypergastrinemia is due to hyperplasia of the antral "G" cells which secrete gastrin (ZE Tye I). Thus is raised the problem of the relationship between common peptic ulcer, "G" cell antral hyperplasia and pancreatic hypergastrinemia. 2. There exists, in the anterior part of the intestine (pancreas, duodenum, stomach, ileum) a system of neuro-humoral cells derived embryologically from the neural crest (Weichert 1967, Gorin and Leger 1969). These pluripotent cells may be the origin of digestive endocrine, or carcinoid tumours, islet cell adenomas, or gastrinomas. Thus may be explained among others the multihormonal secretion of some of these tumours and the frequently multiple sites. 3. Gastrin is secreted by the duodenal "G" cells (Watson 1974). Their physiopathological role is still unknown.