The Etiology of Duodenal Ulcers

Abstract

Since the original work of Mann and Williamson 1 much has been written concerning the experimental production of duodenal ulcers by depriving the duodenum of its normal alkalinity. It, therefore, becomes of interest to know if any one of the 3 secretions, bile, pancreatic juice, or intestinal juices, is specifically responsible for protection against ulcer formation, or whether the presence of all of them is necessary.

In an attempt to determine this point 3 series of experiments were done. In the first series 5 operations were performed under aseptic technic and the common bile duct isolated, tied, and divided in each case. Following this a cholecyst-enterostomy was performed at a point on the small bowel about 18 inches below Treitz's ligament, thereby excluding the bile from the duodenum and draining it into the jejunum at this point. The anastomoses and closures were done with silk. Two of these 5 animals developed an acute duodenal ulcer at 76 and 119 days postoperative respectively. In each case the ulcer was situated exactly at the pyloric ring and was about 3 mm. in diameter. Both died of hemorrhage into the bowel without warning and the ulcer was only discovered at autopsy. Pathologically these ulcers were very different from chronic ulcers produced by duodenal drainage. They were smaller, more punched out, showed no sign of secondary infection, had hemorrhagic bases ulcerating into a vessel in each case, and presented no evidence on the serosal surface by which ulcer formation could have been predicted. Microscopically, they showed very little infiltration and no scar tissue formation. Both animals were in good general condition at the time of death. The 3 others were well nourished and showed no sign of ulcer formation at the date when they were sacrificed, 234, 236, and 239 days postoperative respectively.