Pyloric and prepyloric ulcers

Abstract

In a prospective multicenter trial, 560 patients with peptic ulcer were treated with proximal gastric vagotomy (PGV) without drainage. Four hundred ninety-three patients had duodenal ulcer (DU), 35 pyloric (PU), and 32 prepylorlc ulceration (PPU). Actuarial 5-year recurrence rates were 14%, 35 %, and 33%, respectively, and were significantly higher in PU and PPU than in DU. In a separate study, thickness of the pyloric and antrai wail was assessed in the resection specimens of patients with similarly defined ulcer types and in controls. There was significant thickening of the muscular layer of the pylorus and antrum in patients with PU and PPU compared to those with DU and controls. It appears that this muscular hypertrophy and fibrosis could be one factor responsible for the failure of PGV without drainage in PU and PPU. Preliminary results indicate a possible beneficial effect of adding a drainage procedure ~o PGV when treating pyloric channel ulcers. Our results emphasize that pyloric channel ulcers must be considered as a particular entity of peptic ulcer disease and should no longer be assigned to the duodenal ulcer group.

Asymptomatic free intraperitoneal gas with duodenal stenosis

“…Repetitive healing and recurrence of the underlying duodenal ulcer disease led to scar-related pyloric stenosis and impaired gastric emptying [3][4][5][6]. As a result, a gastric ulcer might have developed due to hypergastrinemia and stimulated adrenergic acid secretion [7].…”

Indication and Surgical Therapy in Uncomplicated Peptic Ulcer Disease

“…In their study on prepyloric ulcers, Muller et al [29] reported a recurrence rate of 34% after vagotomy alone compared to 11 % when the PGV was combined with a pyloroplasty. Andersen et al: [2] investigated the efficacy of PGV with and without drainage: the cumulative 5-year recurrence rate of prepyloric ulcers was 33% with PGV alone and 9% with PGV and drainage.…”

“…In a study of the pathogenesis of this type of ulcer, Lawson [23] advanced the hypothesis that local factors such as chronic atrophic gastritis and a disturbed functioning of the antrum are important determinants, and that acid causes the lesions in the prepyloric antrum altered by inflammation. Histological examinations and morphometric measurements by Muller et al [29] re vealed a significantly thicker wall of pylorus and antrum in patients with prepyloric ulcers than in those whose ulcers where in located intra-or postpyloric sites. Fur thermore they found an increased degeneration of gan glionic cells which indicates dystrophic neuromuscular alterations.…”