Long-term follow-up of patients with gastric outlet obstruction related to peptic ulcer disease treated with endoscopic balloon dilatation and drug therapy.

BACKGROUND

Previous studies suggest that endoscopic balloon dilatation (BD) in gastric outlet obstruction (GOO) related to peptic ulcer disease (PUD) does not achieve long-term remission and most patients require surgery. Most of these studies have not systematically attempted to alter the natural history of the underlying PUD. We reviewed our experience of management of PUD-related GOO with BD and medical treatment of PUD.

OBJECTIVE

The determination of the etiology of benign GOO and the assessment of long-term outcome from endoscopic BD and drug therapy.

DESIGN

An observational study of the management of 23 consecutive patients with PUD-related GOO.

SETTING

A medical gastroenterology unit in the United Kingdom.

PATIENTS

Twenty-three consecutive patients with PUD-related GOO.

MAIN OUTCOME MEASUREMENTS

Symptomatic and endoscopic remission of PUD and GOO.

RESULTS

Twenty-three patients (10 men, 13 women; median age, 71 years; range, 43-94 years) presented with symptoms of GOO secondary to PUD. The initial etiologic assessment was as follows: Helicobacter pylori (12), aspirin or nonsteroidal anti-inflammatory drugs (NSAID) (3), H pylori and aspirin/NSAID (5), idiopathic (2), undetermined (1). All 17 patients who were H pylori-positive received eradication therapy. A reliable posteradication H pylori status was available in 13 and was negative in all. NSAIDs were stopped in all patients. Patients on aspirin for the prevention of atherosclerosis received concurrent antisecretory therapy (AST). In 4 patients, PUD relapsed, despite removal of initial etiology (H pylori in 3, H pylori and NSAID in 1). The PUD in these was redesignated as idiopathic, raising the number of patients with idiopathic PUD to 6. In 2 patients, remission was achieved with AST alone. Twenty-one patients underwent BD. All 23 patients remained in symptomatic remission during a median follow-up period of 43 months (range, 5-90 months). Endoscopic remission was confirmed in all but 1, who refused follow-up endoscopy. Six patients stayed in remission, without the need for maintenance AST after the underlying cause of PUD was removed. In the remaining 17 patients, maintenance AST was required for the following main reasons: idiopathic PUD (6), reflux esophagitis (6), a need for aspirin (5).

CONCLUSIONS

Despite its small size, this study shows that treatment of PUD-related GOO by using endoscopic and medical therapy is associated with a favorable long-term outcome.