Surgery for Peptic Ulcer in the Helicobacter pylori Era

Abstract

disease were designed prior to the identification of Helicobacter pylori as a major cofactor in ulcerogenesis. These operations decrease gastric acid secretion by eliminating vagal stimulation and gastrin production and/or by diminishing the parietal cell mass. The complications and ulcer recurrence rates for each antiulcer operation can be recited by most surgical residents.Most of these data were collected prior to the widespread use of fiberoptic endoscopy and therefore probably represent modest estimates.1 Prospective trials with almost complete endoscopic follow-up have identified ulcer recurrences in 30% to 95% of patients medically treated for peptic ulcer.2,3 Few, if any, patient populations have been systematically screened by endoscopy for recurrent ulcer after surgical therapy for peptic ulcer. In fact, most surgical series have used endoscopic follow-up only in patients with hematemesis, perforation, or persistent, severe dyspepsia.4,5Helicobacter pylori infection of the gastric mucosa is primarily antral and is accompanied by gastritis on histologie examination. Greater than 90% of patients with peptic ul¬ cer have H pylori infections.6 The precise mechanism whereby H pylori infection in the gastric antrum contributes to ulcer forma¬ tion in the duodenum is unclear.7 However, eradication oí H pylori in¬ fection contributes to ulcer healing and reduces ulcer recurrence significantly, as indicated by sev¬ eral randomized prospective stud¬ ies.2,3 Patients having successful eradication of H pylori have ulcer re¬ currence rates of less than 15% at 1 year compared with rates greater than 50% in patients treated with ranitidine alone.2 A National Insti¬ tutes of Health (Bethesda, Md) con¬ sensus statement from February 1994 acknowledges the role of H py¬ lori in peptic ulcer pathogenesis.8It is interesting to reflect on ul¬ cer surgery outcomes in the con¬ text of our knowledge of H pylori.With antrectomy, we were unknow¬ ingly resecting the site of H pylori infection. This offers yet another rea¬ son for the success of vagotomy and antrectomy as a surgical bench¬ mark for peptic ulcer. With other op¬ erations, such as parietal cell va¬ gotomy, the antral source of H pylori infection remains untouched. Not surprisingly, antral gastritis, which is present in greater than 90% of the patients with ulcers, does not im¬ prove after parietal cell vagotomy.9Perhaps the reported lailures and the relatively high recurrence rate of pa¬ rietal cell vagotomy are not due to mysterious uncut vagal branches but are instead due to ongoing H pylori infection in the gastric antrum. Fur¬ thermore, any role for H pylori in re¬ current ulcération after ulcer sur¬ gery remains to be elucidated. Decision making regarding the sur¬ gical therapy of peptic ulcer should be tempered by our evolving under¬ standing of ulcer pathogenesis.

Perforated peptic ulcer: is there a difference between Eastern Europe and Germany?

“…The high proportion of definitive operations is a characteristic feature of Eastern Europe. By contrast, according to the data of recent reports, the number of definitive procedures is diminishing rapidly in the Western countries [10,16,27,28,29].…”

Comparison of four minimally invasive methods of laparoscopic vagotomy in a porcine model

“…These factors have virtually eliminated the need for elective ulcer surgery [1,15]. This surgery was done primarily by vagotomy, which is a safe and effective procedure with low rates of recurrence and mortality [7,8,19].…”