SAN ANTONIO — Treating Helicobacter pylori infection in patients who take NSAIDs does not help prevent the development of peptic ulcer disease, Willem F. Lems, M.D., said at the annual meeting of the American College of Rheumatology.
In his study, 347 patients with culture-confirmed, H. pylori infection and a history of long-term NSAID use were randomized to receive H. pylori eradication treatment or a placebo.
Three months after treatment, peptic ulcers were diagnosed by endoscopy in 6 of 172 patients who had been actively treated, compared with 8 of 175 patients in the placebo group. One patient in the treated group and two patients in the placebo group developed endoscopic duodenal ulcers.
There was no significant difference between the groups in terms of the prevalence of gastroduodenal erosions (41 treated versus 51 placebo). Nor was there any difference in the rate of dyspepsia.
No patient in either group developed a symptomatic ulcer, an ulcer bleed, or ulcer perforation at any time during a full 12-month follow-up.
At the 3-month endoscopic examination, 87% of the treated patients and 21% of the placebo-treated patients were free of H. pylori.
The study adds to a body of literature on H. pylori and NSAID-associated ulcer that has been a bit confusing, said Dr. Lems of VU University Medical Center, Amsterdam.
While H. pylori eradication has been shown definitively to reduce ulcer recurrence in patients not taking NSAIDs, reports on what eradication does for patients on NSAIDs have been conflicting.
Although his study has the scientific strength of being a prospective trial, Dr. Lems said, it also could have been confounded by the fact that patients had to have been on long-term NSAID therapy already. His patients could have been a select group who were already able to tolerate NSAID treatment, and the results of treatment could be different for individuals just starting treatment.
A fairly large percentage of the patients (53%) were either on gastroprotective therapy with a proton-pump inhibitor or were taking a selective cyclooxygenase-2 inhibitor.