What effect does Helicobacter pylori infection have on the risk of peptic ulceration in patients receiving NSAIDs for rheumatoid arthritis?

Abstract

Background: Patients with rheumatoid arthritis (RA) frequently develop dyspepsia which may be due to peptic ulceration. There have been conflicting published data on the possible interactive roles of nonsteroidal anti-inflammatory drugs (NSAIDs) and colonisation of the gastric antrum with Helicobacter pylori in the development of peptic ulceration. Methods: We have prospectively assessed the prevalence of peptic ulcers in dyspeptic RA patients and investigated the factors responsible. We endoscoped 100 RA patients comparing the endoscopic findings to those in 100 age- and sex-matched dyspeptic control subjects. Data on NSAID consumption and Helicobacter colonisation were collected for each patient. Results: Endoscopic evidence of peptic ulceration was found in 29 RA patients and in 16 of the control subjects ( P=0.03). Multiple ulcers (>2) were found in significantly more RA patients than in controls (10 vs. 2). NSAIDs were being used by 60 RA patients and 22 controls ( P<0.001). Helicobacter was found in 41 RA patients and in 33 controls ( P=NS). The consumption of NSAIDs conferred a relative risk (RR) of ulceration of 8.67 (1.19–62.87), while the presence of Helicobacter gave a RR for ulcers of 3.71 (0.37–37.35) in RA patients. The RR for the combination of NSAID consumption and Helicobacter colonisation was 14.44 (2.05–101). The corresponding RRs for the dyspeptic controls were 2.13, 1.57 and 1.42 (all P=NS). Conclusions: Rheumatoid patients have more major and more multiple pathology than age-, sex- and symptom-matched controls. This is due mainly to their increased consumption of NSAIDs. The prevalence of Helicobacter was no greater in RA patients than in controls, but Helicobacter infection increased the risk of NSAID-induced ulceration.