Duodenal colonization by H. pylori is strongly associated with subsequent development of duodenal ulcer in patients with nonulcer dyspepsia

Abstract

Background. The final step of the currently accepted mechanism of duodenal ulcer formation requires the colonization of the duodenum by H. pylori and the subsequent formation of the ulcer crater induced by the organism. On this basis, it would seem logical to hypothesize that patients with nonnlcer dyspepsia carrying the organism in the duodenum be at higher task of developing duodenal ulcer than those who do not. No data are available on this subject. Patiems and Methods. 363 consecutive, dyspeptic patients with an endoscopic diagnosis of nonulcer dyspepsia were characterized for H. pylori infection status at the level of the stomach (3 biopsies from the gastric antrum and 3 from the gastric corpus) and of the duodenum (3 biopsies from the duodenal bulb). At each site, infection was diagnosed if colture was positive and/or if the organism was concomitantly detected at histology (Giemsa staining) and urease testing. H. p2(lori cagPAI status was determined by PCR cagA amplification on isolated strains. All H. pylori positive patients were required to perform follow-up endoscopy one year later, or in the case of worsening clinical symptoms. Results. At basehne, infection was diagnosed in 189 patients (52%) in the stomach and in 50 patients (14%) in the duodenum. 87 patients (46%) were infected with cagA positive (cagA +) H. pylori strains in the stomach and 35 (70%) in the duodenum, a statistically significant difference ( P< 0.005, Chi-sqare test). 167 (79 cagA+, 47 with duodenal colonization) out of 189 H. pylori positive patients (85%) performed follow-up endoscopy after 1 year: a duodenal ulcer was diagnosed in 14; of these, 10 (71%) were cagA positive in the stomach at baseline, whereas 12 (86%) had H. pylori infection in the duodenum (10 cagA+) . This finding implies that stomach colonization by H. pylori cagA positive strains has a sensitivity of 69%, a specificity of 55%, a positive predictive value of 13%, and a negative predictive value of 96% for the development of duodenal ulcer one year after the diagnosis of nonulcer dyspepsia ; by contrast, the sensitivity, specificity, positive predictive value, and negative predictive value of duodenal colonization are 86%, 77%, 26%, and 98%, respectively. Conclusions. Assessment of duodenal colonization by H. pylori in patients with nonulcer dyspepsia is a better predictor for the development of duodenal ulcer than the assessmem of cagA status in the stomach.