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Helicobacter pylori infection and acid secretion in patients with duodenal ulcer in Japan
  1. T CHIBA,
  3. T ITO
  1. Division of Gastroenterology and Hepatology
  2. Department of Internal Medicine
  3. Postgraduate School of Medicine, Kyoto University, Japan
  1. T Chiba. cteya{at}

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Editor,—Helicobacter pylori infection affects gastric acid secretion of the host in various ways. For example, corpus gastritis and subsequent development of mucosal atrophy induced by H pyloriinfection result in decreased acid secretion.1 In contrast, several investigators have reported elevated acid secretion in patients with duodenal ulcer (DU) which is decreased byH pylori eradication with simultaneous reduction of serum gastrin.2 3 Supporting these data, Iijima et al (

) reported that eradication ofH pylori was accompanied by an increase in acid secretion in patients with gastric ulcer (GU) in whom corpus gastritis and/or atrophy are frequently observed, whereas acid secretion decreased after eradication in those with DU. However, in countries such as Japan where corpus gastritis and mucosal atrophy are common among patients infected with H pylori, the situation is not as simple.

We performed a similar study by measuring basal acid output (BAO) and maximum acid output (MAO) using pentagastrin administration before and six months after eradication in Japanese patients with GU (n=21) and DU (n=22). In both patients with GU and DU, serum gastrin levels were significantly higher than those of control subjects (p<0.01) before eradication; they decreased significantly after eradication (GU: 129.7 (19.2) to 94.6 (15.0) pg/ml; DU: 116 (19.8) to 90.3 (16.3) pg/ml; p<0.05). These data are similar to those of Iijimaet al (

). In contrast with their data however we could not find any significant changes in MAO after eradication in DU patients although H pylorieradication resulted in a significant increase in MAO in patients with GU (fig 1). Indeed, as shown in fig 2, changes in MAO varied from patient to patient among DU individuals. Subsequently, we attempted to elucidate the relationship between changes in serum gastrin and MAO more precisely. As expected, in patients with GU, a positive correlation was found between the decrease in serum gastrin and increase in MAO following H pylorieradication (fig 2). These data suggest that recovery of acid secretion by H pylori eradication in patients with GU is responsible for the decrease in serum gastrin levels. In contrast, in patients with DU, no significant correlation was observed between changes in serum gastrin and acid secretion. When we analysed the DU data more precisely however, we found an interesting fact: acid secretion of one group of patients (group C) increased with a simultaneous decrease in serum gastrin. These changes in response toH pylori eradication were similar to those observed in GU patients. Therefore, we divided DU patients into three groups according to changes in MAO by H pylori eradication (group A: MAO decreased more than 1 mEq/h; group B: no change; group C: MAO increased more than 1 mEq/h) and found that group C patients had the lowest serum pepsinogen (PG) I levels and PG I/II ratios among the three groups (PG I: group C 44.7 (1.6), group A 64.5 (2.5), group B 57.8 (2.6); PG I/II: group C 2.52 (0.18), group A 3.98 (0.24), group B 3.60 (0.19); p<0.05). These data indicate that patients in group C had suffered atrophy of the fundic mucosa.

Figure 1

Effects of Helicobacter pylori eradication on maximum acid output (MAO) in Japanese patients with duodenal (DU) and gastric (GU) ulcers. MAO in response to pentagastrin (6 μg) was measured before and six months after H pylori eradication. *p<0.05 v before eradication.

Figure 2

Correlation between decrease in serum gastrin concentration (−Δgastrin) and increase in maximum acid output (ΔMAO) in response to pentagastrin (6 μg) by Helicobacter pylori eradication in Japanese patients with duodenal (DU) and gastric (GU) ulcers. Groups A, B, and C show DU patients in whom MAO decreased (more than 1 mEq/h), did not change, and increased (more than 1 mEq/h) after eradication, respectively.

Data on changes in gastrin stimulated acid secretion after eradication in patients with DU are controversial,2-5 although most reports show a decrease in acid secretion.2 3 As Iijimaet al indicated, the most likely reason for the controversy may be that a considerable number of patients with DU had corpus gastritis, which may somehow cause hypoacidity. We previously reported that gastric acid secretion in Japanese subjects is lower than that in Europeans or North Americans, irrespective ofH pylori infection.6 AsH pylori is reported to induce corpus gastritis more easily in subjects with decreased acid secretion,7 8 we suggested that innate low gastric acid secretion of the Japanese may be responsible for the higher incidence of corpus gastritis and atrophy in Japanese subjects withH pylori infection. This appears to be the case even for patients with DU in Japan, and it may be the reason why acid secretion was not significantly reduced afterH pylori eradication in our DU patients.

It has been a matter of debate whether gastric acid hypersecretion observed in patients with DU is a result of H pylori infection or if the infection accelerates development of DU in subjects who originally had acid hypersecretion. Our data showing that acid secretion was recovered in association with the decrease in serum gastrin levels in some DU patients and that MAO levels in patients with DU after eradication are still higher than those of normal subjects without H pylori infection may support the latter idea. Moreover, this idea may explain the fact that there are more patients with GU than DU among Japanese subjects,9 who exhibit lower acid secretion than Western patients.6

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