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Endoscopic gastrin test andHelicobacter pylori infection
  1. VINCENZO SAVARINO,
  2. CARLO MANSI
  1. Dipartimento di Medicina Interna e Specialità Mediche
  2. Università di Genova,
  3. Viale Benedetto XV 6
  4. 16132 Genova
  5. Italy
  6. Istituto di Medicina Interna e Geriatria
  7. Università di Palermo
  8. Italy
  1. Professor Savarino (email:vsavarin{at}unige.it)
  1. SERGIO VIGNERI
  1. Dipartimento di Medicina Interna e Specialità Mediche
  2. Università di Genova,
  3. Viale Benedetto XV 6
  4. 16132 Genova
  5. Italy
  6. Istituto di Medicina Interna e Geriatria
  7. Università di Palermo
  8. Italy
  1. Professor Savarino (email:vsavarin{at}unige.it)

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Editor,—In their recent article inGut,1 Iijima and colleagues conclude that reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after H pylori eradication. We agree with the recovery of gastric secretory function in the former group of patients, who constantly bear chronic gastritis which improves greatly after disappearance of the germ, with subsequent restoration of gastric glandular tissue.2-4 However, we disagree with their conclusion regarding the latter group, because it is not supported by the experimental data they obtained. It is surprising that they found an increase in acid secretion (although not significant) in duodenal ulcer patients one month after eradication.

This finding is difficult to explain, because basal gastrin levels were significantly reduced compared with those before eradication in the same patients, and others have found a rapid decrease of acid output in relation to the decline of serum gastrin.5 6 The Japanese researchers state that this disparity may depend on the premature assessment of gastrin stimulated acid output (one month), because the same evaluation performed after seven months showed significantly decreased values compared with those before eradication. It must be pointed out, however, that there is a tremendous overlap between acid outputs measured before and after seven months of eradication, and those pertaining to H pylori negative controls. Moreover, the rate of decrease of acid secretion after seven months was only 23% in their study.

This reduction is very low and similar to the level of 16% seen after six months of eradication by Parente et al,7 who themselves acknowledged in their paper that this small percentage casts doubt on the unique role ofH pylori in determining the augmented acid secretion typical of duodenal ulcer. Although the data obtained by Iijima et al and Parenteet al after cure of H pylori infection were significantly different from those before eradication, we believe that statistical significance does not mean physiological relevance in this case.

Apart from the previously mentioned overlapping, some patients even show an increase in acid secretion after seven months, and others have found no change in maximal acid secretion 12 months after eradication of the bacterium.6 It is clear that the deregulation of gastric physiology in duodenal ulcer is caused by a combination of factors and H pylori is only one of them. In addition, it should not be forgotten that 20% of patients with duodenal ulcer have been shown to relapse despite ascertainedH pylori eradication,8 and a high acid output has been found in patients with duodenal ulcer recurrence after the disappearance of H pylori.9

These findings seem to suggest that a genetic predisposition to secrete more acid is present at least in a subset of patients with duodenal ulcer, and is independent of H pyloristatus.10 Therefore, overenthusiastic statements that eradication of H pylori is followed as a rule by normalisation of gastric acid output are deceiving and should be attenuated.

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