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Sporadic fundic gland polyps: what happened before?
  1. P Declich1,
  2. E Tavani1,
  3. S Bellone1,
  4. M Porcellati1,
  5. L Pastori1,
  6. B Omazzi2,
  7. C Gozzini2,
  8. A Bortoli2,
  9. A Prada2
  1. 1Service of Pathology, Rho Hospital, Italy
  2. 2Division of Gastroenterolgy, Rho Hospital, Italy
  1. Correspondence to:
    Dr P Declich
    Service of Pathology, Rho Hospital, Corso Europa n 250 I-20017 Rho, Italy;

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We read with great interest the article by Watanabe et al (Gut 2002;51:742–5) on regression or complete disappearance of sporadic fundic gland polyps (FGPs) in two patients following acquisition of Helicobacter pylori infection. This very interesting article raised a very basic question: “What happened before (and after) the first diagnosis of FGPs?”

We know from previous studies1–3 and personal experience4,5 that the association between FGPs and actual H pylori gastritis is rare, but what remains unanswered is are patients with sporadic FGPs really protected (by some presently unknown mechanism) against H pylori colonisation (that is, H pylori colonisation is really rare in these patients) or are patients with sporadic FGPs prone to H pylori colonisation in a similar manner as the general population, and perhaps the association between H pylori and FGPs seems rare because FGPs disappear when a patient acquires H pylori (and reappear after eradication). So our second question is: “How often do patients with sporadic FGPs acquire H pylori? Is it a rare or common, if unnoticed, event?

From October 1997 to March 2004, we prospectively collected all endoscopic and histological data from 162 patients (mean follow up 34 months) with sporadic FGPs. All of the original slides were reviewed by one of the authors (PD) assessing location, presence, and type of gastritis, intestinal metaplasia, and H pylori colonisation. Furthermore, all preceding and successive gastroenterological examinations were taken into account. The vast majority of our patients (126 of 162 (77.7%)) had no evidence of past or present gastritis, and remained free from H pylori during the observation period. Of these, 74 had also antral biopsies which were all H pylori negative. In 16 patients (9.8%) we found histological evidence of past active antral gastritis with H pylori colonisation years before the first diagnosis of FGPs but only one patient acquired H pylori after the first diagnosis of FGPs, with complete disappearance of polyps. Finally, 19 patients (11.7%) had inactive gastritis with intestinal metaplasia, without H pylori colonisation at the time of the first FGP diagnosis, and in the following period. Therefore, in our experience, the large majority of patients with FGPs appear to be (and remain) free from H pylori colonisation. In only one patient could we document acquisition of H pylori with disappearance of FGPs.

In conclusion, it seems that patients with sporadic FGPs are largely protected from H pylori colonisation and that these patients rarely acquire the infection with disappearance of polyps.


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