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Helicobacter pylori, ghrelin, and obesity
  1. R C Macadam1,
  2. V Borse1,
  3. I Dodo1,
  4. S G Pollard1
  1. 1St James’ University Hospital, Level 8, Clinical Sciences Building, Leeds LS9 7TF, UK
  1. Correspondence to:
    Mr R C Macadam;
    robert.macadambtinternet.com

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Nwokolo et al have demonstrated that following eradication of Helicobacter pylori from asymptomatic patients, plasma ghrelin “increases profoundly” (Gut 2003;52:637–40). Although we find these results interesting, we cannot agree with the conclusion that this may be causally linked to epidemiological observations of the rising incidence of obesity and oesophageal adenocarcinoma in Western populations. In particular, the present study in fact demonstrates that after H pylori eradication, ghrelin merely returns to levels detected in non-obese control patients using the same hormone assay.1 It would seem likely that H pylori infection, leading to oxyntic gland atrophy,2 is associated with at most a mild suppression of plasma ghrelin, which recovers after treatment. This seems unlikely to have a profound effect on calorie intake, particularly as obese patients have a lower mean plasma ghrelin concentration than matched non-obese controls.1 While it is possible, although unproven, that the …

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