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Abstract

Drs. Boeckxstaens and Tytgat raise a crucial issue on the pathophysiology of functional dyspepsia: what is the precise mechanism that originates the symptoms? Our study yields relevant and new information on the mechanism of postprandial symptoms, that constitute a characteristic feature of dysmotility-like dyspepsia.1Caldarella P. Azpiroz F. Malagelada J.-R. Antro-fundic dysfunctions in functional dyspepsia.Gastroenterology. 2003; 124: 1220-1229Abstract Full Text Full Text PDF PubMed Scopus (130) Google Scholar However, the origin of symptoms in ulcer-like dyspepsia remains enigmatic. What makes these patients perceive pain when their stomach is empty of food? As Boeckxstaens and Tytgat point out, it is tantalizing to hypothesize that acid may play a role. The intraluminal milieu of the fasting stomach is acid, and pain alleviates after ingestion of meals that have a diluting and buffering effect on gastric juice. In our study we demonstrated that, in contrast to dysmotility-like dyspepsia, the reproducibility of symptoms in ulcer-like dyspepsia was significantly better with antral than with fundic distention.1Caldarella P. Azpiroz F. Malagelada J.-R. Antro-fundic dysfunctions in functional dyspepsia.Gastroenterology. 2003; 124: 1220-1229Abstract Full Text Full Text PDF PubMed Scopus (130) Google Scholar Hence, following this line of reasoning, we hypothesized that pain in ulcer like-dyspepsia could be related to antral sensitization by acid during fasting. Using a model of intragastric titration,2Saperas E. Azpiroz F. Cucala M. Rodrı́guez R. Malagelada J.-R. Postcibal secretory and symptomatic responses to increased intragastric pressure.Neurogastroenterol Mot. 1994; 6: 295-301Crossref Scopus (4) Google Scholar we tested antral sensitivity to graded distensions with acid versus neutral pH, but we could not find significant differences in patients with ulcer-like dyspepsia as compared to those with dysmotility-like dyspepsia (Salvioli B, Azpiroz F, Malagelada J-R, unpublished observations). We do not claim that the acid hypothesis is wrong, but it may be just more difficult to demonstrate. We agree with Drs. Boeckxstaens and Tytgat that various key aspects in the pathophysiology of functional dyspepsia remain obscure, which will require new potential explanations, or even old ones, to be tested.