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Author’s reply
  1. G De Hertogh,
  2. P Ven Eyken,
  3. K Geboes
  1. Dienst Pathologische Ontleedkunde, UZ Leuven, Leuven, Belgium
  1. Correspondence to:
    Dr G De Hertogh
    UZ St-Rafaël Minderbroedersstraat 12, Leuven 3000, Belgium; gert.dehertogh{at}

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We would like to thank Dr Chandrasoma for his attentive reading and kind comments on our work published in Gut. He has also provided the readers with an admirable synthesis of the most recent research on the development of the different mucosal types in the gastro-oesophageal junction region. By means of this letter, we want to reflect on some of his comments.

The quintessence of Dr Chandrasoma’s vision on cardiac mucosa (CM) is that it is not a normal structure but develops through metaplasia in the context of gastro-oesophageal reflux disease. The presence of a small length of CM in many “normal” adults could be the result of asymptomatic low level reflux. According to his view, the “non-ciliated non-glandular late fetal foregut epithelium” (which we call CM in our study) will develop into either oesophageal squamous epithelium or gastric mucosa with parietal cell containing glands. The necessary corollary of his theory is that there can be no such thing as a normal CM. He also puts forward the notion that the presence of CM in some infants might be due to deviant differentiation of the uncommitted epithelium in the context of reflux or other trauma such as nasogastric intubation. Even if this hypothesis is correct, we think that other possibilities should be considered. One possible situation could be the persistence of the uncommitted epithelium with development of a sort of heterotopic CM (analogous to the heterotopic fundic-type mucosa described in the upper third of the oesophagus). Clearly, much more research is needed.

Obviously, our work is not completely representative of the development of the gastro-oesophageal junction region throughout gestation. Notably, we need extra specimens from third trimester fetuses. At this moment we are gathering this material for future research. As Dr Chandrasoma himself says, the most important reason for the divergent conclusions of his work and ours are the terminology and interpretation of the data. What we call CM is, in Dr Chandrasoma’s opinion, an uncommitted epithelium devoid of glands. He specifically warns against applying the designation “gland” to the tangentially cut tortuous ends of the foveolar pits (our fig 2 and fig 4). We believe glands are present in these illustrations. We formed this conclusion both on a purely morphological basis (the gland cells are cuboidal to triangular and contain a centrally located round nucleus, as opposed to the tall columnar foveolar and pit cells with basically located nuclei) and after histochemical evaluation (the foveolar and pit cells contain a large amount of mostly neutral mucins, whereas the gland cells for a long time contain only a small amount of mostly acidic mucins). We used the term CM for this zone interposed between squamous and fundic mucosa because of its morphological analogy with adult CM (whether normal or abnormal). Its principal characteristic is the presence of mucus producing glands devoid of parietal cells. We stated that CM develops during gestation and is present at birth. We do not know what happens with this CM in infants and children. We cannot comment on the identity of adult CM: has it always been there or did it develop through metaplasia? To prove or disprove Dr Chandrasoma’s theory, evidently much further research has to be done.

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