Atrophic autoimmune gastritis: ‘a muddled or misguided core concept compromises our overall comprehension of the problem’

We thank Lahner et al for their interest in our study: considering their extensive experience in the field of gastric autoimmunity, their contribution is particularly welcome. Overall, most of the authors’ comments are in keeping with the established knowledge of autoimmune gastritis and, therefore, not debatable. We also agree with the interesting citation from Jan Aart Scholte’s work on global governance, which can be applied to any field of science: ‘Definition is not everything, but everything involves definition. A muddled or misguided core concept compromises our overall comprehension of the problem. ’ We shall, therefore, start from discussing definitions. In 2002, an international group of gastrointestinal pathologists (which included Correa) slightly modified the original Correa’ definition and redefined atrophy as ‘loss of native gastric glands’. This definition emphasises that a decrease in the number of glandular units is not essential to a histological definition of gastric mucosal atrophy. Together with glandular fading, metaplastic pseudopyloric metaplasia (PPM) or intestinal metaplasia (IM) decrease the overall amount of the native glands population, resulting in both organic and functional atrophy. The second definition issue relates to the ‘protection’ attributed to PPM against gastric cancer. We agree with Lahner et al on the reparative biological profile of PPM. In our Barrett’s experience, IMnegative columnar metaplasia showed a molecular profile intermediate between native and intestinalised mucosa. This initially tenuous evidence is now supported by international consensus, and it could be applied also to the gastric PPM changes. In principle, we can all agree that in the gastric district, and everywhere else in the body, native is better than metaplastic. 7 Furthermore, in all human districts, it may be overreaching to associate to metaplastic change with a benign or malignant profile. Metaplasia is just metaplasia, even though some metaplastic phenotypes harbour genetic instability prone to a neoplastic progression. As for the result of our study, we could not find in our paper the numbers to which Lahner refers to. Our table 3, insert D, shows that at the initial biopsy (T1) only 8/211 cases did not feature any atrophic changes, and they became 9/211 in the T2 biopsy sets. This minimal difference has no statistical significance and is likely due to chance. In response to the cardinal Lahner’s question ‘is corpusrestricted atrophy always linked to gastric autoimmunity only? ’ we can simply say that no information is currently available other than ‘expert opinions,’ including Lahner’s reference number 7. However, the possible occurrence of corpusrestricted atrophic gastritis unrelated to autoimmunity is an intriguing hypothesis. In autoimmune gastritis, cytotoxic autoreactive H+/K+ATPasespecific T cells target exclusively parietal cells. Therefore, autoimmune gastritis is, by definition, limited to the oxyntic gastric compartment. In contrast, the spread of the inflammatory and atrophic changes from antrum to corpus in Helicobacter pylori infection is well established. Therefore, one could generally assume that H. pylori will not cause a pure corpusrestricted (atrophic) gastritis. There is, however, a situation that is worth exploring. In H. pyloriinfected patients, longstanding proton pump inhibitor therapy may accelerate the oxyntic spreading of antral inflammation and atrophy, while reducing or even eliminating the inflammation in the antrum. The frequency and relevance of such a ‘iatrogenic H. pyloriinduced corpus restricted atrophic gastritis’ remain to be more extensively investigated.