**1. Introduction**

168 Gastrointestinal Endoscopy

Shaheen, N. J. and Richter, J. E. (2009), "Barrett's oesophagus", *Lancet,* vol. 373, no. 9666, pp.

Shaheen, N. J., Sharma, P., Overholt, B. F., Wolfsen, H. C., Sampliner, R. E., Wang, K. K.,

Galanko, J. A., Bronner, M. P., Goldblum, J. R., Bennett, A. E., Jobe, B. A., Eisen, G. M., Fennerty, M. B., Hunter, J. G., Fleischer, D. E., Sharma, V. K., Hawes, R. H., Hoffman, B. J., Rothstein, R. I., Gordon, S. R., Mashimo, H., Chang, K. J., Muthusamy, V. R., Edmundowicz, S. A., Spechler, S. J., Siddiqui, A. A., Souza, R. F., Infantolino, A., Falk, G. W., Kimmey, M. B., Madanick, R. D., Chak, A. and Lightdale, C. J. (2009), "Radiofrequency ablation in Barrett's esophagus with dysplasia", *The New England journal of medicine,* vol. 360, no. 22, pp. 2277-2288. Sharma, P., Bansal, A., Mathur, S., Wani, S., Cherian, R., McGregor, D., Higbee, A., Hall, S.

and Weston, A. (2006a), "The utility of a novel narrow band imaging endoscopy system in patients with Barrett's esophagus", *Gastrointestinal endoscopy,* vol. 64, no.

A., Junghard, O., Lundell, L., Tytgat, G. N. and Vieth, M. (2006b), "The development and validation of an endoscopic grading system for Barrett's esophagus: the Prague

"Dysplasia in short-segment Barrett's esophagus: a prospective 3-year follow-up",

mechanisms, and endoscopic treatment of Barrett's esophagus", *Gastroenterology,* 

Barrett's esophagus. Does it help?", *The Journal of thoracic and cardiovascular surgery,* 

imaging for detection of Barrett's-associated neoplasia", *World journal of* 

Obertop, H. (1998), "Impact of endoscopic biopsy surveillance of Barrett's oesophagus on pathological stage and clinical outcome of Barrett's carcinoma", *Gut,* 

endoscopic resection specimens from 326 patients with Barrett's esophagus and

early esophageal adenocarcinoma", *The American Journal of Medicine,* vol. 123, no. 5,

Adelstein, D. J., Trolli, P. A. and Blackstone, E. H. (2005), "Endoscopic ultrasound errors in esophageal cancer", *The American Journal of Gastroenterology,* vol. 100, no. 3,

Sharma, P., Dent, J., Armstrong, D., Bergman, J. J., Gossner, L., Hoshihara, Y., Jankowski, J.

Sharma, P., Morales, T. G., Bhattacharyya, A., Garewal, H. S. and Sampliner, R. E. (1997),

Streitz, J. M.,Jr, Andrews, C. W.,Jr and Ellis, F. H.,Jr (1993), "Endoscopic surveillance of

Thekkek, N., Anandasabapathy, S. and Richards-Kortum, R. (2011), "Optical molecular

van Sandick, J. W., van Lanschot, J. J., Kuiken, B. W., Tytgat, G. N., Offerhaus, G. J. and

Vieth, M., Ell, C., Gossner, L., May, A. and Stolte, M. (2004), "Histological analysis of

Wong, T., Tian, J. and Nagar, A. B. (2010), "Barrett's surveillance identifies patients with

Zuccaro, G.,Jr, Rice, T. W., Vargo, J. J., Goldblum, J. R., Rybicki, L. A., Dumot, J. A.,

*The American Journal of Gastroenterology,* vol. 92, no. 11, pp. 2012-2016. Spechler, S. J., Fitzgerald, R. C., Prasad, G. A. and Wang, K. K. (2010), "History, molecular

C & M criteria", *Gastroenterology,* vol. 131, no. 5, pp. 1392-1399.

850-861.

2, pp. 167-175.

vol. 138, no. 3, pp. 854-869.

vol. 43, no. 2, pp. 216-222.

pp. 462-467.

pp. 601-606.

vol. 105, no. 3, pp. 383-7; discussion 387-8.

*gastroenterology : WJG,* vol. 17, no. 1, pp. 53-62.

early neoplasia", *Endoscopy,* vol. 36, no. 9, pp. 776-781.

The diagnosis of glandular atrophy of the gastric mucosa (gastric atrophy) remains a challenge in the areas of gastrointestinal endoscopy and pathology. The importance of an endoscopic suspicion of this regressive tissue change is the possibility of alerting the pathologist to its presence. Patients with gastric atrophy, especially in more advanced stages, are more prone to develop intestinal metaplasia, dysplasia and gastric carcinoma, known as the Correa cascade (Correa, 1984, 1992). The most common type of gastric atrophy is that associated with *Helicobacter pylori* (*H. pylori*) infection. In such cases, the glandular atrophy usually occurs in parallel to the course of the inflammatory process that takes place in the gastric antrum (antral gastritis, multifocal gastritis) or in both gastric antrum and body (pangastritis, multifocal gastritis). In contrast, in most cases the chronic atrophic gastritis selective of the gastric body and sparing the antral mucosa is a consequence of an autoimmune inflammatory process. For the purpose of this chapter, the chronic gastritis presenting this histopathological pattern will be called atrophic body gastritis (ABG). Exceptionally, some patients with *H. pylori*-associated gastritis develop gastric lesions with histological pattern very similar to that of ABG which can lead to uncertainty about the differential histologic diagnosis with chronic gastritis of autoimmune origin.

Therefore, the two most important inflammatory diseases of the gastric mucosa, multifocal chronic gastritis and autoimmune gastritis, tend to progress to glandular atrophy of the gastric mucosa. In the first case, gastric atrophy may not occur or it develops more slowly, becoming conspicuous usually in later stages of life. In the second case, which is also more frequent with advancing age, gastric atrophy progresses more rapidly and may induce severe gastric changes also in the younger age groups. This differential course of the development of gastric atrophy in these two inflammatory diseases of the stomach involves different clinical and pathophysiological consequences. Those associated with *H. pylori* infection usually do not involve important pathophysiological changes, while the atrophy resulting from autoimmune disease often leads to well-known pathophysiological changes of the gastric mucosa, often culminating in pernicious anemia. Furthermore, the *H. pylori*dependent glandular atrophy is considered to be a condition predisposing to gastric adenocarcinoma, which has high rates of morbidity and mortality, while the autoimmune-

Atrophic Body Gastritis: A Challenge for the

correlated with the endoscopic reports (Table 2).

and gender

Presumptive Endoscopic and Histologic Diagnosis of Autoimmune Gastritis 171

(Table 1). The 196 patients with a final histologic diagnosis of ABG ranged in age from 11 to 94 years, with a significant predominance of females (76.0%) over males (24.0%). Fifty patients were in a relatively young age range (31 to 50 years), with an even more significant predominance of females, i. e., 83.3% *vs* 16.7% (Figure 1) .The remaining 175 patients were excluded from the study, either because the biopsy specimens of the antral or oxyntic mucosa were not fairly representative for histology or because they could be considered as cases of multifocal atrophic gastritis, regardless of the presence of *H. pylori* infection. Finally, the histological findings of the 196 patients with a diagnosis of atrophic body gastritis were

> All cases of chronic gastritis 2.564 100 Atrophic body gastritis 141 5,5 Unspecified atrophic gastritis 230 9,0

Total of ABG diagnosed 196 7,6

ABG after review of unspecified atrophic gastritis 55 2,2

Table 1. Main histological diagnosis of 6,005 gastroesophageal endoscopies carried out from 2007-2009 in a tertiary care unit of gastrointestinal endoscopy, Belo Horizonte, Brazil

Fig. 1. Distribution of the 196 patients with the final diagnosis of ABG according to the age

Among the 2,564 patients with chronic gastritis, 196 (7.6%) had a conclusive histologic diagnosis of atrophic body gastritis (type A chronic gastritis). Gastric mucosa samples of almost all of these patients showed well preserved antral mucosa, and severe glandular

**Total of cases %** 

dependent glandular atrophy is considered to be a condition predisposing to gastric carcinoids, which, unlike the adenocarcinomas, have low rates of morbidity and mortality. Due to the different regional involvement of the stomach by these two types of chronic gastritis, their histological recognition is relatively easy when tissue samples are properly collected and processed. However, this is not always the case.

Thus, the importance of the differential diagnosis of ABG within this group of chronic gastritis resides in the possibility of its autoimmune origin and in its major clinical consequence, i.e., pernicious anemia. Pernicious anemia and autoimmune gastritis progress in an insidious manner and are usually diagnosed when they have reached florid clinical and morphological characteristics after years of evolution. However, a number of patients with dyspeptic complaints and patients with ABG and pernicious anemia undergo endoscopy in tertiary care settings without a prior knowledge of major illness. (Carmel, R., 1996) Therefore, for some patients seeking a first endoscopy service, the collection of biopsies from the gastric mucosa may be the first opportunity to establish the initial diagnosis of ABG, with or without pernicious anemia. This is important because the evolution of subclinical gastric lesions and systemic symptoms may result in undesirable consequences that become established in a gradual manner. These consequences mainly result from achlorhydria, vitamin B12 deficiency, and the development of hyperplastic polyps and neuroendocrine tumors of the gastric mucosa. For this reason, the diagnosis of ABG acquires importance since it establishes an appropriate clinical and endoscopic followup of the patient.

The objective of this article is to present some data on this topic obtained from a tertiary care unit of gastrointestinal endoscopy and to discuss some pitfalls linked to the routine histopathologic diagnosis of atrophic body gastritis.
