**2. Methods and results**

For the purpose of evaluating the outcomes of endoscopic examination of patients with a final histopathological diagnosis of ABG we surveyed all cases of upper gastrointestinal endoscopy with biopsy sampling of gastric antrum and gastric body performed from 2007 to 2009 at a referral center for digestive endoscopy in the city of Belo Horizonte, Brazil.

A total of 6,005 consecutive gastroesophageal endoscopies with gastric biopsies of the antral and body mucosa of the stomach were reviewed. Among these cases 2,564 (42.7%) had the diagnosis of chronic gastritis as the main pathological condition of the gastric mucosa. Of these, 141 (5.5%) had a diagnosis of atrophic body gastritis (type A gastritis) suggestive of an autoimmune nature. However, a conclusive diagnosis could not be made in the remaining 230 patients (9.0%) whose histology report was mainly descriptive, stating the presence of "chronic gastritis of the body with areas of atrophy" or "body-predominant chronic atrophic gastritis ". Therefore, in most cases of chronic gastritis with body mucosa atrophy it seems that the pathologists did not find sufficient morphological evidence for a more conclusive diagnosis.

All histological slides of the 141 cases of atrophic body gastritis as well as those of the 230 patients with inconclusive diagnosis of gastritis were re-examined by an expert gastrointestinal pathologist (AJAB). When necessary the corresponding paraffin blocks were recovered for new histological sections. After reviewing all cases, the previous diagnosis of the 141 patients with atrophic body gastritis was confirmed. Among the 230 patients with an inconclusive diagnosis, 55 (24%) could be confirmed as cases of atrophic body gastritis

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

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 follow-

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

For the purpose of evaluating the outcomes of endoscopic examination of patients with a final histopathological diagnosis of ABG we surveyed all cases of upper gastrointestinal endoscopy with biopsy sampling of gastric antrum and gastric body performed from 2007 to

A total of 6,005 consecutive gastroesophageal endoscopies with gastric biopsies of the antral and body mucosa of the stomach were reviewed. Among these cases 2,564 (42.7%) had the diagnosis of chronic gastritis as the main pathological condition of the gastric mucosa. Of these, 141 (5.5%) had a diagnosis of atrophic body gastritis (type A gastritis) suggestive of an autoimmune nature. However, a conclusive diagnosis could not be made in the remaining 230 patients (9.0%) whose histology report was mainly descriptive, stating the presence of "chronic gastritis of the body with areas of atrophy" or "body-predominant chronic atrophic gastritis ". Therefore, in most cases of chronic gastritis with body mucosa atrophy it seems that the pathologists did not find sufficient morphological evidence for a more conclusive

All histological slides of the 141 cases of atrophic body gastritis as well as those of the 230 patients with inconclusive diagnosis of gastritis were re-examined by an expert gastrointestinal pathologist (AJAB). When necessary the corresponding paraffin blocks were recovered for new histological sections. After reviewing all cases, the previous diagnosis of the 141 patients with atrophic body gastritis was confirmed. Among the 230 patients with an inconclusive diagnosis, 55 (24%) could be confirmed as cases of atrophic body gastritis

2009 at a referral center for digestive endoscopy in the city of Belo Horizonte, Brazil.

collected and processed. However, this is not always the case.

histopathologic diagnosis of atrophic body gastritis.

up of the patient.

diagnosis.

**2. Methods and results** 

(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 correlated with the endoscopic reports (Table 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 and gender

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

Atrophic Body Gastritis: A Challenge for the

only 9 (4.6%) cases.

**3. Discussion** 

atrophic multifocal gastritis.

atrophy at histology had an inaccurate endoscopy report.

Presumptive Endoscopic and Histologic Diagnosis of Autoimmune Gastritis 173

body mucosa, or fragments that were cut tangentially, could present a morphological pattern similar to that of pyloric mucosa with chronic inflammation, thus leading to a diagnosis of multifocal gastritis instead of ABG (Figure 3). The boundaries between these two histological types of chronic gastritis become even more critical when *H. pylori* is present, which is an unusual occurrence. In the present series of ABG, *H. pylori* was found in

The main endoscopic diagnosis of the 196 cases of atrophic body gastritis were as follows: (a) 76 (38.8%) cases of atrophic pangastritis, (b) 63 (32.1%) cases of pangastritis with apparent atrophy of the gastric body mucosa, (c) 42 (21.4%) cases of light enanthematous pangastritis, (d) 10 (5.1%) cases of pangastritis with gastric polyps, (e) 2 (1.0%) cases with endoscopically

Enantematous pangastritis/likely body mucosa atrophy 63 32,1

Antropyloric-predominant enantematous pangastritis 21 10,7 Body-predominant enentematous pangastritis 01 0,51

**Main endoscopic reports N %**  Atrophic pangastritis 76 38,8

Light enantematous pangastritis 21 10,7

Gastric polyps 10 5,10 Normal gastric mucosa 02 1,02 Unspecified 02 1,02

normal gastric mucosa, and 2 (1.0%) endoscopically unspecified cases (Table 2).

Table 2. Main endoscopic report conclusions of the 196 patients with histologic ABG

For many dyspeptic patients the diagnosis of ABG is the first step indicating the presence of autoimmune gastritis, associated or not with pernicious anemia. Since some of these patients should be monitored periodically from a clinical point of view and regarding the changes in their gastric mucosa, care should be taken not to overlook cases of gastritis with predominant or selective atrophy of the gastric fundus and body on the occasion of the first medical procedures they undergo. Knowing that the final diagnosis of this pathological entity usually depends on a close interaction between endoscopist and pathologist, an indication of the presence of these endoscopic changes to the pathologist directs more attention to the correct diagnosis. This correlation becomes even more necessary if we consider that the histologic processing artifacts, the absence of oxintopeptic glands in the histological sections plus the presence of extensive areas of intestinal and pseudoantral metaplasia, may complicate at first sight the differential diagnosis between ABG and

Table 2 shows that standard endoscopic examination detected signs of gastric mucosa atrophy in 139 (70.9%) patients with ABG, although the affected gastric region was not specified. In the other 57 (29.1%) patients this change was not found although severe glandular atrophy of the body was found at histology. A more precise endoscopic report could direct the pathologist to a more conclusive histologic diagnosis. Most of the 55 patients confirmed as ABG cases among the 230 patients with varying degrees of mucosal

atrophy of the body mucosa (Figure 2 A, C, D). This atrophy was mainly represented by partial or complete replacement of oxyntopeptic glands with glands with intestinal metaplasia and antral-type mucous glands known as pseudoantral or pseudopyloric metaplasia (Figs. 2 D and 3). In several small fragments with poor representation of gastric mucosa, the pseudoantral metaplasia seemed to be a factor responsible for the failure to distinguish between antral and body atrophic mucosa. Small biopsy fragments of atrophic

Fig. 2. Normal gastric mucosa of the antrum (A) and body (B) regions. Note that the foveolar region of the gastric antrum occupies approximately half the mucosa thickness while the mucus-secreting glands are distributed in the basal half of the mucosa. The connective tissue of the lamina propria is visible between the glands. Differently, the body mucosa (B) have short foveolas, and the oxintopeptic glands are numerous and justaposed occupy almost the entire space of conjunctive masking the lamina propria. C and D: body mucosa with severe glandular atrophy from a patients with ABG. Presence of glands with intestinal metaplasia (thin arrow) and pseudoantral metaplasia (thick arrow). The antral mucosa seen in A is from the same patient with ABG seen in C and D

body mucosa, or fragments that were cut tangentially, could present a morphological pattern similar to that of pyloric mucosa with chronic inflammation, thus leading to a diagnosis of multifocal gastritis instead of ABG (Figure 3). The boundaries between these two histological types of chronic gastritis become even more critical when *H. pylori* is present, which is an unusual occurrence. In the present series of ABG, *H. pylori* was found in only 9 (4.6%) cases.

The main endoscopic diagnosis of the 196 cases of atrophic body gastritis were as follows: (a) 76 (38.8%) cases of atrophic pangastritis, (b) 63 (32.1%) cases of pangastritis with apparent atrophy of the gastric body mucosa, (c) 42 (21.4%) cases of light enanthematous pangastritis, (d) 10 (5.1%) cases of pangastritis with gastric polyps, (e) 2 (1.0%) cases with endoscopically normal gastric mucosa, and 2 (1.0%) endoscopically unspecified cases (Table 2).


Table 2. Main endoscopic report conclusions of the 196 patients with histologic ABG
