**13. Summary**

All treatment decisions should be discussed in a multidisciplinary team meeting once every effort has been made to ensure the correct diagnosis has been reached. Patients (and families) should be fully informed and involved in the decision making process. All surgical and endoscopic procedures should be performed by specialists in recognised cancer units. ER should be used as a potentially curative treatment for IMC and focal HGD, and also has an emerging role in aiding histological diagnosis. Following ER the goal should be to ablate the entire Barrett's segment. Due to the technical difficulties and costs associated with PDT, its role is increasingly being superseded by that of RFA. Following initial ablative therapy, further treatments (using the same or different treatment modalities) should be given in an attempt to destroy any remaining metaplastic / dysplastic epithelium. The aim should be complete squamous regeneration, however even if successful, surveillance should be lifelong as glands with malignant potential may persist burried beneathe the regenerated mucosa.

Endoscopic Detection and Eradication of Dysplastic Barrett's Oesophagus 165

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#### **14. References**


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**12** 

 *Brazil* 

**Atrophic Body Gastritis: A Challenge for the** 

**Presumptive Endoscopic and Histologic** 

*Laboratory of Digestive and Neuroendocrine Pathology, Faculty of Medicine,* 

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-

**1. Introduction** 

**Diagnosis of Autoimmune Gastritis** 

Alfredo J. A. Barbosa and Camila G. Miranda

*Federal University of Minas Gerais (UFMG), Belo Horizonte* 

