AIM:Our main objectives were to evaluate the influence of two-year proton pump inhibitors (PPI) therapy in patients with Barrett’s oesophagus on its length, in both types, short and long segment.METHODS:In this single-centre, prospective interventional controlled study were analysed data collected prospectively over two years from patients with Barrett’s oesophagus diagnosed by endoscopy. Patients who received continuous proton pump inhibitors (PPI) for 2 years were included. At each patient visit symptoms were recorded, and at each endoscopy, the length of Barrett’s oesophagus (BE) was measured. Biopsies were taken along the length of the oesophagus at intervals of 1 cm. In total, 50 patients with Barrett’s oesophagus were included in the study: 10 of whom had long-segment Barrett’s oesophagus, and 40 patients had short-segment Barrett’s oesophagus. The mean number of endoscopies performed was 3 per patient.RESULTS:The length of Barrett’s esophagus (BE) was influenced by PPI therapy: Circumferential extension in BE patients short-segment Barrett’s esophagus (SSBE) (before treatment was 1.5 cm and after treatment was 0.8 cm Maximum proximal extension in SSBE group before treatment was 2.3 cm (SD ± 1.1 cm), and 1.1 cm (SD ± 0.9 cm), respectively. Squamous islands were detected in 25% of patients examined after 2 years on PPIs.CONCLUSIONS:PPIs achieve a reduction to the length of Barrett’s oesophagus, in both types, and the development of squamous islands is commonly associated with their use.

BACKGROUND: Cameron lesions are seen in 5.2% of patients with hiatal hernia who undergo esophagogastroduodenoscopic examinations. The prevalence of Cameron lesions seems to be dependent on the size of the hernial sac, with an increased prevalence in the larger-sized sac. In about two-thirds of the cases, multiple Cameron lesions are noted rather than a solitary erosion or ulcer. AIM: The aim of this case report is to present the patient with Cameron ulcers associated with hiatal hernia. CASE PRESENTATION: Our patient presented with postprandial retrosternal pain, especially immediately after eating, vomiting, dyspnea, weight loss, fatigue, signs, and symptoms of severe hypochromic microcytic anemia without signs of acute gastrointestinal bleeding. No history of gastroesophageal disease. Colonoscopy was done and eliminate colic cause of anemia. The endoscopy showed a large hiatal hernia and linear erosions and ulcerations at the level of gastrodiaphragmatic contact (Cameron ulcers) and one non-sanguinant subcardial elipsoid ulceration. After conservative and operative treatment, there was significant clinically and laboratory improvement definitively, after 6 months. Cameron lesion is a rare cause of refractory sideropenic anemia. Diagnosis is very difficult in developing countries, where iron deficiency anemia is more common. A history of disease, clinical course, and laboratory findings are the important facts for diagnosis. CONCLUSION: Endoscopy is the gold standard for diagnosis, although it is not uncommon to overlook these lesions due to their unique location. There are two modalities for the treatment of Cameron lesions: Medical or surgical, which should be individualized for each patient. By severe refractory anemia and large hiatal hernia, associated with clinical signs, surgical approach is very important.

Barrett’s esophagus (BE), as a more frequent complication of gastroesophageal reflux disease, is a metaplastic condition in which the normal squamous epithelium of the esophagus is replaced by specialized intestinal metaplastic epithelium, and that, in about 10% of patients with gastroesophageal reflux disease (GERD) and the main condition for dysplasia and adenocarcinoma. The incidence of adenocarcinoma of the cardia is rapidly increasing at a rate that exceeds that of any other cancer. Recently, acid suppression with proton pump inhibitors (PPIs) has become the cornerstone of treatment for patients with BE. Many worldwide investigations showed that PPI is effective in the regression of BE with low-grade dysplasia and especially for the regression of intestinal metaplasia, incomplete or complete, for long-term use of these medicaments. This chapter reviews the specific endpoints of such treatment, included and our results for this dilemma.