-Background -Proton-pump inhibitors have been used for at least two decades. They are among the most commonly sold drugs in the world. However, some controversy remains about the indications for their use and the consequences of their prolonged use. Objectives -To evaluate and compare the endoscopic and histopathologic gastric changes in chronic users of proton-pump inhibitors to changes in non-users. Methods -A prospective study performed at a tertiary Public Hospital involving 105 patients undergoing upper-gastrointestinal endoscopy. Subjects included 81 proton-pump inhibitor users and 24 non-users (control group).Biopsies of the antral-type mucosa, the antral-fundic transition, and the fundus were evaluated by the Sydney System. The presence of erosion or ulceration, lymphatic follicles, reactive gastropathy, and polypoid or epithelial hyperplasia was also determined. Serum levels of gastrin were measured. Results -We found two polyps, one in each group, both of which were negative for Helicobacter pylori. There were two cases of parietal cell hyperplasia in users of proton-pump inhibitors. Gastrin was elevated in 28 users of proton-pump inhibitors and in four members of the control group. We did not find statistically significant differences in the endoscopic or histopathologic findings between the two groups. Conclusion -Chronic use of proton-pump inhibitors for the duration examined was not associated with significant gastric changes. An interesting finding was that the 4 chronic users of proton-pump inhibitors who had serum gastrin levels above 500 pg/mL also had positive serology for Chagas disease.

Trypanosoma cruzi and Helicobacter pylori (HP) are pathogens that cause chronic diseases and have been associated with hypergastrinemia. The aim of this study was to evaluate the fasting gastrin levels in patients with different clinical forms of Chagas disease (CD), coinfected or not by HP. The enrolled individuals were outpatients attending at the university hospital. HP infection was assessed by serology and 13 C-urea breath test. Fasting serum gastrin concentration was measured by chemiluminescence assay. Gastric endoscopic and histological features were also evaluated. Associations between CD and serum gastrin level were evaluated in a logistical model, adjusting for age, gender and HP status. A total of 113 patients were evaluated (45 with Chagas disease and 68 controls). In the multivariate analysis, increasing serum gastrin levels (OR= 1.02; 95% CI= 1.01-1.12), increasing age (OR= 1.05; 95% CI= 1.02 - 1.09) and HP-positive status (OR = 2.88; 95% CI = 1.10 - 7.51) remained independently associated with CD. The serum gastrin levels were significantly higher in the group of patients with the cardiodigestive form ( P = 0.03) as well as with digestive form ( P = <0.001) of Chagas disease than in the controls. In conclusion, patients with cardiodigestive and digestive clinical forms of CD have increased basal serum gastrin levels in comparison with controls. Moreover, we also demonstrated that H. pylori coinfection contributes to the hypergastrinemia shown in CD.

Background: Acid inhibition from chronic proton pump inhibitor use and a possible increase in gastrin can lead to changes in the regulation of hydrochloric acid production. However, it has not known whether such chronic use changes the presence of gastrin, delta, and enterochromaffin-like cells in the stomach or the relationship between gastrin and delta cells. Aim: To analyze the number of gastrin-producing gastrin cells, somatostatin-producing cells, and histamine-producing cells in patients who were chronic users of proton pump inhibitor, with or without related Helicobacter pylori infection. Methods: Biopsies from 105 patients, including 81 chronic proton pump inhibitor users (experimental group) and 24 controls, were processed immunohistochemically and subjected to counting of gastrin, delta, and enterochromaffin-like cells in high-magnification microscopic fields and in 10 glands. Results: Gastrin cell, delta cell, and enterochromaffin-like cells counts were similar across the groups and appeared to be unaffected by Helicobacter pylori infection. The ratio between gastrin cells and delta cells was higher in the chronic users of proton pump inhibitor group than in controls. Conclusion: Chronic users of proton pump inhibitor does not affect gastrin cell, delta cell, and enterochromaffin-like cell counts significantly, but may alter the ratio between gastrin cells and delta cells.

Background:Morbid obesity is a multifactorial disease that increasingly is being treated by surgery. Aim: To evaluate gastric histopathological changes in obese, and to compare with patients who underwent gastrojejunal bypass and the jejunal mucosa after the surgery. Methods:This is an observational study performed at a tertiary public hospital, evaluating endoscopic biopsies from 36 preoperative patients and 35 postoperative. Results:In the preoperative group, 80.6% had chronic gastritis, which was active in 38.9% (77.1% and 20.1%, respectively, in the postoperative). The postoperative group had a significant reduction in H. pylori infection (p=0.0001). A longer length of the gastric stump and a time since surgery of more than two years were associated with Helicobacter pylori infection. The jejunal mucosa was normal in 91.4% and showed slight nonspecific chronic inflammation in 8.6%. Conclusion:There was a reduction in the incidence of Helicobacter pylori infection in the postoperative group. A longer length of the gastric stump and longer time elapsed since surgery were associated with Helicobacter pylori infection. The jejunal mucosa was considered normal in an absolute majority of patients.

Introdução: A patogênese mais comum da apendicite aguda é a obstrução luminal do apêndice por fecalitos. No entanto, qualquer material que possa obliterar direta ou indiretamente a cavidade apendicular pode causar apendicite aguda. Os tumores apendiculares são relativamente raros, mas podem obliterar o lúmen do órgão, levando à apendicite. Relato de caso: Paciente de 23 anos com quadro de abdome inflamatório agudo foi diagnosticado no pré-operatório com apendicite aguda. No intraoperatório, foi confirmado o diagnóstico de apendicite aguda com apêndice perfurado. O diagnóstico anatomopatológico foi de adenocarcinoma colônico de apêndice e o paciente foi convocado para receber o tratamento adequado. Metodologia: Além do estudo do prontuário do paciente, foi realizada pesquisa bibliográfica sobre o tema, o que permeou a discussão, incluindo prevalência, diagnóstico e manejo dos tumores de apêndice. Conclusão: Ressalta-se neste caso a importância do diagnóstico clínico, radiológico e anatomopatológico da apendicite aguda e da vigilância durante o manejo não operatório. Os relatos de tumores apendiculares estão aumentando, e esse cenário pode ser evitado se os fatores de risco forem identificados.