Effects of long-term PPI treatment on producing bowel symptoms and SIBO.

BACKGROUND: Gastroesophageal reflux disease (GERD), including erosive reflux disease and non-erosive reflux disease (NERD), is a chronic disease with a significant negative effect on quality of life. State-of-the-art treatment involves proton pump inhibitors (PPIs). However, relapse of symptoms occurs in the majority of the patients who require recurrent or continuous therapy. Although PPIs are well tolerated, little information is available about gastrointestinal side effects. AIM: To evaluate the effects of long-term PPI treatment on development of bowel symptoms and/or small intestinal bacterial overgrowth (SIBO). METHODS: Patients with NERD not complaining of bowel symptoms were selected by upper endoscopy, 24-h pH-metry and a structured questionnaire concerning severity and frequency of bloating, flatulence, abdominal pain, diarrhoea and constipation. Patients were treated with esomeprazole 20 mg bid for 6 months. Prior to and after 8 weeks and 6 months of therapy, patients received the structured questionnaire and underwent evaluation of SIBO by glucose hydrogen breath test (GHBT). RESULTS: Forty-two patients with NERD were selected out of 554 eligible patients. After 8 weeks of PPI treatment, patients complained of bloating, flatulence, abdominal pain and diarrhoea in 43%, 17%, 7% and 2%, respectively. After 6 months, the incidence of bowel symptoms further increased and GHBT was found positive in 11/42 (26%) patients. By a post hoc analysis, a significant (P < 0·05) percentage of patients (8/42) met Rome III criteria for irritable bowel syndrome. CONCLUSIONS: Prolonged PPI treatment may produce bowel symptoms and SIBO; therefore, the strategy of step-down or on-demand PPI therapy should be encouraged in GERD.

Is screening for and surveillance of atrophic gastritis advisable?

Gastric cancer remains a leading cause of cancer-related deaths in many parts of the world. At present, prevention seems to be the most effective means to reduce its the incidence and mortality rate. Gastric atrophy is considered the first relevant step in the histogenesis of gastric adenocarcinoma. However, whether screening for and surveillance of atrophic gastritis is advisable is debated. The prevalence and pattern of chronic atrophic gastritis varies greatly from country to country, being higher and mainly diffuse pangastritis or localized in those countries with a high gastric cancer incidence. The only method available to detect gastric atrophy is histopathological examination of endoscopic specimens, but there is no consensus about diagnosis. Serum gastric secretion may be a marker of gastric atrophy, although it has high specificity but low sensitivity. Gastric atrophy is mainly related to chronic Helicobacter pylori (H. pylori) infection. Thus, the only effective strategy for gastric cancer prevention is eradication of H. pylori infection to arrest atrophy progression in selected populations. In conclusion, there is insufficient evidence to suggest screening for and surveillance of atrophic gastritis in the general population; however, this strategy should be applied in countries with a high incidence of gastric cancer.

Large Brunner's gland adenoma: case report and literature review.

Brunner's gland adenoma (BGA) is a very rare benign tumour of the duodenum, which is usually asymptomatic and discovered incidentally at endoscopy. Occasionally, this lesion may be large, causing upper gastrointestinal haemorrhage or intestinal obstruction. The case had a large Brunner's gland adenoma, presenting melena that was managed by endoscopic excision.