Cite this article as: Bor S, Kalkan İH, Çelebi A, et al. Alginates: From the ocean to gastroesophageal reflux disease treatment. Turk J Gastroenterol 2019; 30(Suppl 2): S109-36.

Non-alcoholic fatty liver disease (NAFLD) is an umbrella term to describe the entire spectrum of this common liver disease. In patients with NAFLD, especially those with non-alcoholic steatohepatitis (NASH), most often have one or more components of the metabolic syndrome, but this is not universal. Although most patients with NAFLD share many clinical features, only a subset of patients develops significant liver inflammation and progressive fibrosis. On the other hand, not all patients with NASH exhibit insulin resistance. NASH can be seen in patients who are lean and have no identifiable risk factors. Many clinical studies have tried numerous drugs and alternative medicine, however, investigators have failed to identify a safe and effective therapy for patients with NASH. As summarized, the heterogeneity of pathogenic pathways in individual patients with NASH may warrant the development of an individualized treatment according to the underlying pathogenic pathway. The differentiation of pathogenetic targets may require the development of diagnostic and prognostic biomarkers, and the identification of genetic susceptibilities. At present, evidence-based medicine provides only a few options including life-style modifications targeting weight loss, pioglitazone and vitamin E in non-diabetic patients with biopsy-proven NASH.

Objective. Recently, mucosal changes of small bowel were defined by developing new imaging techniques including capsule endoscopy (CE) in portal hypertensive patients. However, the clinical impact of these changes is unknown. In this study, we aimed to determine the additional cause of blood loss in portal hypertensive patients. Material and methods. A total of 444 portal hypertensive patients, hospitalized in our clinic between 2005 and 2007, were evaluated. Patients with obscure bleeding were enrolled to this prospective case–control study. CE was performed in 21 patients who met inclusion criteria. Gastroscopy, colonoscopy and computerized tomography/small bowel enema were performed in all patients. Results. Fourteen cirrhotic and seven noncirrhotic portal hypertensive patients were enrolled to this study. Mean age of patients was 47.9 ± 15.6 years, and 13 of 21 were male. Small bowel varices were found in 7 patients (1 active bleeding) and other mucosal abnormalities in 10 patients (vascular ectasia, erosion and edema, 1 active bleeding). Although two of them were normal, jejunal malignant mass was found in two patients (1 active bleeding). Of 21 patients, 19 (90.5%) patients had portal hypertensive abnormalities (including varices). However, ileal varices rate was 57.1% (4 patients) in noncirrhotic portal hypertensive patients and 21.4% (3 patients) in cirrhotics. Conclusion. Ninety percent of patients had portal hypertensive abnormalities in small bowel and one-third of them had small bowel varices. Small bowel varices and vascular ectasia were the main causes of obscure bleeding in portal hypertensive patients.

Objective. Familial Mediterranean fever (FMF) is the most common form of autoinflammatory diseases. We aimed to evaluate the small bowel mucosa by capsule endoscopy (CE) in FMF patients for investigation of other possible causes of abdominal pain. Material and methods. The study group consisted of 41 patients with FMF. A standard questionnaire was used to record the gastrointestinal symptoms, other clinical findings, Mediterranean fever gene (MEFV) mutations, and history of medications including non-steroidal anti-inflammatory drugs (NSAIDs). Gastroscopy, colonoscopy and small bowel CE were performed in all patients, and biopsies were taken from terminal ileum and duodenum. Results. The mean age of the patients was 34 ± 11 years, 63% of them were female, and 76.5% of them were carrying MEFV exon 10 mutations. Only one patient used NSAIDs in addition to colchicine. In endoscopic investigations, gastric erosion was detected in only one patient, and no significant findings were detected in colonoscopy. CE showed small bowel mucosal defects in 44% (erosions in 26.8%, ulcer in 17.1%) and edema in 29.3% of the patients. Most (64%) of the ulcer and erosions were localized to jejunum, and only 24% were in ileum. Mitotic changes as an indirect finding of colchicine toxicity were not different from the changes observed in samples of independent group of patients with irritable bowel syndrome. Conclusion. Mucosal defect was observed in half of the FMF patients, which may be associated with underlying inflammation or chronic colchicine exposure. Detection of nonspecific chronic inflammation without mitotic changes supports that mucosal defects may be associated with the autoinflammatory process.

This study evaluated the risks and outcomes of capsule retention during capsule endoscopy (CE) for investigating small bowel disease. Capsule retention is the most serious complication of CE. Before CE, the gastrointestinal tract was evaluated for blockages with computerized tomography. Analysis of CE was made retrospectively. Capsule endoscopy was used to investigate obscure bleeding (90.2%; n = 324) or other symptoms (9.8%; n = 35). The capsule retention rate was 11/359 (3.1%); it was retained in a malignant lesion area (adenocarcinoma or melanoma) in two patients (18.2%), in the small bowel in an ulcerated area in five patients (45.5%), and in the oesophagus/stomach in four patients (36.4%) due to dysmotility. None of the patients had symptoms of obstruction. Scanning patients before CE did not predict capsule retention. Retention is a complication of CE, but occurs as a result of the underlying disease. The risk of retention is increased in patients with motility disorders, suspected small bowel ulcers or malignancies.