The Prevalence, Risk Factors, and Clinical Correlates of Erosive Esophagitis and Barrett's Esophagus in Iranian Patients with Reflux Symptoms.

Background. Erosive esophagitis (EE) and Barrett's esophagus (BE) are the two important complications of gastroesophageal reflux disease. We aimed to investigate the prevalence of and the risk factors for EE and BE in an Iranian group of patients with reflux symptoms. We also examined the relationship between reflux symptoms and endoscopic findings. Methods. A total of 736 patients with gastroesophageal reflux disease (GERD) symptoms were enrolled and all underwent upper gastrointestinal endoscopy. Diagnosis of Barrett's esophagus was confirmed by pathologic examination and Helicobacter pylori (H. pylori) infection was demonstrated by rapid urease test. Results. Two hundred eighty-three and 34 patients were found to have EE and BE, respectively. Multivariate analysis showed that hiatal hernia (P < 0.001) and H. pylori infection (P < 0.002) were the two significantly related risk factors for esophagitis. Only age was related to BE, with BE patients being more likely to be older (P < 0.001) than others. Conclusions. Prevalence of EE and BE in Iranian reflux patients is similar to that seen in western countries. H. pylori infection and the presence of hiatal hernia may be strong risk factors for esophagitis as does older age for Barrett's esophagus. Finally, reflux symptoms have no significant relationship with endoscopic findings.

The effect of helicobacter pylori eradication on liver fat content in subjects with non-alcoholic Fatty liver disease: a randomized open-label clinical trial.

BACKGROUND: The role of Helicobacter pylori (HP) in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) is unclear. OBJECTIVES: The aim of this study was to evaluate the effect of HP eradication on liver fat content (LFC), liver function tests (LFT), lipid profile, and homeostasis model assessment-IR (HOMA-IR) index in NAFLD. PATIENTS AND METHODS: Dyspeptic patients with increased serum aminotransferase levels were enrolled in the study. The exclusion criteria were factors affecting serum aminotransferase or HP treatment strategy. Participants with persistent elevated serum aminotransferase level and ultrasound criteria for identification of fatty liver were presumed to have NAFLD. "NAFLD liver fat score" was used to classify NAFLD. Those with "NAFLD liver fat score" greater than -0.64 and positive results for urea breath test (UBT), were included. Lifestyle modification was provided to all participants. HP eradication was performed in intervention arm. LFC, fasting serum glucose (FSG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), triglyceride (TG), cholesterol (CHOL), high and low-density lipoprotein (HDL, LDL), and HOMA-IR were checked at baseline and after that, at intervals of eight weeks and twenty four weeks. RESULTS: One hundred (49 males) patients with the mean age of 43.46 (± 11.52) were studied. Repeated measure ANOVA showed a significant reduction in LFC, anthropometric measurements, and laboratory parameters (except for HDL) in the both groups during the study; however, no significant difference was observed between the groups. CONCLUSIONS: It seems that HP eradication per se might not affect LFC, LFT, lipid profile, and insulin resistance in dyspeptic NAFLD patients.

Antigliadin antibody in sporadic adult ataxia.

BACKGROUND: The most common neurologic manifestation of gluten sensitivity is ataxia, which accounts for up to 40% of idiopathic sporadic ataxia. Timing of diagnosis of gluten ataxia is vital as it is one of the very few treatable causes of sporadic ataxia and causes irreversible loss of Purkinje cells. Antigliadin antibody (AGA) of the IgG type is the best marker for neurological manifestations of gluten sensitivity. This study was conducted to measure the prevalence of gluten ataxia in a group of Iranian patients with idiopathic ataxia. METHODS: For 30 patients with idiopathic cerebellar ataxia, a questionnaire about clinical and demographic data was completed. Serum AGA (IgA and IgG) and antiendomysial antibody (AEA) were assessed. Gluten ataxic patients underwent duodenal biopsy. Magnetic resonance imaging was done for all patients to see if cerebellar atrophy is present. RESULTS: Only 2 patients had a positive IgG AGA (6.7%) who both had a positive AEA while none of them showed changes of celiac disease in their duodenal biopsies. Only presence of gastrointestinal symptoms and pursuit eye movement disorders were higher in patients with gluten ataxia. CONCLUSION: Prevalence of gluten ataxia in Iranian patients with idiopathic ataxia seems to be lower than most of other regions. This could be explained by small sample size, differences in genetics and nutritional habits and also effect of serologic tests in clinical versus research setting. Further researches with larger sample size are recommended.