Effect of gastric helicobacter pylori colonization in the development of erosive esophagitis in patients with hiatal hernia.

Background/Aims: There may be various factors that determine gastroesophageal reflux disease (GERD) as a result of hiatal hernia (HH) (such as the size of the hernia, age, other host and environmental factors) and the presence of protective factors to explain the absence of reflux disease should not be ignored. Helicobacter pylori (Hp) infection can prevent the development of GERD or cause it. This study aimed to determine whether Hp colonized in the stomach and hernia affects the development of erosive esophagitis (EE) in patients with HH. Materials and Methods: In this case-controlled study, 111 patients with HH were eligible for the study. Study group with EE (n = 61, 55%) and control group without EE (n = 50, 45%) were formed. Groups were compared for gastric Hp and Hp in the hernia. Results: While the frequency of Hp in the antrum was 55.7% in the group with EE, it was 30% in the control group (p = 0.01, OR: 2.94 in 95% CI 1.34-6.46). The rates in terms of HP frequency in the corpus were 43.6% and 32.1%, respectively, (p = 0.45). Hp colonization in HH was detected in 18 cases (29.50%) and 14 cases (28%), respectively, (p = 0.86). In regression analysis, antral Hp was found to be effective in the development of EE (p = 0.01). Conclusion: As a result of this study, we think that antral Hp may have a causative role in the development of reflux esophagitis, but the presence of Hp in HH does not have an effective role in reflux esophagitis formation.

Does regression in treatment-induced liver fibrosis reflect noninvasive tests? Assessing treatment results of hepatitis B patients who took potent antiviral drugs for 5 years.

BACKGROUND: Chronic liver disease may be reversed through treatment, and it is crucial to have a definitive diagnosis of liver fibrosis for this treatment. Aims: In this study, we aimed to determine whether regression of liver fibrosis in naive patients undergoing strong antiviral therapy is reflected in noninvasive tests. MATERIALS AND METHODS: We systematically reviewed and monitored medical records of patients with chronic hepatitis B who underwent liver biopsy for patient qualification. We selected patients with a liver fibrosis score of two or more who had not previously received antiviral treatment. We used previously described formulas to compute the indirect indicators of fibrosis for the patients and noted the values of Aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio (AAR), age-platelet index (API), fibrosis index-based 4 factor (FIB-4), AST-platelet ratio index (APRI), mean platelet volume (MPV) and platelet count (PLT). RESULTS: We found a significant difference between the three measurements for APRI, AAR and FIB-4 scores and MPV and PLT distributions in patients who were administered entecavir and tenofovir (Friedman P < 0.05). In the post-hoc binary comparison for both entecavir and tenofovir, we found significant differences between the baseline measurements and the 3rd- and 5th-year measurements in terms of APRI, AAR, FIB-4, MPV, and PLT. CONCLUSION: Liver biopsy is considered the gold standard for the treatment and follow-up of hepatitis B but may not be appropriate in all cases. Non-invasive tests may be effective in monitoring antiviral therapy. We demonstrated that non-invasive tests improved with antiviral therapy, which may be a reflection of treatment-regression in liver histopathology.