Approved by the following research ethics committee: Gazi University Ethics Committee. Number N o 53 -26/01/2015. ABSTRACTPurpose: Ocular inflammation is a frequent extraintestinal manifestation of inflammatory bowel disease (IBD) and may parallel disease activity. In this study, we evaluated the utility of a choroidal thickness measurement in assessing IBD activity. Methods: A total of 62 eyes of 31 patients with IBD [Crohn's disease (CD), n=10 and ulcerative colitis (UC), n=21] and 104 eyes of 52 healthy blood donors were included in this study. Choroidal thickness was measured using enhanced depth imaging optical coherence tomography. The Crohn's disease activity index (CDAI) and the modified Truelove Witts score were used to assess disease activity in CD and UC, respectively. Results: No significant differences in mean subfoveal, nasal 3000 µm, or temporal 3000 µm choroidal thickness measurements (P>0.05 for all) were observed between IBD patients and healthy controls. Age, smoking, CD site of involvement (ileal and ileocolonic involvement), CDAI, CD activity, and UC endoscopic activity index were all found to be significantly correlated with choroidal thickness by univariate analysis (P<0.05). Smoking (P<0.05) and the CD site of involvement (P<0.01) were the only independent parameters associated with increased choroidal thickness at all measurement locations. Conclusions: Choroidal thickness is not a useful marker of disease activity in patients with IBD but may be an indicator of ileal involvement in patients with CD.

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Gastric cancer (GC) develops through a multistep process known as the gastritis-atrophy-metaplasia-dysplasia-cancer sequence associated with alterations in the expression of host oncogenes and tumor suppressor genes after several decades. Helicobacter pylori (H. pylori) infection is the most consistent risk factor for GC, and its elimination is, therefore, the most promising strategy to reduce the incidence of this malignant disorder. However, the results of the relevant studies are controversial as to whether the H. Pylori eradication effectively induces the regression of gastric preneoplastic lesions. The inconsistencies are likely due to the heterogeneity in studies with respect to the number of biopsy samples taken, the method of histologic classification of findings, sample size, and the duration of the follow-up. Additionally some probable or well-defined factors other than H. Pylori may influence the progression of gastric preneoplastic lesions. Lastly, the real existence of a "point of no return" may partially explain the controversial findings. Here, we present an index case, and review data about the role of H. pylori during gastric carcinogenesis, and subsequently discuss information available from recent studies to evaluate the benefit of the H. pylori eradication for the regression of gastric precancerous lesions.

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