Cruciferous vegetable consumption and gastric cancer risk: A meta‐analysis of epidemiological studies

The relationship between consumption of cruciferous vegetables (CV) and risk of gastric cancer has been investigated by many studies, but remains controversial. We carried out a meta‐analysis to summarize available evidence from epidemiological studies on this point. Relevant published reports of CV intake and gastric cancer were identified using MEDLINE (PubMed), EMBASE, and Web of Science databases through to the end of September 2012. We pooled the relative risk from individual studies using a fixed‐ or random‐effects model and carried out heterogeneity and publication bias analyses. Sixteen case–control and six prospective studies were included in our analysis. When all studies were pooled, we yielded a significantly inverse association between CV (relative risk = 0.81; 95% confidence interval, 0.75–0.88) intake and gastric cancer risk, with little heterogeneity (Q = 27.27, P = 0.292, I² = 12.0%). Specific analysis for cabbage intake yielded similar result. When separately analyzed, case–control studies of CV intake yielded significant results and the results of prospective studies showed borderline statistical significance. Moreover, significant results were consistent for high‐quality studies, for North American, European, and Asian studies, for studies on males, and for studies on non‐cardia gastric cancer. Findings from this meta‐analysis provide evidence that high intake of CV was inversely associated with the risk of gastric cancer and non‐cardia gastric cancer in humans. Further studies on other specific CV, food preparation methods, and stratified results by anatomic cancer site and histological type should be extended in the future.     

Increased expression of extracellular matrix metalloproteinase inducer (EMMPRIN) and MMP10, MMP23 in inflammatory bowel disease: Cross‐sectional study

It has been reported that EMMPRIN is involved in the regulation of immune response and the induction of MMPs production by fibroblasts. The aim of this study was to describe the intestinal gene expression and protein production of EMMPRIN, MMP23 and MMP10 in patients with ulcerative colitis (UC) and Crohn’s disease (CD) and compared them with a control group. Gene expression of EMMPRIN, MMP10 and MMP23B was measured by RT‐PCR. In order to determine EMMPRIN and MMP protein expression, colonic tissues were immunostained. The results of the study showed EMMPRIN gene expression was upregulated in rectal mucosa from active (a)UC versus aCD patients (P = .045), remission (r)CD group (P = .0009) and controls (P < .0001). We detected differences between rUC and aCD (P = .004), rCD (P < .0001) or control group (P < .0001). EMMPRIN showed a higher expression in mucosa (intraepithelial lymphocytes), submucosa and adventitia (endothelial cells) from aCD patients. MMP23 levels were increased in aUC and aCD compared to rUC and rCD and the control group (P = .0001). EMMPRIN+/MMP23+─expressing cells were localized mainly in mucosa, muscular and adventitia from active UC patients. MMP10 gene expression was increased in aUC versus CD patients and the control group (P = .0001). MMP10 gene expression is associated with inflammation in UC patients (P = .0001, r² = .585). EMMPRIN+/MMP10+─producing cells were found mainly in all intestinal layers and perivascular inflammatory infiltrates from aUC patients. In conclusion, EMMPRIN, MMP23 and MMP10 were upregulated in patients with active UC versus remission UC , CD and control groups suggesting that, they are involved in the inflammatory process.     

Beyond Helicobacter: dealing with other variants of gastritis—an algorithmic approach

In daily practice, the presence of inflammation in gastric biopsies prompts a mental algorithm, an early question being whether the lesion present is Helicobacter‐associated. If Helicobacter organisms are not found, then there is a further algorithm, governed by the predominant type of inflammatory cells present, and the presence of other features such as intraepithelial lymphocytosis, a subepithelial collagen band, granulomas, coexisting chronic inflammation, focality, and superimposed reactive changes including erosions and ulcers. Each of these generates its own differential diagnosis. If no inflammation is present, then the two major changes specifically looked for are the changes associated with hypergastrinaemia, by far the most common cause of which is treatment with proton pump inhibitors, and reactive changes. These may be present with and without accompanying inflammation, and, when the epithelial changes dominate, the term gastropathy is preferred. In this article, we present an approach to non‐Helicobacter inflammation and gastropathies.