Colorectal cancer progression originates when accumulated genetic and epigenetic alterations cause genomic instability and a malignant phenotype. Subsequent molecular pathway deregulation leads to histopathologic changes that are clinically evident as aberrant crypt foci (ACF) and visualized by high-magnification chromoscopic colonoscopy. ACF are biomarkers of increased colorectal cancer risk, particularly those with dysplastic features. Genetic profiling using genomic instability, loss of heterozygosity, and methylation analysis has revealed a minority population of ACF genotypically analogous to cancer.

Background and aimTesting for Helicobacter pylori (Hp) infection is recommended for work-up of unexplained iron deficiency anemia (IDA), although the evidence supporting this recommendation is scant. The aim of this study was to investigate the association between Hp infection and unexplained iron deficiency (ID) or IDA in the older adult population without significant upper gastrointestinal source of blood loss.MethodsRetrospective single-center cohort study; 523 out of 1253 consecutive patients who underwent esophagogastroduodenoscopy with no significant upper and/or lower gastrointestinal source for blood loss or risk factors for IDA. Comparisons were made between the Hp-positive and Hp-negative groups using Fisher exact test, chi-square test and Student’s t-test. Univariate and multiple logistic regression analyses were used to identify significant risk factors associated with ID and IDA.ResultsOne hundred and three subjects (19.7%) had Hp infection and 420 (80.3%) were negative for Hp. Sixty-eight (22.1%) out of 307 subjects with available serum iron profile had unexplained ID and 28 (5.4%) out of 510 subjects with available hemoglobin profile had unexplained IDA. No association was found between ID/IDA and Hp infection in univariate and multiple logistic regression analyses.ConclusionWe found no association between unexplained ID or IDA and Hp infection in older adult population without peptic ulcer disease or significant upper gastrointestinal source of blood loss.

1. In the present study, we evaluated the role of cyclo-oxygenase (COX)-1 and COX-2 on gastric acid secretion in rabbit isolated parietal cells and gastric glands by examining [(14)C]-aminopyrine uptake, prostaglandin (PG) E(2) synthesis and COX-1, COX-2 and proton pump expression at baseline and after treatment with various concentrations of specific COX-1 (SC-560), COX-2 (5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methyl-sulphonyl)phenyl-2 (5H)-furanone; DFU) and non-specific COX (indomethacin) inhibitors. 2. In parietal cells, SC-560 and indomethacin, over the concentration range 10(-8) to 10(-4) mol/L, dose-dependently increased basal and 10(-4) mol/L histamine-stimulated aminopyrine uptake and inhibited PGE(2) synthesis, whereas DFU (10(-8) to 10(-5) mol/L) had no effect. However, at 10(-4) mol/L, DFU augmented histamine-stimulated aminopyrine uptake by 135% and inhibited PGE(2) synthesis by 39%, indicating an inhibition of COX-1 at this higher concentration. 3. The SC-560-, DFU- and indomethacin-induced augmentation of histamine-stimulated aminopyrine uptake was reduced to basal levels after 10(-5) mol/L lansoprazole treatment in parietal cells and gastric glands, whereas 10(-4) mol/L ranitidine only partially inhibited such augmentation. 4. Only COX-1 was detected in parietal cells. However, both COX-1 and COX-2 were expressed in gastric glands, with relative protein density of COX-1 being sixfold higher than that of COX-2. Protein levels of COX-1 in parietal cells and those of COX-1 and COX-2 in gastric glands remained unchanged, regardless of inhibitor treatment, either alone or with histamine. 5. Parietal cell proton pump expression was significantly enhanced by 10(-5) mol/L SC-560 and 10(-4) mol/L indomethacin (by 29 and 31%, respectively) and pump activity was enhanced by 61 and 65%, respectively. In contrast, 10(-5) mol/L DFU had no effect. 6. In conclusion, the data indicate that inhibition of COX-1- but not COX-2-derived PGE(2) synthesis is involved in augmentation of non-steroidal anti-inflammatory drug-induced gastric acid secretion in parietal cells by enhancing expression and activation of the proton pump.

No abstract

No abstract