Detection of Helicobacter pylori in bladder biopsy specimens of patients with interstitial cystitis by polymerase chain reaction

The cause of interstitial cystitis (IC) is still unknown. Several features suggest that it may be an infectious disease and it has compelling similarities to chronic gastritis. The identification of Helicobacter pylori as the cause of chronic gastritis focused attention on this organism. Many studies have been done investigating the role of H. pylori in the etiology of IC. Previous studies mostly determined the presence of H.pylori with antibodies in the serum samples of IC patients, but these methods may lead to false positive or negative results. We therefore investigated the presence of H.pylori in bladder biopsy specimens by using polymerase chain reaction (PCR), which is accepted as the most sensitive and specific test for detecting this organism. A total of 32 patients with IC were enrolled into the study. The PCR assay was performed on cold cup bladder biopsies of IC patients. Both positive and negative controls were included in each set of PCR reactions. Gastric biopsy specimens of peptic ulcer patients with proven H. pylori infection were used as positive controls. Bladder biopsies of all IC patients were negative for H. pylori DNA. PCR showed the presence of H. pylori in the positive controls in each cycle demonstrating that the PCR assay was working properly. Thus, there is no evidence that IC is the result of H. pylori infection. This study does not negate the possibility that other infectious agents may play a role in the etiology of IC

Hyperbaric oxygen therapy is as effective as dexamethasone in the treatment of TNBS-E-induced experimental colitis

Introduction Hyperbaric oxygen (HBO) has been demonstrated to be useful as an adjunctive therapy for Crohn's disease. In the present study, HBO was tested as a treatment for trinitrobenzenesulfonic acid-ethanol (TNBS-E)-induced distal colitis, and its effects were compared with dexamethasone therapy. Methods A total of 48 Sprague-Dawley rats were separated into six groups: the control, and those treated with vehicle, TNBS-E, HBO, dexamethasone, or combined HBO + dexamethasone. The HBO treatment group was exposed to 100% HBO at 2 ATM for 75 min twice daily at 6-h intervals in a HBO chamber, both on the day of colitis induction and 3 days thereafter. Treatment with intraperitoneal dexamethasone twice daily was started 1 h before the induction of colitis and was continued for 7 days in the dexamethasone group. The rats were decapitated 8 days after the induction of colitis, and the colonic tissue wet weight, macroscopic and microscopic lesion score, and tissue myeloperoxidase (MPO) activity were determined. Results HBO therapy decreased the activity of experimental colitis measured by the tissue wet weight, macroscopic score, microscopic score, and MPO activity. The dexamethasone treatment significantly reduced the colitis activity as determined by the tissue MPO activity and wet weight. There were also decreases in the macroscopic and microscopic activity scores with the dexamethasone therapy; however, these changes were not statistically significant. The combined therapy with HBO and dexamethasone provided no additional benefit over HBO therapy alone. Conclusion HBO therapy can be a valuable therapeutic option in treatment of patients with inflammatory bowel disease. HBO therapy in the refractory patients deserves further, larger clinical studies

Critical pH Level of Lye (NaOH) for Esophageal Injury

Aim/Background Lye (NaOH) ingestion in humans often results in alkaline damage to the esophagus, but knowledge about this process is limited. Here, we explore the effects of lye on esophageal epithelial structure and function using rabbit esophageal epithelium as a model of lye ingestion. Methods Rabbit esophageal epithelium was mounted in Ussing chambers so that the electrical potential difference (PD), short-circuit current (I (sc)), and transepithelial resistance (R (T)) could be monitored before, during, and after mucosal exposure to lye (NaOH) at pHs ranging from 7.4 to 12.1. Histopathology and dextran fluxes were also performed and correlated with the electrical data. Results Mucosal exposure to lye at pHs < 11.5 had no damaging effects on the esophagus. However, at pHs a parts per thousand yen11.5, damage was both time- and pH-dependent, as noted by increases in PD and I (sc), and declines in R (T). Further, the electrical changes were paralleled morphologically by epithelial liquefaction necrosis and increases in dextran flux. Also, by pretreating tissues with ouabain, the early lye-induced rise in PD and I (sc) was shown to result from a combination of increased active (sodium) transport and passive (sodium) diffusion which indicates that, even early on, the damaging effects of lye include changes in both apical cell membranes and tight junctions of this epithelium. Conclusion Lye (NaOH) injury to the esophageal epithelium is both pH- and time-dependent, but requires a minimum pH of 11.5. At pHs a parts per thousand yen11.5, lye produces liquefaction necrosis, an injury that involves both cellular and junctional barriers, and which markedly increases epithelial permeability to ions and uncharged molecules. Based on these results, non-industrial cleaning products in the home are likely to be safer if they have a concentration of lye below pH 11.5