Heterotopic gastric mucosal patches in the proximal esophagus should not be overlooked during endoscopy because they may lead to important complications in relation to their acid secretion, which may vary according to their parietal cell mass.

Oesophageal strictures developing after caustic ingestion in children are a serious problem, and several protocols to prevent stricture formation have been proposed. A prospective clinical trial was conducted for preventing strictures in caustic oesophageal burns in a single clinic, and the results are presented. All children with caustic ingestion who had oesophagoscopy for diagnosing the severity of the burn were included in the study. Eighty-one children were included in the series, with ages ranging between 3 months and 12 years. The patients were given nothing by mouth until oesophagoscopy. IV fluids, broad-spectrum antibiotics, ranitidine, and a single-dose steroid were given. Oral burns were positive in 66 patients. Oesophagoscopy revealed a normal oesophagus in nine patients, grade 1 burn in 24, grade 2a in 21, grade 2b in 23, grade 3a in two, and grade 3b in one. Patients with grade 1 and 2a burns were discharged after oesophagoscopy. Patients with grade 2b and all grade 3 burns were given nothing by mouth for a week except water when swallowing their saliva, and were fed via total parenteral nutrition. After the 1st week, if there was no problem with swallowing, liquid foods were introduced. No intraluminal tubes were used. At the end of the 3rd week, a barium meal was administered and an upper gastrointestinal series taken. Dilatation was performed at 2-week intervals for strictures, which developed in one grade 2a patient, six grade 2b patients, and the grade 3b patient. Only one of these patients is currently on an oesophageal dilatation program. Limiting oral intake and avoiding foreign bodies in the oesophagus seem to provide a good success rate; however, further prospective studies are needed to decrease the incidence of corrosive oesophageal strictures.

Angiogenesis is an important component of pathogenesis of inflammatory bowel disease (IBD). Chronic inflammation and angiogenesis are two closely related processes. Chronic intestinal inflammation is dependent on angiogenesis and this angiogenesis is modulated by immune system in IBD. Angiogenesis is a very complex process which includes multiple cell types, growth factors, cytokines, adhesion molecules, and signal transduction. Lymphangiogenesis is a new research area in the pathogenesis of IBD. While angiogenesis supports inflammation via leukocyte migration, carrying oxygen and nutrients, on the other hand, it has a major role in wound healing. Angiogenic molecules look like perfect targets for the treatment of IBD, but they have risk for serious side effects because of their nature.

Bismuth salts exert their activity within the upper gastrointestinal tract through action of luminal bismuth. Bismuth exerts direct bactericidal effect on Helicobacter pylori by different ways: forms complexes in the bacterial wall and periplasmic space, inhibits different enzymes, ATP synthesis, and adherence of the bacteria to the gastric mucosa. Bismuth also helps ulcer healing by acting as a barrier to the aggressive factors and increasing mucosal protective factors such as prostaglandin, epidermal growth factor, and bicarbonate secretion. To date, no resistance to bismuth has been reported. Also synergism between bismuth salts and antibiotics was present. It was shown that metronidazole and clarithromycin resistant H. pylori strains become susceptible if they are administered together with bismuth. Bismuth-containing quadruple therapy was recommended both by the Second Asia-Pacific Consensus Guidelines and by the Maastricht IV/Florence Consensus Report as an alternative first choice regimen to standard triple therapy, in areas with low clarithromycin resistance, and it is recommended as the first-line therapeutic option in areas with a high prevalence of clarithromycin resistance. Greater than 90% eradication success can be obtained by bismuth-containing quadruple therapy. Choosing bismuth as an indispensable part of first-line therapy is logical as both metronidazole and clarithromycin resistances can be overcome by adding bismuth to the regimen.

This study was planned for searching possible changes of the total coagulation and fibrinolysis system in inflammatory bowel disease (IBD) in order to obtain some clues for explaining the relation between IBD and hypercoagulability. A total of 24 patients with ulcerative colitis, 12 patients with Crohn disease, and 20 healthy controls were studied. Platelets; prothrombin time (PT); partial thromboplastin time (PTT); fibrinogen; D-dimer; fibrinogen degradation products; protein C; protein S; antithrombin; thrombin time; von Willebrand factor; coagulation factors V, VII, VIII, IX, XI, and XIII; plasminogen; antiplasmin; tissue plasminogen activator; plasminogen activator inhibitor 1; and prothrombin fragments 1 + 2 were studied. Most of the procoagulants (platelets, fibrinogen, von Willebrand factor, coagulation factor IX, and plasminogen activator inhibitor 1) were found increased together with decreases in some anticoagulants (protein S and antithrombin) in IBD. Also the activation markers of coagulation (D-dimer, fibrinogen degradation products, and prothrombin fragments 1 + 2) were all increased. The parameters of the total coagulation-fibrinolysis system were increased in IBD, regardless of the form and the activity of the disease.

Isolated case reports in which symptomatic hearing loss develops suddenly during the course of inflammatory bowel disease (IBD) have been reported, but the presence of subclinical sensorineural hearing loss (SNHL) associated with IBD has been investigated in only two preliminary studies. In order to research this further, we aimed to investigate the presence of subclinical SNHL in IBD by comparison with a control group and to examine possible relations between the bowel disease parameters and hearing loss.Otoscopy, tympanometry, and pure tone audiometry were carried out in 39 patients with IBD (21 Crohn's disease [CD], 18 ulcerative colitis [UC]) and 25 healthy age- and sex-matched controls. All patients and control subjects had normal otoscopy findings and tympanometry was unremarkable, excluding middle ear disease and conductive hearing loss. Analysis of each frequency examined showed that the average hearing thresholds were increased significantly in the study group compared to those of the control group at higher frequencies (2, 4, and 8 kHz). When these parameters were compared with the control group according to subgroups of IBD, a significant difference was determined for the UC group at frequencies of 2, 4, and 8 kHz and for the CD group only at the frequency of 4 kHz. Although there was a trend of increment in SNHL as the age of the patient and duration and extent of UC increased, no significant correlation was observed between SNHL and these parameters or sex, activity, involvement site, medication history of IBD, and coexistence of other extraintestinal manifestations. In conclusion, it was demonstrated that a subclinical SNHL may be associated with UC and somewhat with CD, affecting mainly the high frequencies. In light of this finding, it may be advisable to investigate labyrinth functions as well as other extraintestinal manifestations in patients with IBD.

Irritable bowel syndrome is a common problem in the population, but gluten enteropathy is not associated with the vast majority of subjects with irritable bowel syndrome as expected. The need for screening gluten enteropathy among these patients is still unclear, and screening with serology only without small bowel biopsy may lead to false positive results.

We aimed to evaluate the carcinogenesis risk in inflammatory bowel disease via p53 mutation and its relation with hyperproliferation (cyclin-D1) and angiogenesis (with vascular endothelial growth factor [VEGF] and microvessel density) and whether these events play important roles in pathogenesis of inflammatory bowel disease. Colonic tissue samples of 26 ulcerative colitis, 6 Crohn's disease, and 8 amoebic colitis patients as well as samples of 10 healthy controls were stained with p53, cyclin-D1, CD34, and VEGF monoclonal antibodies by immunohistochemistry and evaluated semiquantitatively. Expression of p53 was higher in ulcerative colitis than in the healthy control and amoebic colitis groups (4.15 +/- 2.07, 1.4 +/- 1.5, 1.3 +/- 1.5; P < 0.001). The Crohn's disease group had the highest p53 expression (4.6 +/- 1.6). The Crohn's disease, ulcerative colitis, and amoebic colitis groups all had higher VEGF expression than did the healthy controls (respectively, 4.3 +/- 1.2, 2.92 +/- 2.0, 2.3 +/- 1.5, 0.6 +/- 0.97; P < 0.001). Also, microvessel density was statistically higher in all three colitis groups than in healthy controls. Cyclin-D1 expression in all four groups was similar. The study showed that p53 mutation was present in nonneoplastic mucosa of inflammatory bowel disease patients. Detecting strong p53 overexpression with VEGF overexpression may help in differentiating inflammatory bowel disease from other colitis.