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Background: Coeliac disease patients show a number of gastrointestinal motor abnormalities, including a decrease in lower oesophageal sphincter pressure. The prevalence of endoscopic oesophagitis in these subjects however is unknown. Aim: To evaluate whether untreated adult coeliac patients had an increased prevalence of reflux oesophagitis and, if so, to assess whether a gluten free diet exerted any beneficial effect on gastro-oesophageal reflux disease (GORD) symptoms. Patients and methods: We retrospectively studied 205 coeliac patients (females/males 153/52, median age 32 years) who underwent endoscopy for duodenal biopsy and 400 non-coeliac subjects (females/males 244/156, median age 37 years) referred for endoscopy for upper gastrointestinal symptoms. Each patient was given a questionnaire for evaluation of GORD symptoms prior to and 4-12 months after endoscopy. Coeliac patients were given a gluten free diet. Oesophagitis patients of both groups, following an eight week course of omeprazole, were re-evaluated for GORD symptoms at four month intervals up to one year. Significance of differences was assessed by Fisher's exact test. Results: Oesophagitis was present in 39/205 (19%, 95% confidence interval (CI) 13.8-25.0%) coeliac patients and in 32/400 (8%, 95% CI 5.5-11.1%) dyspeptic subjects. At the one year follow up, GORD symptoms relapsed in 10/39 (25.6%, 95% CI 13-42.1%) coeliacs with oesophagitis and in 23/32 (71.8%, 95% CI 53.2-86.2%) non-coeliac subjects with oesophagitis. Conclusion: Coeliac patients have a high prevalence of reflux oesophagitis. That a gluten free diet significantly decreased the relapse rate of GORD symptoms suggests that coeliac disease may represent a risk factor for development of reflux oesophagitis. [ABSTRACT FROM AUTHOR]

Background: Studies on intestinal T cell clones from the mucosa of patients with coeliac disease have led to the identification of immunogenic gliadin epitopes. One is HLA-DQ8 restricted, its recognition by T cells being increased by introduction of negatively charged residues operated by tissue transglutaminase. Aim: To test HLA-DQ8 restricted epitope in both native (QYPSGQGSFQPSQQNPQA) and deamidated (QYPSGEGSFQPSQENPQA) forms in an organ culture system of treated coeliac mucosa from HLA-DQ8 positive and HLA-DQ8 negative patients. Patients and methods: Jejunal biopsies obtained from 10 patients with coeliac disease (six HLA-DQ8 positive and four HLA-DQ8 negative) were cultured in vitro with a peptic-tryptic digest (PT) of gliadin, or with the native (peptide A) or deamidated (peptide B) peptide. Intraepithelial CD3[sup +] and lamina propria total CD25[sup +] and CD3[sup +]CD25[sup +] cells were counted, lamina propria intercellular adhesion molecule 1 (ICAM-1) expression was evaluated, as well as that of Fas molecules on epithelial cells. Results: In HLA-DQ8 positive, but not in HLA-DQ8 negative, coeliacs the density of intraepithelial CD3[sup +] cells, lamina propria total CD25[sup +], and CD3[sup +]CD25[sup +] cells, as well as expression of ICAM-1 and Fas molecules were significantly increased in biopsies cultured with PT, peptide A, or peptide B compared with biopsies cultured in medium alone. Conclusion: These data show that the DQ8 restricted gliadin peptide is immunogenic only in the intestinal mucosa of HLA-DQ8 positive coeliac patients in both native and deamidated forms. [ABSTRACT FROM AUTHOR]

Gastric mucosal phospholipids, and in particular those of the surface layer, play an important part in mucosal barrier function. This study examined whether the phospholipid composition of the full thickness gastric mucosa is changed in peptic ulcer disease and gastritis. The phospholipid composition of gastric mucosa from endoscopic biopsy specimens in 28 subjects (eight healthy controls, 12 patients with duodenal ulcer, and eight with chronic atrophic gastritis) was studied. In addition, the phospholipid composition of gastric mucosa was compared with that of duodenal mucosa in 10 patients with duodenal ulcer. As expected phosphatidylcholine and phosphatidylethanolamine prevailed in all three groups. Lysolecithin was the smallest component in the duodenal ulcer and chronic atrophic gastritis groups. The phosphatidylethanolamine value was higher in duodenal ulcer and lower in chronic atrophic gastritis compared with the control group. In chronic atrophic gastritis there was an appreciable amount of phosphatidylglycerol that was not present in patients with duodenal ulcer or in the control group. There was no significant difference in phospholipid composition between antral and duodenal sites in duodenal ulcer patients. In conclusion, the phospholipid composition of gastric mucosa changes in human gastrointestinal diseases but its relation to cellular functions needs further study. [ABSTRACT FROM PUBLISHER]

One fifth of all cases of A virus hepatitis (AVH) have symptoms of gastroenteritis at the onset. This study investigated the mediated intestinal absorption of D-xylose (D-xyl) and 3-o-methyl-D-glucose (3-omG) and the non-mediated permeation of lactulose (Lacl, mol wt 342) and L-rhamnose (L-rh, mol wt 164) during acute and remission phases of AVH. Ten patients with AVH were given an oral load containing these sugars (5 g D-xyl: 2.5 g 3-omG, 1 g L-rh, 5 g lacl in 250 ml water) once during the acute phase and again during remission. The same load was given once to a group of 22 healthy controls. The mean concentration of D-xyl in urine and the ratio of D-xyl to 3-omG in plasma and urine were normal in both the AVH phases, ruling out intestinal malabsorption even in the acute phase. This study showed a significant increase in non-mediated permeation to Lacl, but not to L-rh, during the acute phase. These data indicate that the barrier function of the intestine is compromised in AVH infection while the absorptive function is not. An abnormally low concentration of D-xyl and 3-omG in plasma at one hour was found in all patients during the acute phase. This finding cannot be explained by alterations in intestinal absorption, but could be accounted for by increased space distribution of the sugars because of increased diffusion into tissue cells and/or expansion of the extracellular space by fluid retention. [ABSTRACT FROM PUBLISHER]

Background: Current guidelines recommend either UBT or HpSA for monitoring Hp infection. Aim of this multi-center study was to evaluate the agreement between the two tests in patients after treatment. Methods: After 4-6 weeks eradication regimen, patients were tested with both UBT (75mg [sup 13]C-urea) and HpSA (Meridian Diagnostics USA). Cut-off values (DOB30) for UBT were positive (> 5‰), indeterminate (3.01-4.99‰), and negative (0.160). Cut-off values (OD-450nm) for HpSA test were positive (> 0.160), indeterminate (0.159-0.140), and negative (< 0.140). Patients with either discordant or indeterminate tests were re-endoscoped with multiple biopsies for RUT, culture, histology, and immunohistochemistry to semiquantitatively assess the ratio between the coccoid and bacillary forms (C/B) of Hp in gastric mucosa. Patients were considered still infected if at least two of the biopsy-based tests were positive and successfully eradicated if all four tests were negative. Results: 458 patients (46±14 years) were enrolled: 422 (92.2%) had concordant UBT and HpSA (352 negative and 70 positive), 2 (0.4%) indeterminate (1 on UBT and 1 on HpSA), and 34 (7.4%) discordant tests. 28 patients (26 with discordant and 2 with indeterminate tests) underwent endoscopy: the HpSA was inaccurate in 24 cases (19 false negative, 4 false positive, and 1 indeterminate results) while the UBT was inaccurate in 4 (2 false positive, 1 false negative, and 1 indeterminate results). Biopsy-based tests showed no bacillary or coccoid forms in all 5 endoscoped patients, who were negative on UBT and positive on HpSA, but in one in whom the C/B ratio was 3/1 in both antrum and corpus. Conclusions: UBT and HpSA tests give discordant or indeterminate results in 8% of patients after eradicating treatments. When compared to biopsy-based "gold standard" tests, the HpSA test is less accurate than the UBT. Coccoid forms are not the cause of false positive results on HpSA tests. [ABSTRACT FROM AUTHOR]

Gastric cancer can be considered the end result of a multistep process that usually starts as chronic gastritis and progresses through gastric atrophy, intestinal metaplasia and dysplasia. Atrophic gastritis and intestinal metaplasia, long-term consequences of Helicobacter pylori (H. pylori) infection, are regarded as predisposing factors for gastric cancer associated with Helicobacter pylori infection, and their severity appears to influence gastric cancer risk. However it is debatable whether or not bacterial eradication reverses these lesions. Our purpose was to determine the outcome of chronic gastritis after H. pylori eradication in a long-term follow-up. Fifty-four consecutive patients with duodenal ulcer and H. pylori infection were enrolled in the study. All patients received conventional eradication therapy (omeprazole 40 mg bid, amoxocyllin 1 g bid and clarithromycin 500 mg bid). Endoscopic examination with antral and corporal biopsy was done at baseline and at yearly intervals. The follow-up period ranged from 60 to 144 months. Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System. Helicobacter pylori status was determined using a rapid urease test and modified Giemsa stain. Twenty-four patients were successfully treated; infection persisted in 14 and 16 dropped out (during the first five years of follow-up). Inflammation and mean neutrophil activity significantly decreased in patients in whom H. pylori was eradicated. Glandular atrophy improved in 2 and disappeared in 5/17 patients, whereas intestinal metaplasia inproved in 3 and disappeared in 2/12. In the patients in whom H. pylori persisted, inflammatory infiltrate, atrophy and intestinal metaplasia had not significantly decreased during follow-up. In contrast, glandular atrophy worsened in 2 and developed in 5/7 patients. Similarly, intestinal metaplasia did not improve when present and developed in 5/13 cases. In a long-term follow-up, H. pylori eradication does... [ABSTRACT FROM AUTHOR]

The integrity of telomeres, protects the cells from malignant transformation. Telomeres are preserved by telomerase, a multisubunit enzyme comprised of an RNA component (hTR) and a reverse transcriptase protein component (hTERT) which represents the catalitic subunit, hTR is ubiquitously distributed in each tissue while hTERT is undetectable in normal cells and has been reported to be present in 85% of the cancers. Therefore, activation of telomerase has been implicated in cell immortalization and with human carcinogenesis. Aim To investigate the expression of h-TERT m-RNA and protein in gastric biopsies of patients with and without H. pylori infection. Our population was constituted of 36 patients (15 men and 21 women; age range 19-79). H. pylori infection was evaluated by concordance between [sup 13]C-urea breath test and histology (modified Giemsa stain). Gastritis was scored according to up-dated Sydney system, h-TERT m-RNA and protein expression was evaluated by RT-PCR and immunohistochemistry, respectively. Twelve subjects were affected by H. pylori-negative chronic dyspepsia and 24 had H. pylori-positive chronic gastritis. Gastric mucosa was normal in 5/12 of H. pylori-negative patients and showed mild inflammatory infiltrate in the remaining subjects. In H. priori-positive group we observed mild atrophy in 10/24. The grade of inflammation was mild in 14, moderate in 6 and severe in the remaining 3 cases. Intestinal metaplasia was observed only in 4/24 of H. pylori-positive patients, h-TERT m-RNA expression was observed in 24/24 of H. pylori-positive patients while it was undetectable in H. pylori-negative group. The immunoistochemical expression of h-TERT protein was found in the foveolar and glandular epithelia only in the H. pylori-positive group. h-TERT seems to be up-regulated by H. pylori infection. The activation of h-TERT could be a very early event in the multistep process of gastric carcinogenesis H. pylori-related. [ABSTRACT FROM AUTHOR]