Gastric Helicobacter Pylori Infection Research Articles

Helicobacter pylori and autoimmune pancreatitis: role of carbonic anhydrase via molecular mimicry?

Autoimmune pancreatitis is a recently defined nosological entity, which accounts for 4.6-6% of all forms of chronic pancreatitis and is often associated with other autoimmune diseases, particularly Sjogren's syndrome. Possession of the HLA DRB1*0405-DQB1*0401 genotype confers a risk for the development of autoimmune pancreatitis. Autoantibodies against carbonic anhydrase II and lactoferrin are frequently present in affected subjects and are suspected to have a pathogenic role. A link between gastric infection by Helicobacter pylori and autoimmune pancreatitis has been hypothesized. We used in silico protein analysis and search for HLA binding motifs to verify this hypothesis. We found a significant homology between human carbonic anhydrase II and alpha-carbonic anhydrase of Helicobacter pylori, an enzyme which is fundamental for the survival and proliferation of the bacterium in the gastric environment. Moreover, the homologous segments contain the binding motif of the HLA molecule DRB1*0405. Our data strengthen the hypothesis that gastric Helicobacter pylori infection can trigger autoimmune pancreatitis in genetically predisposed subjects.

Primary mucosa-associated lymphoid tissue (MALT) lymphoma of the larynx

Mucosa-associated lymphoid tissue (MALT) lymphoma is usually associated with a chronic inflammatory disease from which lymphoid tissue of MALT type arises as a prerequisite for lymphoma proliferation. No well-characterized chronic inflammatory process has been identified in the larynx. We report a case of primary MALT lymphoma of the larynx associated with extraesophageal reflux, chronic laryngitis, and gastric Helicobacter pylori infection, raising the issue of its physiopathology and treatment. Treatment of this MALT lymphoma of the larynx consisted of complete surgical excision associated with omeprazole, amoxicillin, and clarithromycin. No evidence of disease was observed after 24 months of follow-up. We may assume that chronic laryngitis could be a precursor to MALT lymphoma. This case is the first one to our knowledge of a primary MALT lymphoma of the larynx treated with conservative management combining surgical excision, reflux therapy, and eradication of gastric H. pylori infection.

Oral Fluid Antibody Detection in the Diagnosis of Gastric Helicobacter pylori Infection.

The aim of this study was to evaluate an enzyme - linked immunosorbent assay (ELISA) for the detection of anti - helicobacter pylori (H. pylori) specific IgG antibodies in specimens of oral fluid.All subjects over the age 18 years undergoing endoscopy for any reason were asked to participate in the study. Two groups of 44 patients in each were selected as HP+ and HP-. At the same time, 5 milliliters of unstimulated saliva was collected from these patients, and the antibody titration against H.P. was evaluated by "ELISA" method.In overall, the level of salivary antibody in H.P+ group was significantly more than those in H P- group (P<0.001). In the best cut - off, sensitivity and specificity obtained in this test were respectively 88.6% and 81.8% and positive predictive and negative predictive values were determined as 83% and 87.8%, respectively. Positive Likelihood Ratio and negative likelihood ratio were 6.8 and -0.083, respectively.Oral fluid ELISA is relatively a comfortable, fast and noninvasive test for diagnosis of H. pylori infection.

Risk of the Gastric Cancer Associated with the Interleukin 1β Gene Polymorphism and Helicobacter pylori

Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin is a cytokine markedly inhibiting gastric acid secretion. Interleukin production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was in gastric cancer cases and in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 () in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was in group with Helicobacter pylori infection and in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 () in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.

Immunization with attenuated Salmonella typhimurium producing catalase in protection against gastric Helicobacter pylori infection in mice.

To evaluate the protective effect of live attenuated Salmonella typhimurium expressing catalase against gastric Helicobacter pylori infection in mice, and to explore the underlying mechanisms of the protective immune reaction. The H. pylori catalase gene was introduced into attenuated S. typhimurium strain SL3261. C57BL/6 mice were orally immunized with the SL3261 vaccine strain expressing catalase or with SL3261 alone or phosphate-buffered saline (PBS). Mice were sacrificed 4 weeks after immunization and 5 weeks after H. pylori challenge, respectively. All PBS control mice were infected. Eight of 13 (61.5%) mice immunized with the SL3261 vaccine strain and three of 14 (21%) mice immunized with SL3261 alone showed protection against H. pylori infection. Serum anti-H. pylori IgG2a levels of S. typhimurium-immunized mice were higher than those of PBS controls, both before and after H. pylori challenge, while there were no differences for IgG1 and IgA. Similarly, mRNA expression of interleukin (IL)-2, IL-12 and interferon-gamma in the gastric mucosa of S. typhimurium-immunized mice was significantly higher than that of PBS controls both before and after challenge. Moreover, S. typhimurium-immunized mice were characterized by marked infiltration of lymphocyte and mononuclear cells in the gastric mucosa after challenge. IL-4 and IL-10 were not detected in any of the three groups. IL-6 expression was increased in the PBS group compared with the S. typhimurium-immunized groups after challenge. This study demonstrates that oral immunization of mice with catalase delivered by an attenuated S. typhimurium strain offers protection against H. pylori infection. This protective immunity was mediated through a predominantly Th1-type response and was associated with post-immunization gastritis.

Detection of Helicobacter pylori in nasal and maxillary sinus specimens from patients with chronic sinusitis.

In patients with chronic sinusitis, the colonization of nasal and maxillary sinus tissues by Helicobacter pylori (HP) was investigated using polymerase chain reaction, urease test (CLO test), culture, and immunohistochemical analysis. A prospective clinical study. The subjects were 11 patients aged 20 to 72 years with chronic sinusitis who had undergone sinus surgery under local anesthesia. In 7 of 11 patients, the HP status of the stomach was also studied. Nasal and maxillary sinus tissues were studied using polymerase chain reaction, urease test, culture, and immunohistochemical analysis. Helicobacter pylori infection of nasal and maxillary sinus tissues was defined by at least two positive results of different tests. Three (16%) of 19 nasal and maxillary sinus specimens from two patients were shown to be HP-positive (positive by polymerase chain reaction and immunohistochemical analysis and weakly positive by the CLO test). In one of these two patients, HP infection of the stomach was confirmed. In the other, a positive findings on immunohistochemical analysis suggested HP infection of the stomach. Immunoreactive structures were seen by immunohistochemical analysis in the nasal, maxillary sinus, and gastric specimens of these two patients but were partially degraded. Helicobacter pylori may exist in the nasal and maxillary sinus tissue specimens of some patients with chronic sinusitis with gastric HP infection.

Microarray analysis of epithelial gene expression profiles during gastric Helicobacter pylori infection

Microarray analysis of epithelial gene expression profiles during gastric Helicobacter pylori infection

Metaplasia of the duodenum shows a Helicobacter pylori–correlated differentiation into gastric-type protein expression

The origin of gastric metaplasia of the duodenum (GMD) remains enigmatic. We studied expression of mucins and trefoil peptides in GMD to gain insight into its phenotype and origin. We examined duodenal tissue of 95 patients (0 to 83 years old, 26 with gastric Helicobacter pylori infection) for the presence of GMD. Expression was examined immunohistochemically of secretory mucins (MUC2, MUC5AC, MUC5B, and MUC6), trefoil peptides (TFF1, TFF2, and TFF3), and sucrase-isomaltase (SI). GMD, found in 37 patients, correlated positively to gastric H. pylori infection, age, and villus atrophy. MUC2 and TFF3, expressed in normal goblet cells, were absent from 100% and 87% of GMD, respectively. GMD ubiquitously expressed MUC5AC, whereas MUC5AC expression in adjacent goblet cells was closely correlated with the extent of GMD. TFF1, TFF2, and MUC6 were found in 84%, 92%, and 65% of GMD, respectively. MUC5B was absent from epithelium and GMD. SI, expressed by villus enterocytes, was absent from GMD. Brunner's glands ubiquitously expressed MUC5B, MUC6, and TFF2. GMD was characterized by the expression of gastric-type proteins MUC5AC, MUC6, TFF1, and TFF2 and the absence of intestinal markers MUC2, TFF3, and SI. In terms of the location of metaplastic cells, our results suggest that epithelial cells migrating toward villus tips switch to gastric-type secretory cells. Positive correlation with infection suggests an inductive role H. pylori in the development of GMD. HUM PATHOL 34:156-165. Copyright 2003, Elsevier Science (USA). All rights reserved.

Is Helicobacter pylori infection associated with chronic idiopathic urticaria?

BackgroundChronic idiopathic urticaria (CIU) is one of the most frequent skin diseases, however its causes remain unknown in the vast majority of cases. There is increasing evidence for systemic effects of gastric Helicobacter pylori infection, which may result in extra gastrointestinal disorders. Although CIU can result from several causes, a possible relationship between chronic urticaria and Helicobacter pylori has been recently suggested ObjectiveThe aim of this study is to determine the prevalence of Helicobacter pylori infection in a series of patients with CIU, and measure the effectiveness of eradication therapy on the skin disease MethodWe assess Helicobacter pylori infection by 13C urea breath test (UBT) in 21 CIU patients. Amoxicillin, clarithromycin, and omeprazole were given to infected patients for seven days. The results of therapy were assessed by urea breath test one month after therapy. Urticaria and gastrointestinal symptoms were assessed on enrolment and for six months after eradication ResultsPrevalence of Helicobacter pylori infection was of 71.4 % (15/21). There were no differences concerning age (31.83 vs. 33.82 years) and duration of symptoms (38.40 vs. 35.38 months) in patients with respectively positive and negative UBT. Helicobacter pylori eradication rate was of 80% (12/14). Three patients had clinical improvement with total resolution of urticaria starting immediately after eradication therapy, being able to completely withdrawn antihistamine and corticosteroids therapy without complaints. In relation to the rest of the patients, these three had smaller duration of urticaria disease (14.3 vs. 43.7 months; p = 0.038) and greater titters in the UBT results (42.39 vs. 25.81; p = 0.073) DiscussionAlthough some authors found convincing evidence of the involvement of Helicobacter pylori as one possible cause of chronic urticaria, our results have failed to confirm the existence of this etiological association. The most remarkable finding was that those patients who had clinical remission of disease were the ones with greater UBT titters suggesting a role for the amount of colonization by Hp in the pathogenesis of urticaria disease

Helicobacter pylori infection is associated with greater impairment of cytochrome P-450 liver metabolic activity in anti-HCV positive cirrhotic patients.

Helicobacter pylori gastric infection has been associated with various digestive and extradigestive diseases. In liver disease bacterial infections have been associated with impairment of cytochrome P-450 liver metabolic activity. Moreover, infection by Helicobacter spp. seems to be linked with the development of hepatocellular carcinoma (HCC) in mice. Our aims were to evaluate the influence of H. pylori infection on cytochrome P-450 liver metabolic activity as assessed by means of monoethylglycinexylidide (MEGX) test and to assess the prevalence of H. pylori infection in patients with HCC. Ninety-six hepatitis C virus (HCV) -positive cirrhotic patients, 36 of whom had HCC, were tested for H. pylori infection by means of anti-H. pylori IgG. Patients underwent the MEGX test. Characteristics of the patients were then analyzed on the basis of the presence of H. pylori infection. Seroprevalence of H. pylori infection was similar between cirrhotic patients without (68%) or with (63.8%) HCC. Mean MEGX values were significantly (P < 0.0001) lower in H. pylori infected patients (18.2 +/- 13.9 ng/ml) as compared to the noninfected ones (46.9 +/- 17.1 ng/ml), independently of Child-Pugh's classification. These differences persisted even after subdividing patients according to the presence of HCC. In conclusion, in anti-HCV positive cirrhotic patients H. pylori infection is associated to an impairment of cytochrome P-450 liver metabolic activity. Seroprevalence of H. pylori infection in HCC patients is similar to that observed in tumor-free cirrhotics.

The effect of colonisation by Helicobacter pylori in Praomys (Mastomys) natalensis on the incidence of carcinoids.

An animal model of experimental gastric Helicobacter pylori infection has been developed in the Z strain of Praomys (Mastomys) natalensis; this animal has been reported to develop gastric carcinoids and adenocarcinoma spontaneously. In the present study, male and female Mastomys were killed at 1, 2, 4, 8 and 16 weeks after H. pylori inoculation. Colonisation of H. pylori was maintained in the stomachs of all animals for up to 16 weeks. H. pylori were mainly found in the antrum. Lymphoid infiltration appeared in the antral lamina propria and submucosa in all male and female animals from 4 to 16 weeks after inoculation. On microscopic examination after immunostaining for H. pylori, the organisms were detected in the antral mucus layer of the gastric epithelium. Serum immunoglobulin G specific for H. pylori could be detected 2 weeks after inoculation in female and 4 weeks after inoculation in male Mastomys, and persisted throughout the 16-week study period. At 18 months after inoculation, H. pylori positive rates for male and female Mastomys were 15 of 21 and 7 of 27, respectively. Carcinoids developed in 27 of 100 inoculated and in 49 of 100 uninoculated male, and in 5 of 100 inoculated and in 21 of 100 uninoculated female animals at 18 months after inoculation. Adenocarcinoma developed in 1 of 100 male Mastomys in both the inoculated and uninoculated groups, but in none of the female animals in either the inoculated or uninoculated groups. These results indicate that antrum-predominant colonisation by H. pylori caused the decrease in incidence of carcinoid formation in Mastomys.

Helicobacter pylori induces apoptosis of rat gastric parietal cells.

Gastric Helicobacter pylori infection may lead to multifocal atrophic corpus gastritis associated with loss of epithelial cells as well as glandular structures. The current work investigated H. pylori effects on cell death of isolated, nontransformed rat parietal cells (PC). Highly enriched rat PC (>97%) were isolated from gastric mucosa and cultured in serum-free medium over 24 h. The cells were cocultured over 8 h with cytotoxin-associated immunodominant protein (cagA)(+)/vacuolating toxin (vacA)(+) or with cagA(-)/vacA(-) H. pylori laboratory strains and also with H. pylori mutants deleted in several genes of the cag pathogenicity island. Staphylococcus aureus or Campylobacter jejuni were used as controls. Apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and electron microscopy. Interleukin (IL)-8 and cytokine-induced neutrophil chemoattractant (CINC)-1 secretion was measured by ELISA. Activation of nuclear factor-kappaB (NF-kappaB) was studied in nuclear extracts of PC by electrophoretic mobility shift assay. Apoptosis of PC was induced in a concentration- and time-dependent manner by cagA(+)/vacA(+) H. pylori strains but not by cagA(-)/vacA(-) negative strains or by the cagE knockout mutant. S. aureus and C. jejuni had no effect. PC showed no IL-8 or CINC-1 secretion on exposure to cagA(+)/vacA(+) H. pylori. cagA(+)/vacA(+) strains induced activation of NF-kappaB complexes in nuclear extracts of PC, which were composed of p65 and p50 subunits. No significant stimulation of NF-kappaB activation was detected by incubation of PC with the cagE knockout mutant. Preincubation of PC with antisense but not missense oligodeoxynucleotides against the p65 subunit significantly reduced DNA binding to the kappaB recognition sequence. The p65 oligonucleotides as well as the proteasome inhibitor N-CBZ-isoleucin-glutamin-(o-t-butyl-)-alanin-leucin and the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine completely prevented PC apoptosis induced by cagA(+)/vacA(+) strains. In summary, cagE presence appears to be essential for H. pylori-induced apoptosis of gastric parietal cells, and this effect is dependent on the activation of NF-kappaB and production of nitric oxide.

Long-term clinical outcome of elderly patients with reflux esophagitis: a six-month to three-year follow-up study.

Although the prevalence of reflux esophagitis is known to increase with age, data on the long-term outcome of esophagitis in elderly patients are scarce. We sought to evaluate the clinical outcome of elderly patients with esophagitis 6 months to 3 years after diagnosis and to identify specific prognostic indicators of a poor outcome. This was a long-term (6 months to 3 years) follow-up study. Patients older than 65 years of age diagnosed as having reflux esophagitis healed after acute treatment (2 to 4 months) were included in the study. Clinical examinations and upper gastrointestinal endoscopy were performed every 6 months for the first year and annually thereafter. After healing, no therapy was prescribed; in the event of symptom recurrence, a maintenance therapy consisting either of H2 blockers or proton pump inhibitors (PPI) was prescribed. At baseline and during follow-up, the following clinical parameters were recorded: gender, age, the presence of symptoms (heartburn, acid regurgitation, epigastric/chest pain), type and dose of the maintenance therapy, nonsteroidal antiinflammatory drug use; gastric Helicobacter pylori infection, diagnosis of hiatal hernia, and/or Barrett's esophagus. The chi-square test, the Kaplan-Meier test, and Cox's proportional hazards regression analysis were used for statistical analyses. Included in the final analysis were 138 patients (M/F, 81/57; mean age, 79.7 years; range, 66-97). The numbers of patients in need of maintenance therapy were 47 of 69 (68.1%) after 6 months, 29 of 58 (50%) after 12 months, 17 of 39 (43.6%) after 24 months, and 12 of 26 (46.1%) after 36 months of follow-up. A significantly higher esophagitis relapse rate was found in patients not treated compared with subjects who were in maintenance therapy: 59% versus 8.5% (P <.0001) at 6 months, 65.5% versus 20.7% at 12 months (P <.002), 63.6% versus 11.7% at 24 months (P =.003), and 57.1% versus 8.3% at 36 months (P =.02). No significant difference in relapse rate was found in patients treated with H2 blockers versus PPIs (21.7% versus 10%). The Cox model demonstrated that no maintenance treatment (P =.00001), the presence of typical symptoms (P =.00001), the presence of hiatal hernia (P =.03), and a high severity grade of esophagitis at baseline (P =.009) were risk factors for relapse of esophagitis. In elderly subjects, esophagitis relapse occurs in a high percentage of cases, particularly in patients not treated with antisecretory drugs. The presence of typical symptoms, hiatal hernia, and a severe grade of esophagitis are risk factors for relapse. The most effective measure for minimizing the occurrence of relapse is a maintenance therapy with antisecretory drugs.

Changes of coronary risk factors after eradication of Helicobacter pylori infection.

Several epidemiological studies have shown a positive correlation between chronic gastric infection with Helicobacter pylori (HP) and coronary artery disease. A number of reports also claimed that there are strong relationships between HP infection and coronary risk factors. However, clinical studies concerning the changes of coronary risk factors after eradication of HP infection are few and contradictory. We conducted a prospective study aiming to compare sugar, lipid and fibrinolytic profiles before HP eradication with those after HP eradication. HP infection was confirmed by endoscope-based examinations and eradicated by a standard OAC (omeperazole-amoxicillin-clarithromycin) regimen. We measured and compared pre- and post-eradication blood sugar, lipid profiles (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride) and fibrinolytic profiles (tissue-plasminogen activator, plasminogen activator inhibitor-1, fibrinogen, and D-dimer levels). Forty-eight patients (male:female, 25:23; mean age, 50.8 +/- 11.3 years) with gastric HP infection were enrolled in this study. Although HP infection was confirmed to have been successfully eradicated, no significant changes of blood fasting sugar, lipids or fibrinolytic profiles were found in patients after treatment. Coronary risk factors including fasting sugar, lipid and fibrinolytic profiles were not changed after successful HP eradication treatment. The relationship between HP infection and coronary artery disease needs to be clarified.

Helicobacter pylori-related iron deficiency anemia: a review.

Several clinical reports have demonstrated that Helicobacter pylori gastric infection has emerged as a new cause of refractory iron deficiency anemia, unresponsive to iron therapy, and not attributable to usual causes such as intestinal losses or poor intake, malabsorption or diversion of iron in the reticulo-endothelial system. Although the interaction between infection and iron metabolism is now well consolidated, our understanding of the pathogenetic mechanism underlying the anemia is still wanting. Microbiological and ferrokinetic studies seem to suggest that Helicobacter pylori infected antrum could act as a sequestering focus for serum iron by means of outer membrane receptors of the bacterium, that in vitro are able to capture and utilize for growth iron from human lactoferrin. The proposed hypothesis does not answer why this complication is such a rare disease outcome in a common human infection but it may be used as a template for further controlled studies to determine the mechanisms of this atypical, medically important putative sequelae of H. pylori infection.

Impairment of cytochrome P-450-dependent liver activity in cirrhotic patients with Helicobacter pylori infection.

Helicobacter pylori gastric infection has been associated with various digestive and extra-digestive diseases. The systemic influence of gastric H. pylori infection seems to be mediated by the release of various cytokines. In liver disease, bacterial infections have been associated with the impairment of liver metabolic function. To evaluate the influence of H. pylori infection on liver function as assessed by means of the monoethylglycinexylidide test, which depends upon liver blood flow and cytochrome P-450 activity, and the 13C-galactose breath test, which depends on cytosolic enzymatic activity and is correlated with hepatic functional mass. Moreover, to evaluate whether H. pylori-associated modifications of liver function may be related to tumour necrosis factor-alpha serum levels. Thirty-five patients with liver cirrhosis of various aetiologies, who underwent monoethylglycinexylidide and 13C-galactose breath tests, were retrospectively evaluated for H. pylori infection by means of anti-H. pylori immunoglobulin G. The main clinical, biochemical and functional characteristics of the patients as well as their tumour necrosis factor-alpha serum levels were then analysed on the basis of the presence of H. pylori infection. Twenty-one patients tested positive for H. pylori infection (60%), and 11 tested negative (31.4%). No clinical or biochemical differences were observed between H. pylori-infected and non-infected patients. H. pylori infection showed no difference in distribution according to Child-Pugh classes (A, 55%; B and C, 67%). The monoethylglycinexylidide test results were significantly lower at each sampling time in H. pylori-positive patients compared to H. pylori-negative patients (MEGX15, P=0.027; MEGX30, P=0.014; MEGX60, P=0.028), while 13C-galactose breath test showed no significant differences considering both cumulative percentage dose and percentage dose/h. The median tumour necrosis factor-alpha serum levels were no different between H. pylori-positive (16.1 pg/mL, 95% confidence interval, 8.7-28.7) and H. pylori-negative (12.3 pg/mL, 95% confidence interval, 8.7-23.4) patients. In cirrhotic patients, H. pylori infection seems to selectively affect cytochrome P-450 liver activity, while hepatic functional mass does not seem to be impaired. Tumour necrosis factor-alpha does not seem to be the mediator of this impairment. Further studies are needed to evaluate the impact of H. pylori eradication on parameters of liver function.

Relationship between gastric helicobacter pylori infection and iron deficiency anemia in subjects with cellac disease

Relationship between gastric helicobacter pylori infection and iron deficiency anemia in subjects with cellac disease

Relationship between gastric helicobacter pylori infection and iron deficiency anemia in subjects with cellac disease

Relationship between gastric helicobacter pylori infection and iron deficiency anemia in subjects with cellac disease

7235 Endoscopic ultrasonography in gastric malt and gastritis.

A close association between gastric Helicobacter pylori infection and MALT lymphoma of the stomach has been described and H. pylorieradication can result in histological regression of the gastric lymphoma in most cases. Recent studies suggest that EUS may provide informations useful to predict the lymphoma response to antibiotic therapy: deeper the gastric wall infiltration lower the response rate. AIMS:to compare the gastric wall structure in early gastric MALT lymphoma and chronic H. pylori -associated gastritis. METHODS:10 pts. with low grade gastric MALT lymphoma occasionally diagnosed by biopsies taken in the presence of an endoscopic pattern of gastritis and 10 pts. with H. pylori -associated gastritis were evaluated. Both groups have negative endoscopic appearance (no severe lesions except erythema or aspect of mild atrophy). EUS was performed with a radial (Olympus GF-UM 20 7.5-12 MHz) echoendoscope with the water-filled technique. Thickness of the entire gastric wall and of the mucosa and submucosa layers was measured in antrum, corpus and fundus. RESULTS:structure of the wall with respect to echogenicity, layering and thickness is similar in the two groups (i.e. low-grade MALT lymphoma and gastritis). CONCLUSION:Patients with histological diagnosis of lowgrade gastric lymphoma but no evidence of any endoscopic lesions showed an EUS pattern with normal frequencies (7.5-12 MHz) superimposable to the one observed in H. pylori -associated gastritis. This subset of MALT lymphoma patients may have an early disease with the highest chances of prolonged remission with antibiotic therapy.

Usefulness of 13C-Urea Breath Test in the Diagnosis of Gastric Helicobacter Pylori Infection

Helicobacter pylori chronically infects half of the human population and is associated with gastritis, peptic ulcer and gastric cancer. (13)C-urea breath test (UBT) is the main in vivo tool for the diagnosis of H. pylori infection. In this study, the safety and the accuracy of UBT were evaluated. A group of 492 dyspeptic patients was studied by UBT, the results were expressed as the difference over baseline at 30 min (DOB30). All patients were evaluated for systemic, gastrointestinal or allergic-type adverse reactions after ingestion of 75 mg (13)C-urea and citric acid in aqueous solution. The first 256 patients enrolled also underwent endoscopy and gastric biopsy. Patients positive on histology were considered infected. UBT was well tolerated and none of the 492 patients had any systemic or allergic-type adverse reaction. Among the 256 patients studied with histology, 116 were H. pylori positive on biopsies. Using 4 %o as cut-off value for DOB30,115 out of the 256 patients were positive on UBT, with only 2 false positive and 3 false negative. With this threshold, the sensitivity, specificity, and accuracy of the UBT were 97.4%, 98.5%, and 98.0%, respectively. (13)C-UBT has proven to be a safe and simple, yet accurate, test for the non-invasive diagnosis and monitoring of H. pylori infection.