Taking the low (stretch) road

Helicobacter pylori infection can be detected by several invasive tests based on gastroscopy and by noninvasive methods such as serologic assays. Noninvasive tests can be used not only in addition to invasive tests but also by themselves to screen for H. pylori infection in patients who are not in urgent need of endoscopy. Lately, rapid qualitative serologic tests have been developed. In the present study, the accuracy of a novel rapid whole-blood test, Pyloriset Screen, detecting immunoglobulin G (IgG) and IgA antibodies against H. pylori was evaluated. A total of 207 consecutive adult outpatients referred for upper endoscopy were enrolled. Gastric biopsy specimens were taken from the antrum and corpus for histologic examination and rapid urease testing. Cultures were available for 113 patients. Serum samples collected from all patients were tested for H. pylori antibodies by two enzyme immunoassays (EIAs) (Pyloriset EIA and an in-house EIA), a rapid latex agglutination test (Pyloriset Dry), and Pyloriset Screen. Patients were considered H. pylori positive if helicobacters were seen on histologic examination (77 patients) or, if in combination with histologically verified (although helicobacter-negative) gastritis, their IgG antibody titers were elevated in the two EIAs (five patients). The Pyloriset Screen test had a sensitivity of 95%, a specificity of 94%, a positive predictive value of 91%, and a negative predictive value of 97%. Among 63 patients under the age of 45 years, the Pyloriset Screen test did not miss a single H. pylori diagnosis, and only 1 patient had a false-positive result. Pyloriset Screen could be used reliably to screen for H. pylori infection.     

The Trp64Arg mutation of the beta3-adrenergic receptor is associated with hyperglycemia and current body mass index in Jamaican women

Helicobacter pylori is a major etiologic agent in gastroduodenal disorders. In this study, immunoglobulin A (IgA) antibodies to H. pylori antigens were evaluated in serum and gastric juice specimens obtained from patients with gastritis or peptic ulcers by utilizing antibody capture enzyme-linked immunosorbent assays (ACELISAs). Urease alpha subunit (UA), urease beta subunit (UB), the 66-kDa heat shock protein (HSP), and the 25-kDa protein (25K) were used as antigens for the ACELISAs. The antibody titers of the ACELISAs reflect the ratio of H. pylori-specific IgA to total IgA. The ratio is stable, although the antibody concentration fluctuates in gastric juice. By using ACELISAs it was possible to evaluate quantitatively not only serum IgA antibodies but also gastric juice secretory IgA (S-IgA) antibodies. In both serum IgA and gastric juice S-IgA ACELISAs, the titers of antibody to HSP and 25K were remarkably correlated with the histologic grade of gastritis, whereas those to UA and UB were not strongly correlated with histologic grade. Thus, it is useful for estimating the histologic grade of gastritis to quantify serum IgA and gastric juice S-IgA antibodies to HSP and 25K.     

Technical report: Cystic air spaces in the lung: change in size on expiratory high-resolution CT in 23 patients

BACKGROUND: Urticaria is a common disease that is always a challenge to the dermatologist due to its evasive etiology. PATIENTS AND METHODS: One hundred and seven chronic urticaria patients were studied. Routine laboratory investigations were performed and Helicobacter pylori (H. pylori) immunoglobulin G (IgG) antibody determinations, autoimmune reactivity, infections, allergies, and hyperreactivities were investigated. RESULTS: Pathologic findings were seen in 92 patients. Concomitant diseases suggesting autoimmune reactivity were detected in nine patients and, in 16 patients, infections including maxillary sinusitis, streptococcal tonsillitis, and tooth infection were found. Elevated total IgE level was detected in 37 out of 75 patients and positive skin prick test results in 47 out of 91 patients. Fifty-five patients had a history of recent dyspeptic symptoms. A diagnosis of adult celiac disease was made in two patients and, additionally, IgA antigliadin antibodies were seen in four patients. H. pylori IgG antibodies were found in 40 out of 107 patients. Active gastritis was verified by esophagogastroduodenoscopy in 30 out of 32 patients with positive Helicobacter staining in 24 samples. An elevated IgE level was detected in 64% of H. pylori-positive and in 39% of H. pylori-negative patients. CONCLUSIONS: In this study, several findings suggesting aberrant immunologic activation were detected in chronic urticaria patients. Inflammation in the gastrointestinal tract, e.g. caused by H. pylori infection, may have an important role in the etiology of chronic urticaria.     

Diagnosis of otitis media with effusion by acoustic reflectometry

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.     

Relationship between Helicobacter pylori infection, histological gastritis, and functional dyspepsia

BACKGROUND/AIMS: It is still controversial as to whether or not Helicobacter pylori (H. pylori) infection, histological gastritis, and functional dyspepsia (FD) are intercorrelated. We prospectively evaluated patients with functional dyspepsia in an attempt to clarify this issue. METHODOLOGY: Eighty-eight consecutive patients with functional dyspepsia (age range: 18-84 years) who did not show disease(s) other than gastritis were investigated. In a questionnaire they were asked to report the presence or absence of 8 upper gastrointestinal (GI) symptoms and to score them from 0 (absence) to 3 (severe), whereupon a sum score was calculated. Forty age-matched subjects with a sum score of <3 served as controls. Biopsy specimens for histology, bacterial culture, and rapid urease test were taken. A C13-urease breath test was also performed in 122 subjects. RESULTS: H. pylori infection was present in 43% of patients with functional dyspepsia and 35% of control subjects (not significant (n.s.)). None of the symptoms were correlated with H. pylori infection. The median symptom sum score was 8.5 in H. pylori-positive and 9.5 in H. pylori-negative patients with functional dyspepsia (n.s.). Histological gastritis was strongly associated with H. pylori infection but was not correlated with any of the symptoms. CONCLUSIONS: In a prospective population of patients with functional dyspepsia, H. pylori infection or gastritis are not associated with specific or severe symptoms. Our data imply that H. pylori gastritis is not an important condition in the pathogenesis of dyspeptic complaints.     

Temporal stability of antisocial personality disorder: blind follow-up study at 8 years

We studied the relation between Helicobacter pylori and residual gastritis in 28 patients with gastric cancer on whom distal partial gastrectomy with Billroth I reconstruction was performed over a 13-month period. They were subjected to serologic testing along with endoscopic and histologic examinations before operation and at 3, 6, and 12 months after operation. Anti-H. pylori immunoglobulin G (IgG) and serum gastrin levels were measured by serologic tests. The presence or absence of gastritis was determined endoscopically, and gastric mucosal hexosamine levels were determined. Gastritis was measured quantitatively by histologic examination in specimens taken from the gastric mucosa using Rauws' score. After the initial histologic evaluation we divided the H. pylori-positive patients into two groups: those with a Rauws' score of 0 to 3 ("weak" gastritis group), and those with a Rauws' score of 4 to 10 ("strong" gastritis group), allowing us to compare the results of our three postoperative histologic examinations of the two groups for possible significant differences. Our endoscopic examinations showed gastric mucosal inflammatory changes in both H. pylori-positive and H. pylori-negative patients at 3, 6, and 12 months after operation, but there was no significant difference between these two groups at any point. During the histologic examinations, however, anti-H. pylori IgG assay had become negative in several patients in the "weak" gastritis group at 3 months after operation and was found to have become negative in 78% of all patients in that group 12 months after operation. In contrast, in the "strong" gastritis group H. pylori infection was still evident in the patients 12 months after operation, suggesting that "strong" histologic gastritis may have some connection to H. pylori infection, whereas "weak" histologic gastritis has no such connection. The gastric mucosal hexosamine level was higher in the "weak" gastritis group than in the "strong" gastritis group both before operation and at 6 and 12 months, indicating some relation between gastric inflammatory changes and hexosamine levels in gastric mucosa. It further suggested the possibility that H. pylori plays a role in destroying gastric mucosa by depleting mucin, thus acting as one (though not the only) cause of residual gastritis after distal partial gastrectomy. In conclusion, we found evidence that there is a relation between residual gastritis and H. pylori infection, but H. pylori is not the sole cause of residual gastritis after gastric surgery. A causal relation is difficult to detect by simple analysis of histologic findings or by endoscopic observation or clinical symptoms alone.     

Salivary-specific immunoglobulin G in the diagnosis of Helicobacter pylori infection in dyspeptic patients

OBJECTIVES: Helicobacter pylori infection is arguably the most common chronic bacterial infection in humans. The high prevalence and the association with peptic ulceration and gastric cancer indicate that simple, noninvasive methods for diagnosis of the infection are needed. In this study, the accuracy of salivary diagnosis for H. pylori infection was assessed. METHODS: Saliva and serum samples of 152 dyspeptic patients were tested for H. pylori IgG and IgA by an in-house ELISA. All patients underwent gastroscopy with biopsy. RESULTS: One hundred thirty-one patients (86%) were found to be H. pylori positive on histology. Duodenal ulcer was found in 67 patients; 85 had no macroscopic lesion. Salivary and serum H. pylori IgG as well as serum H. pylori IgA titers were significantly higher in H. pylori-positive than in H. pylori-negative patients. The sensitivity and specificity of salivary H. pylori IgG were 82% and 71%, respectively; the positive and negative predictive values were 95% and 40%, respectively; and the accuracy 81%. The corresponding figures for serum H. pylori IgG were 97% and 91%; 98% and 83%; and 96%. Those for serum H. pylori IgA were 80% and 52%; 91% and 30%; and 76%. The sensitivity of salivary H. pylori IgG in detecting duodenal ulcer was 83% (56/67) that of serum H. pylori IgG was 97% (65/67) (odds ratio = 0.15; confidence interval = 0.02-0.8; p = 0.02). CONCLUSIONS: Salivary H. pylori IgG was a fairly sensitive and accurate indicator of gastric H. pylori colonization, with a high positive predictive value in our population. Data, however, suggest that salivary H. pylori IgG measurements do not compare favorably with serology.     

Identification of cDNAS encoding plastid-targeted glutathione peroxidase

OBJECTIVE: Helicobacter pylori (H. pylori) is a major factor in determining the risk for development of gastric adenocarcinoma through the intermediate steps of atrophic gastritis and intestinal metaplasia. Because H. pylori infection is highly prevalent in asymptomatic populations and only a few people develop cancer, additional factors may influence the risk for development of cancer, once infection is established. Some factors may pertain to differences among bacterial strains. Because infection by H. pylori strains possessing cagA (cytotoxin-associated gene A), a gene encoding a high-molecular-weight immunodominant antigen (CagA), is associated with enhanced induction of gastritis, the aim of our study was to evaluate potential differences in the prevalence and intensity of atrophy and intestinal metaplasia between CagA-positive and CagA-negative H. pylori-infected patients. METHODS: Eighty H. pylori-infected patients among 120 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were studied. Six bioptic specimens were taken from the gastric antrum: five for histological examination, and one for urease test. The H. pylori status was determined by histology, CLO test, and serology (in a standardized ELISA) for serum IgG and IgA directed to H. pylori. The CagA status was determined by Western blotting to detect serum IgG antibodies to CagA. Gastritis was classified according to the Sydney System. A score from 0 to 3 was assigned to each of the following morphological variables: atrophy, intestinal metaplasia, and mononuclear and neutrophilic cell infiltration. The association between CagA status and histological features was assessed by means of the chi2 test for trend. RESULTS: Among the 80 H. pylori-infected patients 53 (66%) were CagA seropositive and 27 (34%) were CagA seronegative. The mean age of the two groups was similar. CagA-positive patients had significantly higher scores for atrophy (p = 0.006), intestinal metaplasia (p = 0.01), and mononuclear (p < 0.001) and polymorphonuclear (p = 0.002) cell infiltration than did CagA-negative patients. No differences in contrast, were found for H. pylori density. CONCLUSION: Infection with CagA-positive H. pylori strains is associated with an increased prevalence and intensity of antral atrophy and intestinal metaplasia, in addition to higher degrees of gastritis. Our results seem to suggest that the CagA status could be a helpful parameter to define a subgroup of H. pylori-infected patients at increased risk of developing gastric adenocarcinoma.     

Urinary procoagulant activity and tissue factor levels in patients with diabetes mellitus

BACKGROUND: Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis. PATIENTS AND METHODS: A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined. RESULTS: Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia. CONCLUSION: Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.     

Healing of chronic antral gastritis: effect of sucralfate and colloidal bismuth subcitrate

BACKGROUND: Colloidal bismuth subcitrate (CBS) causes endoscopic and histological improvement in gastritis and eradication of Helicobacter pylori in patients with non-ulcer dyspepsia (NUD). The effect of sucralfate, a cytoprotective drug, on endoscopic and histologic gastritis and H pylori clearance is not clear. We studied the effect of CBS and sucralfate on these features in patients with NUD. METHODS: Sixty three patients with NUD and H pylori infection were randomized to receive one of the following for four weeks: (i) CBS (240 mg twice daily) (Group 1); (ii) placebo I, similar in size, color and shape to CBS (Group 2); (iii) sucralfate (2.0 g twice daily) (Group 3) and (iv) placebo II, similar to sucralfate (Group 4). Symptoms, endoscopic and histological findings and H pylori status were assessed before and after treatment. RESULTS: Similar symptomatic improvement was observed with each treatment, indicating a placebo effect. Significant endoscopic and histological improvement was observed with CBS only. CBS was better than sucralfate in inducing endoscopic and histological improvement. Clearance rate of H pylori was 46.6% with CBS, 16.6% with its placebo, 33.3% with sucralfate and 13.3% with its placebo. CONCLUSION: CBS is more effective than sucralfate in inducing endoscopic and histologic healing of H pylori-related gastritis among NUD patients.     

Association of Helicobacter pylori infection with elevated serum lipids

Helicobacter pylori causes a chronic gastric infection, which has been associated with coronary heart disease. To evaluate the mechanisms of this association, we studied whether the infection affects serum lipid levels as previously shown in acute infections. We analysed the serum samples of 880 males who participated in a reindeer herders' health survey in Northern Finland in 1989. H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and triglyceride, total cholesterol and high-density lipoprotein cholesterol concentrations by routine enzymatic methods. A total of 52% of the subjects were positive for both H. pylori specific IgG and IgA and 31% were antibody-negative. The serum triglyceride and total cholesterol concentrations were significantly higher in the males with positive IgG and IgA antibody titres for H. pylori than in the males with no signs of infection (1.20 vs. 1.03 mmol/l, P < 0.001 and 6.59 vs. 6.11 mmol/l, P < 0.001, respectively). The associations remained statistically significant in non-smokers after the adjustment for age, body mass index (BMI) and social class. The finding supports the hypothesis that chronic infections may modify the serum lipid profile in a way that increases the risk of atherosclerosis.     

Helicobacter pylori and gastroduodenal lesions in 547 symptomatic young adults

OBJECTIVES: Helicobacter pylori (H. pylori) is involved in the pathogenesis of gastric inflammatory disorders. Both antral chronic gastritis and H. pylori infection prevalence increase with age. The aim of the study was to assess the prevalence of H. pylori infection in young adults and to study the relationship between endoscopical and histological features and H. pylori infection. METHODS: The study concerned 547 young patients (age: 18-25 years), undergoing endoscopy for upper gastrointestinal symptoms. The severity and the activity of chronic gastritis was graded by histological examination of antral biopsies. The diagnosis of H. pylori infection was based on histology and culture or urease test. RESULTS: Fifty-three percent of the patients had a normal endoscopy; 44 ulcers were found: 34 duodenal ulcers and 10 gastric ulcers. H. pylori infection was detected in 34% of cases. The prevalence of H. pylori infection was 29.8% in non-ulcer patients, 50% in gastric ulcers and 91% in duodenal ulcers (P < 0.01). Duodenal ulcer, aspect of antral mosaic mucosa and nodular gastritis, were closely related to the presence of H. pylori. There was a significant relationship between H. pylori infection and both the severity (P < 0.01) and the activity (P < 0.01) of the antral chronic gastritis. The prevalence of follicular gastritis was 22% : it was present in 60% of H. pylori positive patients and 2.4% of H. pylori negative patients. H. pylori infection was more frequent in patients from Africa than in Europeans (P < 0.01). There was no significant association between H. pylori infection and different types of diets, settlements (rural vs urban) or symptoms. CONCLUSION: These results show that in the young population studied, duodenal ulcer, nodular gastritis, antral mosaic mucosa, active chronic gastric and follicular gastritis are closely related to H. pylori infection. They suggest that in the subgroup of non ulcer symptomatic patients, H. pylori prevalence is higher than in the general population.     

Positive association between Helicobacter pylori infection and food allergy in children

BACKGROUND: In children Helicobacter pylori has been involved as a pathogenetic factor in gastritis and duodenal ulcer and as a cofactor in protein-losing enteropathy, chronic diarrhoea, short stature, and gastritis lymphoproliferative disease. A subset of an H. pylori strain possesses an antigen, CagA, as a virulence factor. In the present study we determined anti-H. pylori IgG and anti-CagA IgG titres in children with food allergy. METHODS: Ninety paediatric patients were studied: 30 with food allergy, 30 with atopic asthma, and 30 with inflammatory bowel disease. Anti-H. pylori IgG and anti-CagA IgG were determined in all children by means of a commercial enzyme immunoassay (ELISA). RESULTS: The anti-H. pylori IgG titre was significantly higher in allergic patients than in the other two groups. The anti-CagA IgG titre did not differ significantly between the patients. CONCLUSIONS: These findings show a positive association between H. pylori infection and food allergy in children. We hypothesize that virulence factors other than CagA may be involved in the pathogenesis of H. pylori infection in paediatric patients with food allergy.     

Skull base aspergillosis granuloma originating from the sphenoid sinus: a case report

To clarify the prevalence of Helicobacter pylori infection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody to H pylori was determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody to H pylori in the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (P < 0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, P < 0.001). H pylori colonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25 H pylori seropositive patients who underwent endoscopy and biopsy. Results suggest that H pylori infection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis and H pylori infection are needed.     

Proposed recommendations for research on biochemical markers for problematic drinking

Successful eradication of Helicobacter pylori infection in children has required long treatment regimens that may result in noncompliance with failure to eradicate this organism. Despite full compliance with shorter therapeutic regimens, such as amoxycillin and omeprazole for 2 wk, the H. pylori eradication rate is poor in children. OBJECTIVES: The aim of this study was to evaluate the efficacy of, and compliance with, a 2-wk treatment with metronidazole, omeprazole, and clarithromycin in eradicating H. pylori disease in children. METHODS: Over a 15-month period, children diagnosed to be H. pylori positive by Steiner's stain of gastric antral biopsy specimens were treated with metronidazole, omeprazole, and clarithromycin. Follow-up upper GI endoscopy was performed 6-8 wk after completion of therapy. RESULTS: Of 15 patients with H. pylori-positive antral gastritis, 11 had duodenal ulcer disease; three patients with severe abdominal pain and one with vomiting had H. pylori gastritis only. H. pylori eradication was seen in 11 of 11 (100%) patients with duodenal ulcer disease and in three of four (75%) with gastritis only; the overall success rate was 93%. Duodenal ulcer disease healed when H. pylori was eradicated in all but one patient, who at presentation had a penetrating ulcer with a duodenobiliary fistula. Fourteen of 15 patients (93%) were fully compliant, and no adverse reactions were reported. CONCLUSIONS: Two weeks of therapy with metronidazole, omeprazole, and clarithromycin is effective H. pylori therapy in children. It is well tolerated, and full compliance can be achieved.     

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.     

A review of esthetic alternatives for the restoration of anterior teeth

Helicobacter pylori infection is an important cause of peptic ulcer disease and chronic gastritis. Infection with this bacterium stimulates the production of immunoglobulin (Ig) G antibody. Salivary IgG antibody tests to detect H pylori infection offer a convenient and noninvasive method of diagnosis. To evaluate an IgG salivary antibody kit, saliva was collected from 157 out-patients with dyspepsia referred for endoscopy to a tertiary centre. A salivary IgG ELISA antibody assay was performed using the Helisal Helicobacter pylori (IgG) assay kit, and at least four gastric biopsies were obtained. H pylori infection was confirmed by demonstration of the organism on Warthin-Starry silver stain (sensitivity 85%, specificity 55%). The prevalence of infection with H pylori was 30%. When the analysis was redone, excluding those treated with eradication therapy, the results were similar (sensitivity 86%, specificity 58%). The positive predictive value of the assay was 45% and the negative predictive value was 90%. Despite the ease of sampling, the assay used has limited diagnostic utility, lacking the predictive value to indicate which patients referred with dyspeptic symptoms to a tertiary care setting are infected with H pylori.     

Cloning, genomic structure, and expression of mouse ring finger protein gene Znf179

OBJECTIVE: H. pylori causes chronic gastritis, which may progress to peptic ulcer, gastric atrophy, or gastric cancer. However, little is known about the role of H. pylori infection in reflux esophagitis and the relationship between reflux esophagitis and atrophic gastritis needs to be clarified. We sought to identify the possible interrelationships among Helicobacter pylori infection, reflux esophagitis, and atrophic gastritis, to signal areas in which researchers should consider focusing their attention. METHODS: A broad-based Medline search was performed to identify all related publications addressing H. pylori infection, atrophic gastritis, gastroesophageal reflux disease (GERD), secretion of gastric acid, and gastric motility published between 1966 and July 1997. RESULTS: Whereas some studies have shown no significant association between H. pylori infection and reflux esophagitis, others have observed that the prevalence of H. pylori infection was lower in patients with GERD, implying a protective role. Eradication of H. pylori leads to occurrence of reflux esophagitis in some cases, but the mechanisms inducing posteradication reflux esophagitis are unknown. H. pylori infection may lead to atrophic gastritis (and hence hypochlorhydia) through both bacterial and host factors, although gastric atrophy and subsequent intestinal metaplasia are hostile to H. pylori because of hypochlorhydria. Although it has been reported that long-term proton pump inhibitor therapy for refractory reflux esophagitis may induce or enhance the development of gastric atrophy in H. pylori-infected patients, this relationship has been disputed. CONCLUSIONS: H. pylori infection may be negatively associated with reflux esophagitis, but this requires confirmation. Research then needs to focus on whether this is explained through motility- or acid-related mechanisms. The potential costs of maintenance antireflux therapy may need to be taken into account when evaluating the cost effectiveness of anti-H. pylori therapy.     

Urease-specific monoclonal antibodies prevent Helicobacter felis infection in mice

Experiments were performed to determine the antigenic specificity of a monoclonal antibody (immunoglobulin A [IgA] 71) previously demonstrated to neutralize the ability of Helicobacter felis to colonize mice. Immunoprecipitation of radiolabeled H. felis outer membrane proteins with IgA 71 revealed specificity for a 62-kDa protein. Another of our monoclonal antibodies, IgG 40, precipitated a protein of similar molecular weight. IgA 71 but not IgG 40 also precipitated purified recombinant H. pylori urease. The antigenic specificity of both antibodies was confirmed to be urease by the ability of each to select Escherichia coli clones expressing the H. felis urease genes. The two antibodies were shown to bind nonoverlapping epitopes in a competition enzyme-linked immunosorbent assay. Both IgA 71 and IgG 40 could effectively neutralize H. felis infectivity by incubating the bacteria with the antibodies prior to oral administration to naive mice. The mechanism of protection does not appear to be inhibition of urease activity, as IgA 71 does not inhibit the conversion of urea to ammonia by H. pylori urease in vitro. These results support a protective role for the secretory humoral immune response in Helicobacter immunity and provide further evidence that the urease enzyme can serve as a protective antigen.     

Helicobacter pylori may cause "reflux" gastritis after gastrectomy

Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.