Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Helicobacter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed1994

Are tryptase and cathepsin D related to Helicobacter pylori infection and mucosal gastrin in peptic ulcer?

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others, Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method. Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated with Helicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa to Helicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.

Adult↗
PubMed2000

Low seroprevalence of Helicobacter pylori infection in patients with stress ulcer bleeding--a prospective evaluation of patients on a cardiosurgical intensive care unit.

OBJECTIVE: The pathogenesis of stress ulceration in seriously ill patients is uncertain and the pathogenic role of Helicobacter pylori infection is unknown. We therefore assessed the seroprevalence of patients of a cardiosurgical intensive care unit (ICU) with clinically important stress ulcer bleeding. We compared this prevalence with a control group matched for this kind of surgical intervention, missing history of peptic ulcer disease, age and gender. DESIGN: Prospective survey. SETTING: Cardiosurgical ICU in a university teaching hospital. PATIENTS AND PARTICIPANTS: Two thousand five hundred seventy cardiosurgical patients with intravenous ranitidine stress ulcer prophylaxis were screened for clinically important stress ulcer bleeding. Helicobacter pylori seropositivity was measured in all patients with a clinically important bleeding and in a control group of 245 consecutive cardiosurgical patients, matched for the kind of cardiosurgical intervention, age and gender. RESULTS: In 56 of 2,570 (2.1%) patients signs of clinically important bleeding were seen. Endoscopical examination revealed stress ulcer bleeding in 42 cases. The incidence of stress ulcer bleeding was 1.6%. The seropositivity of the group with ulcer bleeding was 45.2 % whereas 62.4 % of the patients in the control group were Helicobacter pylori positive (p = 0.08). CONCLUSIONS: Our results suggest that the Helicobacter pylori infection does not play a pathogenic role in stress ulcer bleeding. Prophylactic cure of Helicobacter pylori can not be recommended in this setting.

Adult↗
PubMed1999

Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings.

The role of Helicobacter pylori infection in the development and exacerbation of reflux esophagitis was investigated. The prevalence of Helicobacter pylori infection, the severity of atrophic gastritis, and esophageal motility (determined by esophageal manometry by an infusion catheter method) were assessed in patients with mild (n = 46) and severe (n = 27) reflux esophagitis and subjects without reflux (n = 28). Compared with the prevalence of Helicobacter pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups (60.7%, 47.8%, and 14.8%, respectively) was significantly (P < 0.05) lower. Atrophic gastritis was milder in both reflux groups than in the non-reflux group. The degree of gastritis was also milder in the severe reflux group than in the mild reflux group. The esophageal sphincter pressure was significantly (P < 0.05) lower in the reflux groups than in the non-reflux group, and the amplitude of primary peristalsis was significantly (P < 0.05) lower in the severe reflux group than in the non-reflux group. There were no significant differences between reflux patients with and without Helicobacter pylori infection in the parameters of esophageal manometry. These data imply that a low prevalence of Helicobacter pylori infection may result in a milder grade of atrophic gastritis, and consequently, exacerbate reflux esophagitis.

Analysis of Variance↗
PubMed1999

Evaluation of a new serologic test for diagnosis of Helicobacter pylori infection in children.

A new semiquantitative enzyme immunoassay (Platelia Helicobacter pylori; Sanofi Diagnostics Pasteur, France) was evaluated and compared with two other serological assays (Gap-test IgG; Bio-Rad, France; and Cobas Core; Roche, Switzerland) for the diagnosis of Helicobacter pylori infection in children. The three tests were compared with the examination of biopsy samples obtained from 160 dyspeptic subjects (mean age, 9 +/- 4.7 years). Discrepant results were studied using an immunoblot technique. The response obtained for the Platelia assay in children was significantly lower than that obtained in a previously described population of 92 adults (Helicobacter pylori-negative mean ratios, 0.376 vs. 0.504, P<0.000783; Helicobacter pylori-positive mean ratios, 1.95 vs. 2.67, P<0.000003). Thus, the optimal cut-off for children (0.80) was lower than the one recommended for adults (1.10). According to the Receiver Operating Characteristic (ROC) curve analysis and to the Wilcoxon value, the Platelia and Cobas Core assays showed the highest discriminatory properties (Wilcoxon value, 0.94 for both) compared with the Gap-test IgG (Wilcoxon value, 0.91). When the newly established cut-off value (0.80) was used, the performance of Platelia was equivalent to that of Cobas Core (sensitivity: 94.4% for each; respective specificities, 86.8% and 90.6%). The Gap-test IgG had a lower sensitivity (maximum, 79%) and a higher specificity (maximum, 95.3%), but there were difficulties in interpretation because its grey zone encompassed 12% of the sera. In conclusion, the results showed good performance of the Platelia Helicobacter pylori assay and confirmed the merit of a specific cut-off value for use of this test in children.

Adult↗
PubMed2000

Infection with Helicobacter pylori and leukocyte response in patients with myocardial infarction.

To test whether Helicobacter pylori may contribute to the inflammatory response following myocardial infarction, the levels of IgG antibodies to Helicobacter pylori and some parameters of leukocyte activity were measured in 63 patients and 61 comparable controls. Helicobacter pylori-positive patients showed a significantly higher expression of the adhesion molecule LFA-1 on neutrophils than Helicobacter pylori-negative patients (433+/-29.0 vs. 398.8+/-38.9 mean fluorescence channels; P<0.0001), whereas no significant difference for any parameters tested was found in control subjects. These data suggest a role of Helicobacter pylori in inducing a leukocyte response following myocardial infarction.

Aged↗
PubMed2001

Serologic diagnosis of Helicobacter pylori infection in outpatients aged 45 years or less.

The diagnostic accuracy of serological tests for Helicobacter pylori was studied in 145 consecutive outpatients aged 45 years or less referred for gastroscopy. Helicobacter pylori infection can be detected by serological tests, including rapid whole-blood tests. The low prevalence of the disease in young people may have a negative effect on the positive predictive value of a test. In this study, the presence of Helicobacter pylori was assessed by a biopsy urease test and histological examination, and by several serological tests: a rapid whole-blood test on fingerstick blood, a latex agglutination serum test, a commercial enzyme immunoassay (EIA) test, and an in-house EIA for detection of antibodies of both the IgG and IgA classes. Helicobacter pylori infection was diagnosed with invasive tests in 21 (14.5%) patients. The sensitivity, specificity, and positive and negative predictive values of the EIA-based tests, compared to histological examination, were 100%, 96-97%, 81-84%, and 100%, respectively. The positive predictive value of the latex agglutination test was 78%, whereas it was only 47% for the whole-blood rapid test used. Although the results of the whole-blood rapid test were unsatisfactory, the quantitative EIA-based tests could reliably detect Helicobacter pylori among young patients, in whom the prevalence of the infection is low.

Adult↗
PubMed2004

Regression of rectal mucosa-associated lymphoid tissue lymphoma but persistence of Helicobacter pylori infection of gastric mucosa after administration of levofloxacin: report of a case.

PURPOSE: Several articles have reported regression of rectal lymphoma of mucosa-associated lymphoid tissue after anti- Helicobacter pylori therapy. It remains unclear, however, whether lymphoma of rectal mucosa-associated lymphoid tissue is related to Helicobacter pylori infection. METHODS: A 60-year-old woman visited our hospital with a complaint of hematochezia. On colonoscopy a pale, ulcerated protrusion approximately 3.5 cm in diameter was found in the rectum. Pathologic diagnosis of a biopsy specimen was low-grade mucosa-associated lymphoid tissue lymphoma. The patient received a ten-day course of levofloxacin, and the cycle was repeated three times over seven months. RESULTS: Although persistence of Helicobacter pylori infection was confirmed, the tumor regressed completely. CONCLUSION: Our findings in this case suggest that rectal lymphoma of mucosa-associated lymphoid tissue may be related to unknown microorganisms other than Helicobacter pylori. Levofloxacin may be effective for treatment of rectal lymphoma of mucosa-associated lymphoid tissue regardless of Helicobacter pylori infection.

Anti-Infective Agents↗
PubMed2005

Comparison of proton pump inhibitor-based triple therapy with losec and the generic drug, Omepradex, for efficacy of Helicobacter pylori eradication.

Triple therapy with a proton pump inhibitor (PPI), amoxicillin, and clarithromycin is widely accepted in Israel for Helicobacter pylori eradication. Recently, a generic drug for omeprazole was introduced to the market, but its efficacy as a PPI was questioned. The aim of the study was to compare eradication efficacy of triple therapy-based regimens with Losec (Astra-Zeneca, Sweden) and the generic form, Omepradex (Dexxon, Israel). People belonging to Clalit Health Services (CHS), the biggest health insurance provider in Israel, and receiving omeprazole (Losec or Omepradex) for 7 days (assumed to be Helicobacter pylori eradication purposes), between 1.1.2001 and 31.12.2001, were retrieved from the CHS central computer. Of 450 patients (287 in the Losec group and 163 in the Omepradex group), 97 (21.6%) underwent 13C-urea breath test (13CUBT) for validation of Helicobacter pylori successful eradication and participated in the study. They were all treated with triple therapy with omeprazole, amoxicillin, and clarithromycin, and were stratified according to the PPI used: Group A, Losec; and Group B, Omepradex. Positivity of 13CUBT was computed. Sixty-one (21.25%) and 36 (22.08%) patients in Groups A and B, respectively, underwent 13 CUBT for validation of successful Helicobacter pylori eradication (NS). In Group A 41 of 61 patients (67.21%) had a negative 13CUBT, in comparison with 26 of 36 (72.22%) in Group B (NS). Using logistic regression analysis all confounding factors were found to be noncontributory to the discrimination between negative (successful eradication) and positive (failed eradication) 13CUBT. There is no statistically significant difference between Losec and the generic drug Omepradex as part of a PPI-based triple therapy for eradication efficacy of Helicobacter pylori.

Adult↗
PubMed2007

Experimental infection of pigs with 'Candidatus Helicobacter suis'.

'Candidatus Helicobacter suis' is a spiral-shaped bacterium that colonizes the stomach of more than 60% of slaughter pigs. The role of 'Candidatus Helicobacter suis' in gastric disease of pigs is still unclear. Experimental studies in pigs are lacking because this bacterium is unculturable until now. An inoculation protocol using 'Candidatus Helicobacter suis' infected mouse stomach homogenate was used to reproduce the infection in pigs. Control animals were inoculated using negative mouse stomach homogenate. Pigs were inoculated three times with one-week intervals and euthanized 6 weeks post inoculation. Tissue samples were taken from different mucosal stomach regions to detect 'Candidatus Helicobacter suis' by PCR and urease test. Mucosal inflammation was evaluated on formalin-fixed tissue samples. Lesions in the pars oesophagea were scored macroscopically. Infection was successful in all challenged animals, with the antrum and the fundus being predominantly positive. Infection was associated with infiltration of lymphocytes and plasma cells in the antral mucosa, evolving to follicular gastritis. No apparent inflammation of the fundic stomach region was detected in the infected animals. A clear link between 'Candidatus Helicobacter suis' and pars oesophageal lesions could not be found.

Animals↗
PubMed2000

Gastric pathology associated with Helicobacter pylori.

A bacterium is associated with a specific gastritis. Neutrophils infiltrate the necks of the glands, just deep to the infected foveolae. This infiltration rarely, if ever, occurs without H. pylori infection. Foveolar epithelial damage is common, with loss of cell structure. Electron microscopy suggests that the bacteria cause this damage as they attach to the superficial cell membrane. These features, defined by Whitehead et al as active changes, appear specific for H. pylori infection. The neutrophils and specific epithelial changes disappear within days of starting treatment for Helicobacter. They rapidly recur if the treatment is unsuccessful. Without treatment, the changes remain for decades and are severe in 10% to 20% of cases. Other changes occur in the mucosa. Reduced mucus secretion occurs in damaged or proliferating epithelium. This reduced secretion occurs near healing ulcers or with other types of inflammation but is often severe when Helicobacter is present. It returns to normal within weeks of treating the infection. The bacteria adhering to the cell membrane may cause this change directly. Lymphoid infiltration occurs with any type of chronic inflammation or immune reaction. The infiltration is not specific for Helicobacter, and it reduces slowly in months or years after eradication of H. pylori. Peptic ulceration, particularly duodenal ulceration, although not specific, is particularly common with H. pylori infection. The long-term inflammation probably causes other gastric pathology. Atrophy is common. Epithelial metaplasia occurs in about 20% of patients, usually mild. Other features, such as scarring, epithelial dysplasia, and in situ malignant change, are less common. They show little improvement after eradicating H. pylori. The part played by the bacteria in their cause remains uncertain. Pathologists see a long-standing chronic gastritis clearly related to a bacterium. The inflammation often is severe and commonly damages the mucosa, with ulceration, atrophy, metaplasia, and occasional premalignant changes. Physicians would treat inflammation of this degree in most other parts of the body. This disease is usually symptomless. There is some controversy, but eradicating Helicobacter often fails to improve nonulcer dyspepsia. This failure results in a continuing argument over whether or not to treat the infection. Meanwhile the pathology continues. A temporary solution to the problem is suggested: Patients infected with Helicobacter can give informed consent. Patients can be told about the infection, the pathology, the poor relationship to symptoms, and side effects of therapy, and they can decide.

Biopsy, Needle↗
PubMed2002

[Acquisition of secondary resistance after failure of a first treatment of Helicobacter pylori infection in children].

AIMS: To assess the frequency of acquisition of secondary Helicobacter pylori resistant-strains after a first course of antimicrobial treatment. PATIENTS AND METHODS: A retrospective study was performed during the 1994-2000 period, in 15 girls and eight boys, mean age 10.9 +/- 4.8 years (1.4-17 years), with Helicobacter pylori gastritis (culture and antimicrobial susceptibility) presenting a failure of first course treatment, with during one week a proton pump inhibitor and amoxicillin together with either clarithromycin (n = 14) or metronidazole (n = 9). Two endoscopies were performed, the first at the time of diagnosis and the second after the failure of bacterial eradication demonstrated by a positive 13C urea breath test six weeks after the end of treatment. Antimicrobial susceptibility of all Helicobacter pylori strains was tested after each endoscopy and before starting a second course of the treatment. RESULTS: Comparison of antimicrobial susceptibility before and after the first course of treatment showed that Helicobacter pylori strains were all sensitive to amoxicillin, clarithromycin-resistant in eight children (34.7%) before treatment vs 12 (52.1%) after treatment, p = 0.42, ns, metronidazole-resistant in 13 (56.5%) vs 12 (52.1%), p = 0.80, ns, and both clarithromycin and metronidazole-resistant in four (17.3%) vs seven (30.4%), p = 0.63, ns. Among the 14 children treated by a triple therapy including clarithromycin, three (21.4%) developed a secondary resistance to clarithromycin and in one metronidazole resistance was no more detected. Among the nine children treated with a triple therapy including metronidazole, none developed a secondary resistance to metronidazole and one developed a secondary resistance to clarithromycin. CONCLUSION: This study shows the absence of amoxicillin-resistant strains, a high initial clarithromycin-resistant strains level (primary resistance), increasing after a first course of treatment, and for metronidazole a high initial level of resistance not influenced by treatment. Secondary clarithromycin-resistance of Helicobacter pylori strains following the first course of treatment could account for failure of bacterial eradication and suggests the importance of antimicrobial susceptibility.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Prolonging proton pump inhibitor-based anti-Helicobacter pylori treatment from one to two weeks in duodenal ulcer: is it worthwhile?

AIMS: To compare the efficacy of one-week versus two-week treatment with lansoprazole, amoxycillin and clarithromycin in inducing healing of Helicobacter pylori-positive duodenal ulcers as well as to investigate the role of several factors, determinant in the ulcer healing process. PATIENTS AND METHODS: Seventy-one active duodenal ulcer patients were randomised to receive one- or two-week treatment with lansoprazole (30 mg bid), clarithromycin (500 mg bid) and amoxycillin (1 g bid), not followed by any additional acid suppressive therapy. Ulcer healing and Helicobacter pylori infection were assessed by endoscopy and urea breath test 4 weeks after the end of treatment. Before entering the trial and four weeks after the end of treatment, dyspeptic symptoms were recorded and scored by a validated questionnaire. The potential effects of a number of clinical variables on the ulcer healing process were evaluated by means of univariate and multivariate analyses. RESULTS: Duodenal ulcer was healed in 80.5% patients treated for one week and in 91.4% patients treated for 2 weeks according to intention-to-treat analysis (p=NS). Ulcer healing was more frequent in the Helicobacter pylori cured patients compared to those with persisting infection (90.9% vs 68.5%; p=0.04). Multivariate analysis did not reveal any significant predictor of duodenal ulcer healing. CONCLUSIONS: Two-week treatment with lansoprazole, amoxycillin and clarithromycin, without continuation of antisecretive therapy, is better, although the difference is not statistically significant, than one-week treatment in healing Helicobacter pylori-positive duodenal ulcer disease. The eradication of Helicobacter pylori is the most important factor related to ulcer healing.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Effects of CYP2C19 gene polymorphism on cure rates for Helicobacter pylori infection by triple therapy with proton pump inhibitor (omeprazole or rabeprazole), amoxycillin and clarithromycin in Japan.

BACKGROUND: Omeprazole is mainly metabolized by cytochrome P450 2C19 (CYP2C19) in the liver. Rabeprazole, on the other hand, is mainly metabolized to thioether-rabeprazole via a non-enzymatic pathway and partially metabolized to demethylated-rabeprazole by CYP2C19 in liver CYP2C19 status may affect cure rate for Helicobacter pylori infection with proton pump inhibitor triple therapy. AIM: To investigate whether genetic polymorphism of CYP2C19 and selected proton pump inhibitors (omeprazole or rabeprazole) were associated with cure rate for Helicobacter pylori infection using triple therapy with omeprazole or rabeprazole, amoxicillin, and clarithromycin. METHODS: A total of 170 Helicobacter pylori-positive patients with chronic gastritis were randomized to receive one of the following Helicobacter pylori eradication regimens; OAC (omeprazole 20 mg bd, amoxycillin 750 mg bd and clarithromycin 400 mg bd for 1 week) and RAC (rabeprazole 20 mg bd, amoxycillin 750 mg bd and clarithromycin 400 mg bd for 1 week). The CYP2C19 genotype; wild-type or two mutant genes (ml in exon 5 and m2 in exon 4), or both, were identified by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: In DAC regimen, cure rate (per protocol analysis) was 73.3% in homozygous extensive metabolizers, 86.1% in heterozygous extensive metabolizers, and 85.0% in poor metabolizers. In RAC regimen, the cure rate was 81.0% in homozygous extensive metabolizers, 82.9% in heterozygous extensive metabolizers, and 87.5% in poor metabolizers. Cure rate was not significantly different between the CYP2C19 genotypes in both regimens. CONCLUSION: Triple therapy with proton pump inhibitor (omeprazole or rabeprazole), amoxycillin, and clarithromycin is sufficiently effective in cure of Helicobacter pylori infection regardless of CYP2C19 status.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Randomised study of the efficacy of omeprazole and clarithromycin with either amoxycillin or metronidazole in the eradication of Helicobacter pylori in screened primary care patients.

BACKGROUND: Population Helicobacter pylori screening and treatment has been advocated as a means of reducing mortality from gastric cancer. The optimum Helicobacter pylori eradication therapy to use in this setting is uncertain. AIMS: To compare efficacy of seven days of omeprazole, clarithromycin and either metronidazole, or amoxycillin in Helicobacter pylori positive subjects detected by population screening. PATIENTS: Helicobacter pylori positive patients from the placebo group of a population screening and treatment trial were invited to take part in the investigation. METHODS: Patients were randomised to receive either omeprazole, clarithromycin and metronidazole or omeprazole, clarithromycin and amoxycillin, and Helicobacter pylori eradication was verified with a 13C-urea breath test at least four weeks after completion of therapy. RESULTS: A total of 221 patients took part in the study and 210 completed the protocol. Treatment was successful in 93/111 [84%) patients allocated to omeprazole, clarithromycin and metronidazole and in 96/110 (87%) allocated to omeprazole, clarithromycin and amoxycillin in an intention-to-treat analysis (p=0.46). Per protocol eradication rates were 93/107 (87%) in the metronidazole, and 96/103 (93%) amoxycillin group (p=0.129). CONCLUSIONS: There was no significant difference between the two regimens. The eradication rates achieved are comparable with previous studies in both dyspepsia and peptic ulcer patients.

Adult↗
PubMed2001

Helicobacter pylori: diseases, tests and treatment.

Gastroduodenal disease associated with Helicobacter pylori infection are reviewed as well as the diagnostic approach. Generally, there are by and large two ways in which a diagnosis of infection by Helicobacter pylori can be made: by using either an invasive or non-invasive procedure. The invasive procedures involve endoscopy and biopsy Biopsy is essential since the mucosa may often appear macroscopically normal but, nevertheless, be inflamed. Once a biopsy is obtained histological examination, culture, polymerase chain reaction, detection of the presence of urease activity can be detected. The non-invasive tests that can be used to diagnose the infection are: serology, detection of labelled metabolic products of urea hydrolysis either in the breath (13CO2, 14CO2), the urine or the blood, detection of Helicobacter pylori antigen in stool specimen. At present, no single test is sufficiently reliable to definitely detect colonisation by Helicobacter pylori, and a combination of two is recommended, if feasible. Choice of the test to be used is not straightforward and relies on a series of situations, i. e., clinical setting and local expertise and availability, that the clinician must consider to obtain the best diagnostic yeld. The challenge of Helicobacter pylori eradication is not very easy to obtain. The possible scenario and the use of a new proton pump inhibitor (esomeprazole) are reviewed and discussed.

Dyspepsia↗
PubMed2002

Treatment of Helicobacter pylori infection. Indications and regimens: an update.

The management of Helicobacter pylori infection is still surrounded by controversy and uncertainties. Indications and correct application of current regimens for Helicobacter pylori infection are still considered a matter of debate. Regarding indications, only peptic ulcer and mucosa associated lymphoid tissue lymphoma are considered clear indications for treatment. In other conditions, such as atrophic gastritis, post gastric cancer resection, first-degree relatives of gastric cancer patients, dyspeptic patients, patients with gastro-oesophageal reflux disease and non-steroidal anti-inflammatory drug users, the value of Helicobacter pylori eradication is still controversial. The regimens for first-line and second-line treatment of Helicobacter pylori infection have been recommended by the Maastricht 2 Consensus Report. Although all the treatments are considered to be effective, physicians still do not agree on what first-line regimen should be used. Furthermore, a consensus on the duration of the antibiotic treatment is still lacking, although Maastricht guidelines for treatment of Helicobacter pylori infection recommend a one-week therapy. Also regimens, as a third-line treatment, and methods to improve compliance and clinical outcome are still a matter of debate. All these points will be considered in the present review

Amoxicillin↗
PubMed2002

Comparison of two new rapid serology tests for diagnosis of Helicobacter pylori infection in Chinese patients.

BACKGROUND: Rapid serology test is a simple and convenient way for diagnosing Helicobacter pylori infection. However performances of these tests are usually less satisfactory than expected, particularly in developing countries. AIM: To evaluate the performances of two newly developed rapid serology tests for Helicobacter pylori infection. PATIENTS: Consecutive Chinese dyspeptic patients undergoing upper gastrointestinal endoscopy. METHODS: Gastric biopsies were obtained from antrum and corpus for rapid urease test and histological examination. Diagnosis of Helicobacter pylori infection was based on two or more positive results in rapid urease test, histology and [13C] urea breath test. Patients' sera were tested against two rapid serology tests: ASSURE Hp Rapid Test (Genelabs Diagnostics, Singapore) and SureStep (Applied Biotech, San Diego, CA, USA). RESULTS: A total of 148 patients were evaluated and Helicobacter pylori infection was diagnosed in 78 (53%) patients by gold standard. The sensitivities of ASSURE Hp and SureStep were, respectively, 94% and 71% (p=0.0003). Specificities of the two test kits were both 90%. The overall accuracy of ASSURE Hp was significantly higher than SureStep (92% versus 80%, p=0.004). CONCLUSION: Both rapid serology tests appear to be specific in diagnosing Helicobacter pylori infection in the Chinese populations. However the ASSURE Hp test is more sensitive and accurate than the SureStep test.

Adult↗
PubMed2003

Endoscopic 13C-urea breath test for the diagnosis of Helicobacter pylori infection.

BACKGROUND: Endoscopic 13C-urea breath test may avoid contamination of oral urease and rapidly discriminate Helicobacter pylori-positive and Helicobacter pylori-negative patients. AIMS: To compare the accuracy of endoscopic 13C-urea breath test with conventional invasive methods in diagnosis of Helicobacter pylori infection. PATIENTS: One hundred patients who attended for routine upper gastrointestinal endoscopy were included. METHODS: 13C-urea was applied to the stomach through the working channel of endoscope at the end of endoscopic examination. Breath samples were collected before endoscopy and 2, 4, 6, 8, 10 min after consumption of 100 or 50 mg 13C-urea. Helicobacter pylori infection was defined as those with positive culture or positive results of both histology and CLO test. RESULTS: The accuracy of 100 mg endoscopic 13C-urea breath test was significantly higher than that of culture and CLO test (100% vs. 88% and 92%, p = 0.02 and 0.03, respectively). The accuracy of 50 mg endoscopic 13C-urea breath test was higher than that of histology and CLO test (98% vs. 90% and 96%, respectively), although the differences were not statistically significant. CONCLUSIONS: Endoscopic 13C-urea breath test has a higher accuracy compared with biopsy-based modalities. It may be a good choice to diagnose Helicobacter pylori infection if endoscopy is indicated for a dyspeptic patient.

Adult↗