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.     

Discrepancy between Helicobacter pylori stool antigen assay and urea breath test in the detection of Helicobacter pylori infection

Background. The reference diagnostic methods available for detection of Helicobacter pylori infection are either invasive (histology) or expensive and highly sophisticated (Urea Breath Test). A new enzyme immunoassay, which can be easily performed in any laboratory, has been developed to detect Helicobacter pylori in stool specimens (HpSA - Meridian Diagnostics, Cincinnati, USA). Aim of the study was to compare HpSA to Urea Breath Test.Patients and methods. A total of 125 patients (52 never treated for Helicobacter pylori infection and 73 after Helicobacter pylori eradication therapy) referring to our Department, underwent both tests within two weeks.Results. Contrasting results between the two tests were found in 30% of cases: in 19% of the untreated patients and in 37% of the treated patients (p<0.001). The main discrepancy consisted in positive HpSA associated with negative Urea Breath Test. Mean HpSA value in such conditions was 0.273 optical density, while in patients with both positive tests, it was 1.192 optical density. In untreated, but not in treated patients, raising the HpSA cut off value significantly decreased the percentage of conflicting results.Conclusions. Some disagreement was detected between HpSA and Urea Breath Test results, especially in treated patients. Possible explanations for our findings are a low HpSA cut off value together with the identification of Helicobacter pylori coccoid forms by the immunoassay but not by the urease based Urea Breath Test. The higher percentage of discrepancy detected in treated patients might support this hypothesis.     

Lower concentrations of clarithromycin suppress urease activity, motility, and binding to gastric epithelial cells in Helicobacter pylori isolates

Background. Our previous study showed that histological scores of gastric mucosal inflammation and Helicobacter pylori density decreased even in patients who failed to eradicate Helicobacter pylori after antimicrobial therapy including clarithromycin. This may reflect indirect suppressive effects of lower concentrations of clarithromycin on Helicobacter pylori, as suggested in other Gram-negative rod infections.Aims. To investigate whether clarithromycin suppresses virulence factors of Helicobacter pylori at sub-minimal inhibitory concentration.Methods. Six clarithromycin-susceptible Helicobacter pylori isolates and 7 clarithromycin-resistant isolates were obtained from patients with peptic ulcer disease. These isolates were analysed for urease activity, motility, and ability to bind to gastric epithelial cells after they were incubated with or without clarithromycin at sub-minimal inhibitory concentrations.Results. Incubation of Helicobacter pylori isolates with clarithromycin at sub-minimal inhibitory concentrations reduced urease activity, motility, and binding to gastric epithelial cells in a dose-dependent manner. These findings were observed both in clarithromycin-susceptible and resistant strains.Conclusions. Suppressive effects of clerithromycin on virulence factors of Helicobacter pylori at sub-minimal inhibitory concentrations may be associated with observed attenuation of gastric inflammation and Helicobacter pylori density in patients who failed in bacterial eradication after triple therapy including clarithromycin.     

Prevalence peptic lesion in asymptomatic, healthy volunteers

Aim. To investigate the presence of lesions of the upper gastrointestinal tract of asymptomatic, healthy volunteers undergoing clinical pharmacology studies.Material and Methods. A series of 53 volunteers (45 male, 23 Helicobacter pylori negative and 30 Helicobacter pylori positive) underwent upper gastrointestinal endoscopy. Helicobacter pylori status was assessed using two methods (rapid urease test and histology) from antral and corpus biopsies.Results. Peptic lesions were found in 24 (45%) subjects: erosive oesophagitis, gastric/duodenal ulcers and gastric/duodenal erosions were found in 23%, 9% and 36% of these volunteers, respectively. Helicobacter plyori-positive subjects had significantly (p<0.05) more gastroduodenal lesions than Helicobacter pylori negative individuals (12/30 vs 3/23). The presence of peptic ulcers and erosive oesophagitis was similar in Helicobacter pylori-positive and -negative individuals.Conclusions. The possibility that peptic lesions might exist in otherwise asymptomatic, asymptomatic, healthy individuals cannot be ruled out. Helicobacter pylori-positive individuals have a significantly higher incidence of gastric and duodenal lesions than Helicobacter pylori negative subjects.     

Effect of Helicobacter pylori infection on gastric cell proliferation and genomic instablity in a paediatric population of Southern Italy

Background. The incidence of gastric cancer is high in areas with a high prevalence of Helicobacter pylori infection. Cell transformation and tumour progression occur over a long period of time and markers of genomic instability usually precede morphological changes.Aim. To evaluate the effect of Helicobacter pylori infection on cell proliferation, DNA status and oncogene expression in children.Patients and Methods. Morphometric and immunohistochemical techniques were used to analyse DNA content, p53 and c-myc oncogene expression and cell proliferation on gastric biopsies of 53 children (27 Helicobacter pylori-negative and 26 Helicobacter pylori-positive).Results. Gastric mucosa was normal in 11 % of Helicobacter pylori-positive and in 33% of Helicobacter pylori-negative subjects. Most children had chronic non-atrophic gastritis regardless of Helicobacter pylori infection, and only a minority of children affected by Helicobacter pylori had mild atrophic gastritis. Cell proliferation was significantly higher in children with Helicobacter pylori-positive gastritis than in those with Helicobacter pylori-negative gastritis. No metaplasia, dysplasia, p53 overexpression or altered DNA content was found in any child. Interestingly, 46% of children with and 29% without Helicobacter pylori infection had c-myc overexpression closely related to the cell proliferation rate.Conclusion. Helicobacter pylori infection in children may coexist with a normal gastric mucosa, and it is not associated with genomic instability markers in cases of chronic gastritis.     

Cure of Helicobacter pylori-positive active duodenal ulcer patients: double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy

Aims. To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection.Patients and Methods. A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated.Results. Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0. 0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pylori-cured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46/58 patients previously treated with the triple therapy and in 10/40 patients treated with the dual therapy (p<0.0001). Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients.Conclusions. Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.     

Role of Helicobacter pylori infection in pernicious anaemia

Background. Pernicious anaemia is associated with atrophic body gastritis and considered an autoimmune disease. Whether Helicobacter pylori is involved in the induction of pernicious anaemia is uncertain.Aims. To investigate the prevalence of Helicobacter pylori infection in pernicious anaemia patients and to ascertain whether the Helicobacter pylori positive patients had distinctive clinical and gastric morphofunctional characteristics.Patients and Methods. A series of 81 consecutive pernicious anaemia patients underwent serological, functional and endoscopic/histological investigations.Results. A total of 49 (60.5%) patients were Helicobacter pylori-positive (males 61.2% vs females 38.8%). No difference was observed in clinical and morphofunctional characteristics between Helicobacter pylori-positive and negative patients, whereas distinctive functional/histological features between histologically Helicobacter pylori-positive (n=8) and serologically Helicobacter pylori-positive (n=41) cases were detected. In the histologically Helicobacter pylori-positive group, Pepsinogen I was higher [13 [0–58] vs 5 [0–26] ng/ml; P=0.0025]) and positivity for anti-parietal cell antibodies was lower [42.9% vs 76.9, P=0.0867). Antral histological variables of the gastritis score were significantly higher in the histologically Helicobacter pylori-positive than in the serologically Helicobacter pylori-positive patients, but this latter group had a higher score of body atrophy (2.63± 0.12 vs 1.71 ± 0.29; P=0.0051). Body inflammation was also significantly higher in the histologically Helicobacter pylori-positive group (chronic inflammation: 1.43±0.2 vs 1.05±0.06; P=0.0271; inflammation acitivity:: 0.57±0.3 vs 0.15±0.06, P=0.0220). Antral mucosa was normal in 24/41 (58.5%) of the serologically Helicobacter pylori-positive patients, but only in 1/8 (12.5%) of the histologically Helicobacter pylori-positive patients (p=0.232).Conclusions. Almost two thirds of pernicious anaemia patients have evidence of Helicobacter pylori, but only those with an active Helicobacter pylori infection have distinctive functional and histological features. These findings support the hypothesis that Helicobacter pylori infection could play a triggering role in a subgroup of pernicious anaemia patients.     

Helicobacter pylori is not a risk factor for hepatic encephalopathy

Background. Helicobacter pylori infection has been described as a risk factor for hepatic encephalopathy in patients with chronic liver disease although the topic remains controversial.Aims. To determine whether Helicobacter pylori infection is an independent predictive factor for encephalopathy in patients with liver cirrhosis.Methods. Clinical, epidemiological, analytical and nutritional parameters of 205 patients were collected. Helicobacter pylori infection was determined by serology. Encephalopathy (grade 11 or higher) was clinically assessed during follow-up. The relationship between each parameter and encephalopathy was analysed by Kaplan-Meier curves and the Log rank test. The most significant parameters underwent multivariate analysis by Cox regression.Results. Twenty-five variables were related to encephalopathy in the bivariate analysis. Multivariate analysis selected five independent factors: previous bouts of encephalopathy (Odds ratio 3.79; 95% confidence interval 1.94–7.38), albumin (Odds ratio 0.86; 95% confidence interval 0.80–0.92), tricipital skin fold (Odds ratio 0.79; 95% confidence interval 0.66–0.95] chronic pulmonary disease (Odds ratio 2.78, 95% confidence interval; 1.31–5.92), and on-going alcoholism (Odds ratio 2.62; 95% confidence interval 1.16-5.88].Conclusions. Helicobacter pylori is not an independent risk factor for hepatic encephalopathy.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease

Background. It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid.Aims. To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions.Methods. Duodenal (anterior, superior, inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and ¹³C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment.Results. Duodenal gastric metaplasia regression was observed in all ( ) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0.001).Conclusions. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Validity of various diagnostic tests to evaluate cure ofHelicobacter pylori infection

Many diagnostic methods have been developed and used for detectingHelicobacter pylori to evaluate the success of treatment ofH. pylori infection. We investigated and compared the suitability of the rapid urease test (RUT), polymerase chain reaction (PCR),¹³C-urea breath test (¹³C-UBT), and serology with culture for evaluating cure ofH. pylori infection. Forty-sevenH. pylori-positive gastric ulcer patients received dual therapy of lansoprazole (30 mg u.i.d.) and clarithromycin (200 mg b.i.d.). Four weeks after the completion of treatment, RUT, PCR,¹³C-UBT, and culture were performed and the negative rates of these tests were compared. Anti-H. pylori IgG antibodies were measured by enzyme-linked immunosorbent assay (ELISA) before and 4 weeks after completion of the treatment to evaluate changes of titers during the treatment. The negative rate of RUT (55%) was significantly greater than that of culture (27%). Significant declines in titers were seen in the patients who had negative culture results, while the decline in the titer was not significant in the patients who had positive results. PCR assay and¹³C-UBT were suitable for the evaluation ofH. pylori eradication, but RUT was not suitable, because of its sensitivity. By monitoring anti-H. pylori IgG antibody titers, therapeutic failure can be detected early after completion of treatment.     

Usefulness of the Immunological Rapid Urease Test for Detection of Helicobacter pylori in Patients Who are Reluctant to Undergo Endoscopic Biopsies

Cardiovascular diseases and liver cirrhosis are in the list of Helicobacter pylori-related extragastric diseases. Patients with cirrhosis and cardiovascular diseases under the control of aspirin have increased risk of gastrointestinal bleeding. The immunological rapid urease test (IRUT) provides a rapid and safe diagnostic test for H. pylori using gastric mucus collected at endoscopy. We investigated its usefulness in 93 patients with these extragastric diseases including 46 with H. pylori infection assessed by urea breath test and serology. Twenty H. pylori-infected patients received eradication therapy and the IRUT was assessed to evaluate the efficacy of bacterial eradication. The sensitivity, specificity, and positive and negative predictive values for IRUT were 96%, 90%, 90%, and 96%, respectively. The results of IRUT completely agreed with those of urea breath test following anti-H. pylori therapy. The IRUT has acceptable diagnostic performance in such cohorts reluctant to undergo endoscopic biopsies due to the risk of bleeding.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: for-year follow-up study

Background. About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied.Aim. To study: a) whether gastric acid hypersecretion “per se” is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients.Patients. The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients.Methods. Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, ¹³C-urea breath test after 42 months; clinical questionnaires were completed every 6 months.Results. After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEg/h and 64. 1 mEg/h before treatment vs 16 mEg/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs.Conclusions. These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion “per se” is not able to determine the recurrence of duodenal ulcer.     

Comparison of the Clinical Feasibility of Three Rapid Urease Tests in the Diagnosis of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

Rapid urease tests (RUTs) are a fast, accurate, and inexpensive method to diagnose H. pylori infection in the endoscopy suite. Of these, the CLO test is both common and widely used. The aim of our study was to evaluate the accuracy and positive reaction times of two new rapid urease tests (ProntoDry and HpONE) in comparison with the CLO test. Fifty-one patients (26 men, 25 women; mean age, 52.4 years) were included in this study, and all underwent esophagogastroduodenoscopy (EGD). None of the patients had received any prior H. pylori eradication therapy. H. pylori infection status was evaluated by histology, culture, ¹³C–UBT, and RUT. H. pylori infection was considered to be positive if the culture was positive or if two of the other three tests (histology, RUT, and ¹³C–UBT) were positive. If culture was negative and only one of the other three tests was positive, or if all four tests were negative, the result was interpreted as negative. Of these 51 patients, 2 were excluded and 29 (59.1%) were infected with H. pylori. The sensitivities, specificities, positive predictive values, and negative predictive values of the three RUTs were not significantly different. The mean positive reaction times of the three RUTs (CLO test, ProntoDry, and HpONE) were 67.8 ± 12.0, 16.5 ± 2.2, and 17.8 ± 2.1 min, respectively. ProntoDry (P < 0.001) and HpONE (P < 0.001) had significantly faster reaction times than the CLO test, but there was no significant difference between ProntoDry and HpONE. Different media of RUTs may influence the rapidity of a positive reaction time. Both ProntoDry and HpONE were superior to the CLO test in terms of accuracy, reaction time, and cost-effectiveness.     

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output >10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence ofHelicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis).Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P<0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found amongHelicobacter pylori-positive compared toHelicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr wereHelicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence ofHelicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.     

Randomised study ofefficacy 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.     

Helicobacter pylori Infection Is Not Associated with Subclinical Hepatic Encephalopathy in Stable Cirrhotic Patients

The importance of ammonia-producing Helicobacter pylori infection as a cause of subclinical encephalopathy in cirrhosis was investigated. In addition, a single psychometric test that can reliably detect subclinical hepatic encephalopathy was sought. Out-patients with cirrhosis and no overt encephalopathy underwent [¹⁴C]urea breath testing once and psychometric testing on two separate occasions, with an intervening course of clarithromycin/omeprazole if they had subclinical encephalopathy (two of four psychometric tests abnormal). Subclinical encephalopathy was present in 27 of 69 patients (39%), and Helicobacter pylori infection in 14 of 69 (20%). There was no association between the two conditions (P = 0.769). Subclinical encephalopathy resolved in 75% of treated Helicobacter pylori-positive patients and 37.5% of treated Helicobacter pylori-negative patients (P = 0.285). Number connection test-B had high reproducibility among untreated patients (R = 0.655) and high correlation (P 0.01) with three surrogate gold standards. In stable cirrhotic patients, subclinical hepatic encephalopathy was found to: (1) have a high prevalence, (2) not be associated with Helicobacter pylori infection, and (3) be readily detected with the number connection test-B alone.     

Does Serum Nitrite Concentration Reflect Gastric Carcinogenesis in Japanese Helicobacter pylori-Infected Patients?

This study investigated whether the serum nitrite concentration reflects Helicobacter pylori-induced inflammation and atrophic changes of gastric mucosa. Ninety-seven patients underwent biopsy of both antrum and fundus. Samples were analyzed by the rapid urease test and histopathological examination according to the updated Sydney system. Fasting serum samples from each subject were analyzed for specific IgG Helicobacter pylori antibodies, pepsinogen I and II concentrations, and NO₂ ^–/NO₃ ^– content. Eleven patients had H. pylori eradicated with proton pump-based triple therapy. There was a strong positive correlation between the Helicobacter pylori density in the gastric mucosa and the serum nitrite concentration, but a negative correlation existed between the atrophic grade of the gastric mucosa and both serum nitrite concentration and Helicobacter pylori density in the gastric mucosa. Serum nitrite concentrations decreased significantly after successful eradication of Helicobacter pylori. Therefore, serum nitrite concentration may be a useful marker for oxidative DNA damage and apoptosis associated with Helicobacter pylori infection.     

Risk Factors Involved in Patients with Bleeding Peptic Ulcers: A Case–Control Study

Our objectives were to (1) identify the risk factors involved in patients with peptic ulcer disease and determine if they predict bleeding in these patients, (2) determine the association between these risk factors, and (3) analyze the cost effectiveness of various tests for Helicobacter pylori (H. pylori). Two-hundred and thirty patients were included in our study between January 2004 and June 2005 (128 bleeding peptic ulcer disease patients constituted the cases, 102 nonbleeding ulcer patients constituted the controls). H. pylori infection was assessed by urease test and biopsy from gastric antrum. There was no statistically significant difference between these groups regarding sex, age, or location of ulcer. Nonsteroidal anti-inflammatory drug (NSAID) use was higher in the case group (P < 0.001), and the rate of H. pylori infection was lower in these patients (P < 0.05). There was no interaction between NSAID use and H. pylori infection in predicting bleeding ulcer risk (P = 0.08). Sensitivity and specificity for urease test in detecting H. pylori was 75% and 99.7%, respectively. So a positive urease test does not need confirmation with biopsy, which is cost effective.     

Diagnostic performance of gastric imprint smear for determination of Helicobacter pylori infection

BACKGROUND:

Despite the availability of several methods (invasive and noninvasive) for the diagnosis of Helicobacter pylori infection, no test is considered to be the ‘gold standard’. Endoscopy-based tests are regarded as the reference method in most studies.

OBJECTIVE:

To evaluate the diagnostic performance of imprint cytology smears of antral biopsies compared with Gram-stained smears, the rapid urease test and culture methods, separately and in combination.

METHODS:

Antral biopsies were obtained from consecutive patients undergoing upper gastrointestinal endoscopy at a single centre. The biopsies were examined for the presence of H pylori by Gram-stained smear, the rapid urease test, culture methods and imprint cytology smear.

RESULTS:

A total of 273 biopsies were studied. All tests were positive in 36% of the patients. Of 252 biopsies tested, 73% were positive using the imprint cytology technique. Using Gram-stained smear, the rapid urease test and culture methods individually, the sensitivity and specificity of imprint cytology smears for the detection of H pylori were found to be 92.7% and 50%; 92.7% and 49%; and 92.4% and 38.5%, respectively. Combining the three microbiological methods resulted in a sensitivity of 92.1%, a specificity of 51.0% and an efficiency of 71.7% for imprint cytology smears.

CONCLUSIONS:

Endoscopic examination provides useful clinical information. Imprint gastric cytology can be used as a rapid test to establish the diagnosis of H pylori infection at the time endoscopy is performed, enabling the endoscopist to start treatment with immediate effect.     

Helicobacter heilmannii infection in a child after successful eradication of Helicobacter pylori: case report and review of literature

An 11-year-old boy with Helicobacter pylori-associated duodenal ulcer was successfully treated with a combination of lansoprazole, amoxicillin, and clarithromycin. Endoscopy and gastric biopsies were repeated 2 and 12 months later, showing ulcer healing and eradication of H. pylori. However, a 3-year follow-up study demonstrated H. heilmannii in the antral mucosa based on its characteristic morphology and positive urease test and negative culture. The patient had no contact with domestic animals such as cats and dogs. A 7-day course with lansoprazole, amoxicillin, and clarithromycin was performed again, resulting in successful eradication of the organism. Pediatric cases with H. heilmannii infection reported are reviewed.