Does using a warmer influence the results of rapid urease testing for Helicobacter pylori?
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Biopsy↗
Biomedical subjects
D Y Graham
Publications and source records attributed to D Y Graham.
Interobserver variation in the histopathological assessment of Helicobacter pylori gastritis.
The histopathologic detection of Helicobacter pylori in gastric biopsy specimens is considered the gold standard for the diagnosis of H pylori infection. However, few studies have addressed the pathologists' reliability to detect the organism and to assess the degree of the related inflammatory changes. The objectives of this study were to determine the degree of agreement among the findings of four gastrointestinal pathologists in the semiquantitative evaluation of H pylori infection and gastritis. Three slides from specified areas of the stomach of 99 patients with and without H pylori infection were stained with the triple stain, coded, and examined independently by four pathologists. For each specimen, a visual analogue scale graded from 0 (absent/normal) to 5 (maximal intensity) was used to score (1) H pylori (2) neutrophils, and (3) atrophy. Data were analyzed using kappa-statistics. The kappa-coefficient for the detection of H pylori (present vs absent) was approximately .9 (excellent); for the intensity of infection, it was considerably lower on the 6-point scale (approximately .61) and improved slightly on an amalgamated 4-point scale (approximately .71). The agreement on presence or absence of neutrophils was excellent (kappa = .8) in antral biopsies and good (kappa = .67) in corpus biopsies. The kappa for the semiquantitative scoring of neutrophils was poor on the 6-point scale (approximately .43) and fair on the amalgamated scale (approximately .54). The interobserver agreement was the poorest in the evaluation of atrophy (presence, absence, categories, or group categories) with kappa coefficients varying from .08 and .29. This group of pathologists had a high level of concordance on the diagnosis of H pylori infection in any particular patient and a high index in the assessment of the intensity of infection. The agreement was less in the semiquantitative evaluation of active inflammation. When the evaluation concerned a loosely defined feature, such as atrophy, there was essentially no agreement among the pathologists. This study suggests the need for further assessments of pathologists' ability to provide reproducible diagnoses. These results also indicate that more stringent criteria for the diagnosis of "soft" histopathologic features (such as atrophy) are urgently needed.
Atrophy↗
Histological features do not define NSAID-induced gastritis.
Nonsteroidal anti-inflammatory drug (NSAID) use is a common cause of peptic ulcer. This study investigated the nature, frequency, and topographic distribution of histological abnormalities of the gastric mucosa associated with chronic NSAID use. A set of 3 to 11 mapped gastric biopsy specimens were obtained from 108 chronic users of NSAIDs and 61 controls. Each specimen was graded from 0 to 3 for each of the following features: foveolar hyperplasia, smooth muscle fibers, edema, neutrophils, intestinal metaplasia, eosinophils, mononuclear cells, mucosal hemorrhage, atrophy, and Helicobacter pylori. We found that foveolar hyperplasia, considered one of the characteristic features of chemical gastropathy, was absent in 66% of NSAID users. Foveolar hyperplasia was present in 37 NSAID users (34%) and in 10 controls (18%); prominent smooth muscle fibers were found in 51 NSAID users (47%) and 10 of the controls (16%). Concurrent H pylori gastritis obscured the histopathologic changes of NSAID use. All other parameters, including H pylori infection rate (57% v 51%) were similar in NSAID users and controls. We conclude that the histological features characteristic of NSAID users were present only in a subset of patients. No single histological feature can be used to characterize or diagnose chemical gastropathy and no simple set of diagnostic criteria can be applied for this purpose.
Adult↗
One-week triple therapy with omeprazole, amoxycillin and clarithromycin for treatment of Helicobacter pylori infection.
BACKGROUND: Multi-drug regimens are generally required to reliably cure H. pylori infection. We previously demonstrated that a 2-week three-times-a-day regimen of amoxycillin and clarithromycin was effective against H. pylori infection. OBJECTIVES: To evaluate the efficacy and side-effects of a 1-week twice-daily dosing schedule for the treatment of H. pylori infection. METHODS: We studied the efficacy of 1-week of therapy with 20 mg of omeprazole, 1 g of amoxycillin and 250 mg of clarithromycin, all twice daily H. pylori status was determined at entry and 4 or more weeks after completing antimicrobial therapy using histology (Genta stain) and culture. RESULTS: Thirty-one patients with documented peptic ulcer disease and H. pylori infection were treated. The H. pylori infection was cured in 24 (77%, 95% CI = 58-90%) (intention-to-treat). In a per protocol analysis the cure rate was 23 of 29 patients (79%, 95% CI = 60-92%). One patient took only 43% of the study drugs and another withdrew following development of an anaphylactic reaction to study medication. Mild side-effects were reported by 16% including diarrhoea, headache and altered taste. Compliance averaged 95%. Pretreatment clarithromycin resistance averaged 5% and had not been acquired by any strains post-therapy. CONCLUSION: This combination of omeprazole, amoxycillin and low-dose clarithromycin resulted in a relatively low cure rate even in patients with clarithromycin-sensitive isolates. Large comparative studies will be needed to define the optimal duration, dose and dosing interval if this combination of drugs is to become competitive.
Adult↗
High-dose proton pump inhibitor plus amoxycillin for the treatment or retreatment of Helicobacter pylori infection.
BACKGROUND: The combination of 120 mg of omeprazole (40 mg t.d.s.) and amoxycillin has been reported to be effective for treating H. pylori infections. METHODS: Normal volunteers with H. pylori infection received high-dose omeprazole (40 mg t.d.s.) or lansoprazole (60 mg t.d.s.) plus amoxycillin 750 mg t.d.s. for 14 days. The studies were open label and not randomized as those receiving omeprazole plus amoxycillin had previously failed lower dose omeprazole (20 mg b.d.) plus amoxycillin therapy more than 6 months previously. Those receiving lansoprazole plus amoxycillin had not been previously treated. Four to 6 weeks after ending antimicrobial therapy, H. pylori status was determined by Genta stain of gastric mucosal biopsies. RESULTS: Forty-three volunteers entered the study and 41 completed it. The overall success with high-dose proton pump inhibitor plus amoxycillin was 34.9%. For the individual regimens the per-protocol results were 48% (95% CI = 28-69%) with lansoprazole and 12.5% (95% CI = 2-38%) with omeprazole. Compliance was > 95% for both regimens. Side-effects were experienced by four lansoprazole and three omeprazole subjects, and caused two omeprazole subjects to withdraw. Cure rates were similar among different races and ethnic groups, between men and women, and between smokers and non-smokers. The level of the pre-treatment urea breath test also did not predict outcome. CONCLUSION: High-dose proton pump inhibitor plus amoxycillin combinations for treatment of H. pylori infection yielded unacceptable results, as the 95% confidence intervals did not include an 80% cure rate. These combinations do not yield consistent results worldwide and cannot be recommended as primary therapy.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Gastrin-releasing peptide, acid secretion, Helicobacter pylori, and duodenal ulcer: another epiphenomenon?
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Duodenal Ulcer↗
Helicobacter pylori and perturbations in acid secretion: the end of the beginning.
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Duodenal Ulcer↗
Extract of Helicobacter pylori induces neutrophils to injure endothelial cells and contains antielastase activity.
BACKGROUND & AIMS: Previous studies indicate that a water extract of Helicobacter pylori promotes leukocyte adhesion and emigration as well as endothelial barrier disruption (increased vascular protein leakage) in rat mesenteric venules. The aims of this study were to assess whether H. pylori extract-activated neutrophils disrupt endothelial cell monolayers and to identify the mechanisms involved in this process. METHODS: Human neutrophils were incubated with monolayers of human umbilical vein endothelial cells (HUVECs) in the presence or absence of H. pylori extract. RESULTS: H. pylori extract-activated human neutrophils produced endothelial cell detachment from HUVEC monolayers, the severity of which was dependent on the duration of exposure. Endothelial cell detachment was prevented by a monoclonal antibody directed against CD11/CD18 on neutrophils or a monoclonal antibody against intercellular adhesion molecule 1 on endothelial cells. HUVEC monolayer disruption was also prevented by superoxide dismutase, catalase, and a monoclonal antibody against elastase. Further studies indicated that H. pylori extract was capable of inhibiting human neutrophil elastase. The antielastase activity was not diminished by oxidants. CONCLUSIONS: These studies indicate that H. pylori extract-activated human neutrophils can disrupt HUVEC monolayers only when human neutrophils are allowed to adhere to HUVECs and may provide an explanation for the H. pylori extract-induced, neutrophil-dependent vascular protein leakage observed in vivo. The possibility that H. pylori releases antiproteases may explain, in part, why this bacterium is so virulent.
Antibodies, Monoclonal↗
Helicobacter pylori in the drinking water in Peru.
BACKGROUND & AIMS: An association between water sources and the prevalence of Helicobacter pylori infection in Peruvian children was shown previously. The aim of this study was to confirm the presence of H. pylori in drinking water in the same community. METHODS: Forty-eight drinking water samples from different locations in pueblo jovenes (new towns) near Lima were collected. Samples were frozen until technology advanced to the point to the point at which H. pylori might be reliably detected. Immunomagnetic beads coated with anti-H. pylori immunoglobulin Gs were used to concentrate H. pylori, and two polymerase chain reaction assays based on different H. pylori genes were used. One was a polymerase chain reaction for the detection of the H. pylori adhesin subunit encoding gene, and the second was a previously validated H. pylori 16S ribosomal RNA reverse transcriptase-polymerase chain reaction. RESULTS: The expected 375-base pair fragment from the adhesin gene was amplified from 24 water samples. The expected 500-base pair fragment of the 16S ribosomal RNA and the 375-base pair fragment of the adhesin gene were amplified from 11 of the samples. CONCLUSIONS: These results confirm the presence of H. pylori in drinking water in Peru and are consistent with conclusions from a previous epidemiological study of the same population. This provides additional evidence for waterborne transmission of H. pylori in some environments.
Adhesins, Bacterial↗
Adherence of Helicobacter pylori to areas of incomplete intestinal metaplasia in the gastric mucosa.
BACKGROUND & AIMS: Helicobacter pylori is not usually found in areas of intestinal metaplasia. Thus, the development of intestinal metaplasia has been viewed as a mechanism by which the stomach eliminates H. pylori. The aim of this study was to evaluate the frequency of H. pylori adherence to intestinal metaplasia in different populations. METHODS: Mapped gastric biopsy specimens from 378 H. pylori-positive subjects from various geographical regions were examined. Intestinal metaplasia was typed by staining with periodic acid-Schiff/alcian blue and high-iron diamine/alcian blue. RESULTS: In 32 patients, H. pylori was found in intimate contact with intestinal metaplasia. This was documented by electron microscopy. All areas of intestinal metaplasia showing adherence contained sulfomucins and had no brush border. Posttreatment biopsy specimens from 4 patients whose infection was not cured showed persistence of H. pylori in intestinal metaplasia. CONCLUSIONS: These patients may have a strain of H. pylori with unusual adhesion characteristics, or their type of intestinal metaplasia may have biochemical properties that make it hospitable for H. pylori. The exclusive association of H. pylori adherence with incomplete intestinal metaplasia (a putative precursor of carcinoma) and its greater frequency in Koreans (a population at risk for gastric cancer) suggest that this phenomenon may play a role in the hypothetical sequence metaplasia > dysplasia > carcinoma.
Bacterial Adhesion↗
Ulcer site and complications: relation to Helicobacter pylori infection and NSAID use.
BACKGROUND AND STUDY AIM: The aim of this study was to investigate the relationship between the presence and location of ulcers, H. pylori infection, NSAID use, and major upper gastrointestinal tract bleeding. PATIENTS AND METHODS: We studied 100 consecutive patients with duodenal ulcers and 145 consecutive patients with benign gastric ulcers. RESULTS: Ninety-nine percent of the duodenal ulcer patients and 92% of the gastric ulcer patients had H. pylori infection; all gastric ulcer patients without H. pylori infection were using NSAIDs. Gastric ulcers in patients with H. pylori infection who were not using NSAIDs were more likely to be on the lesser curvature (85%) than ulcers in NSAID users who had no H. pylori infection (35%) (p < 0.01). Conversely, only 5% of gastric ulcers in H. pylori-positive patients who were not using NSAIDs were on the greater curvature, compared to 45% in H. pylori-negative NSAID users (p < 0.01), and 23% in patients with both possible etiologies. The frequency of NSAID use was very high in patients presenting with upper gastrointestinal tract bleeding: 21 of 25 with gastric ulcers (84%) and 13 of 21 with duodenal ulcers (62%; p < 0.01 for each, compared to bleeding without taking NSAIDs). Overall, 74% of patients with upper gastrointestinal hemorrhage from peptic ulcer were taking NSAIDs. The prevalence of H. pylori infection was similar among the ulcer patients presenting with and without upper gastrointestinal tract bleeding. CONCLUSIONS: The location of a gastric ulcer on the greater curvature, and presentation with upper gastrointestinal tract bleeding, are separate and valuable clues to the involvement of NSAIDs. NSAID use may now be responsible for most bleeding complications of ulcer disease, regardless of H. pylori status.
Adult↗
Endoscopic retreatment after successful initial hemostasis prevents ulcer rebleeding: a prospective randomized trial.
BACKGROUND AND STUDY AIMS: Rebleeding after initial endoscopic hemostasis remains an important determinant of poor prognosis in patients with ulcer hemorrhage. Prospective identification of patients who are at high risk for rebleeding, and directing further therapeutic measures in these patients, would be expected to improve the prognosis. PATIENTS AND METHODS: We used our previously described scoring system (the Baylor Bleeding Score) to identify patients at increased risk for rebleeding after initially successful endoscopic hemostasis, and randomized them into retreatment and no-retreatment groups. Patients in the retreatment group received additional endoscopic heat probe therapy at 24 hours, the follow-up was otherwise similar. Forty men with major ulcer hemorrhage were randomized, 19 to the retreatment group and 21 to the no-retreatment group. Patients in the two groups had similar Baylor Bleeding Scores, blood transfusion needs (median three vs. two units), ulcer sites (duodenal 57% vs. 43%), stigmata of hemorrhage (actively bleeding 68% vs 67%), and received similar initial endoscopic therapy (heat probe 240 J vs. 300 J). Patients in the retreatment group received additional heat probe therapy (median 165 J) at 24 hours. RESULTS: Rebleeding, requiring significantly more blood transfusion, occurred in 24% of the no-retreatment group patients compared to none of the retreatment group patients (p < 0.05). CONCLUSIONS: Endoscopic retreatment after successful initial endoscopic hemostasis prevents rebleeding in highrisk patients with ulcer bleeding.
Adult↗
Detection of Helicobacter pylori in paraffin-embedded gastric biopsy specimens by in situ hybridization.
Helicobacter pylori is the causative agent of chronic gastritis, peptic ulcers, and is also associated with gastric cancer. Eradication of H pylori infection has proven to be difficult to confirm. The authors developed a nonradioactive in situ hybridization method for detection of H pylori and compared it with conventional methods for diagnosis of the infection. Reverse transcription followed by polymerase chain reaction (PCR) with two 22-base primers was used to amplify a 520 base pair (bp) segment of 16S rRNA from H pylori. The PCR product was labeled with digoxigenin and used as a probe. Specificity of the probe was tested by dot blot hybridization against DNA from 30 different strains of related and unrelated bacteria. Specificity of in situ hybridization assay was proven by the lack of hybridization on sections with gram negative and positive bacteria other than H pylori, with an unrelated probe, without probe, and after RNase treatment. A random sample of 15 biopsy specimens was blindly studied by in situ hybridization method and the results were compared with those of culture and conventional histology. Comparison of in situ hybridization and conventional histology showed agreement in all 15 specimens (5 negative and 10 positive). Between culture and in situ hybridization there was agreement in 13 cases (8 positive, 5 negative). Two cases were negative by culture but positive by in situ hybridization and histology. Nonradioactive in situ hybridization provides a sensitive and specific method for detection of H pylori infection. It should be particularly useful for confirmation of infection in cases equivocal with other methods, and potentially useful in post-treatment evaluation.
Base Sequence↗
Resolution of a metaplastic duodenal polyp after cure of Helicobacter pylori infection.
Although there have been several reports of hyperplastic gastric polyps associated with persistent Helicobacter pylori gastritis, the association of H. pylori infection with metaplastic polyps in the duodenum has not hitherto been described. After a 52-year-old man had a single episode of hematemesis, endoscopy showed a smooth polyp 1 cm in greatest dimension formed by a proliferation of gastric epithelial cells of fundic and antral type found in the duodenal bulb. The outer surface was entirely covered with a single layer of hyperplastic columnar epithelium with many H. pylori organisms. After administration of metronidazole 500 mg, omeprazole 20 mg for 4 weeks, and clarithromycin 250 mg twice a day for 2 weeks, endoscopy showed a decrease in size of the duodenal polyp. At 12 weeks there was complete regression of the polyp. This report documents a new and unusual finding: resolution of a gastric metaplastic polyp in the duodenum associated with cure of H. pylori.
Anti-Bacterial Agents↗
How accurate is the determination of blood in gastric juice? Comparison of peroxidase and porphyrin methods.
BACKGROUND: Mucosal bleeding is frequently used as a measure of gastric mucosal integrity. We compared the orthotolidine method for quantifying haemoglobin in gastric juice with a method based on measurement of fluorescent porphyrins extracted from haem. We also investigated whether acid or pepsin had a deleterious effect on the results of either method. METHODS: We compared the effects of pH (2 or 7), time (up to 180 min), haemoglobin concentration and the addition of pepsin (2.5, 5 or 7.5 kU/mL hog pepsin) on the accuracy of the two methods. RESULTS: With the orthotolidine method there was a time-dependent decline in detectable haemoglobin concentration (P < 0.02) at pH 2 that was not seen at pH 7. The time- and pH-dependent decline in detectable haemoglobin was not seen using the porphyrin assay. CONCLUSION: The widely used orthotolidine method for determination of blood in gastric juice is less reliable than the porphyrin method as it is more likely to be influenced by acidic conditions in the stomach.
Benzidines↗
Metronidazole, ranitidine and clarithromycin combination for treatment of Helicobacter pylori infection (modified Bazzoli's triple therapy).
BACKGROUND: Multi-drug regimens are generally required to reliably cure Helicobacter pylori infection. Metronidazole, clarithromycin and omeprazole has proven to be an effective combination therapy with a cure rate of 90% or greater. METHODS: We evaluated a 14-day combination regimen for H.pylori infection consisting of metronidazole 500 mg b.d., clarithromycin 250 mg b.d. and ranitidine 300 mg b.d. (MRC) instead of omeprazole. Ranitidine alone was continued for an additional 4 weeks. H. pylori status was determined by rapid urease testing, histopathology using the Genta stain, and by culture at entry and 4 weeks after completing antimicrobial therapy. RESULTS: Twenty-seven patients with documented peptic ulcer disease and H. pylori infection were treated. Five had previously failed macrolide-based antimicrobial therapy; none had received metronidazole. All ulcers were healed at week 6 except one patient taking naproxen; his H. pylori infection was cured. Overall, H. pylori infection was cured in 78% (95% CI = 58-91%). In patients with clarithromycin-sensitive isolates, the cure rate was 20 of 23 (87%, 95% C.I. = 66-97%); only one of four patients (25%) with clarithromycin-resistant isolates was cured. In contrast, four of five patients with metronidazole-resistant isolates were cured (80%). In patients with isolates sensitive to both antibiotics, the cure rate was 16 of 18 (89%, 95% C.I. = 65-99%). Mild side effects were reported by 27%, including diarrhoea and altered taste. Compliance averaged 98%. CONCLUSION: These results suggest that the combination of metronidazole, ranitidine and clarithromycin results in high cure rates in patients with clarithromycin-sensitive isolates. Omeprazole may not be required for Bazzoli's triple therapy; and large multicentre comparative trials are indicated.
Adult↗
Helicobacter: a new scientific journal.
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Campylobacter↗
Atrophic changes of gastric mucosa are caused by Helicobacter pylori infection rather than aging: studies in asymptomatic Japanese adults.
BACKGROUND: The current study was designed to evaluate the effect of aging and Helicobacter pylori infection on the gastric mucosa in asymptomatic Japanese adults. MATERIALS AND METHODS: Eighty-five asymptomatic healthy adults were recruited from a health-screening center in Sapporo. All subjects underwent endoscopy and gastric biopsy, and serum was obtained for IgG antibodies to H. pylori, serum gastrin, and pepsinogen levels. RESULTS: The prevalence of atrophic change of the gastric mucosa assessed by pathological findings increased with age (49% in the 30- to 39-year-old group compared to 89% in those 60 years and older, p < .001). The frequency of intestinal metaplasia also increased with age (38% in the 30- to 39-year-old group compared to 82% in those 60 years and older, p < .001). In contrast, the frequency of atrophic gastritis and intestinal metaplasia was extremely low in the H. pylori seronegative group regardless of age. Mean serum gastrin level in H. pylori-positive adults was significantly greater than in those who were H. pylori-negative (114.3 +/- 11.2 compared to 65.8 +/- 6.5 pg/ml, p < .03). The serum pepsinogen I-II ratio was significantly lower in those with H. pylori infection than in those without (3.1 compared to 6.6, p < .0001). CONCLUSIONS: These results suggest that the chronological changes in the gastric mucosa in Japanese individuals are either entirely related to H. pylori infection or the process is greatly accelerated by H. pylori infection.
Adult↗