scholarly journals From Bench to Bedside to Bug: An Update of Clinically Relevant Advances in the Care of Persons withHelicobacter pyloriAssociated Diseases

2000 ◽  
Vol 14 (3) ◽  
pp. 188-198 ◽  
Author(s):  
N Chiba ◽  
ABR Thomson ◽  
P Sinclair
Keyword(s):  
Functional Dyspepsia ◽  
International Workshop ◽  
Symptom Relief ◽  
Subsequent Development ◽  
Noninvasive Test ◽  
Ulcer Disease ◽  
Intention To Treat ◽  
Bismuth Citrate ◽  
H Pylori ◽  
The One

In-depth meetings of the XIth International Workshop on Gastroduodenal Pathology andHelicobacter pyloriled to the presentation and discussion of extensive new data onH pyloriand its diseases. The mode of transmission ofH pyloriremains unclear, and it remains unknown why only a small proportion of infected individuals develop duodenal or gastric ulcer disease and even fewer develop gastric cancer. The role ofH pylorieradication in persons with uninvestigated dyspepsia remains controversial. New clinical trials ofH pyloritreatment show symptom relief and improvement in the quality of life of persons with functional dyspepsia, especially in those with ulcer-like or reflux-like dyspepsia. Clearly the move is toward symptom-based management of persons with dyspepsia, with fewer endoscopies being needed in the otherwise healthy young dyspeptic patients. It remains controversial whether eradicatingH pyloriin duodenal ulcer or functional dyspepsia increases the risk of subsequent development of gastroesophageal reflux disease. The one-week proton pump inhibitor-based triple regimens remain the gold standard ofH pyloritherapy, but some of the ranitidine bismuth citrate plus two antibiotic regimens also achieve an 80%H pylorieradication rate on an intention-to-treat basis. While the urea breath test remains the noninvasive test of choice, interesting new data are available on the use of stool antigen testing to diagnoseH pyloriinfection. The number ofH pylori-associated gastroduodenal diseases grows to include possible liver, vascular, immune and skin conditions.

scholarly journals A Randomized Trial Comparing Seven-Day Ranitidine Bismuth Citrate and Clarithromycin Dual Therapy to Seven-Day Omeprazole, Clarithromycin and Amoxicillin Triple Therapy for the Eradication ofHelicobacter pylori

2003 ◽  
Vol 17 (9) ◽  
pp. 533-538 ◽  
Author(s):  
Sander Veldhuyzen van Zanten ◽  
Naoki Chiba ◽  
Alan Barkun ◽  
Carlo Fallone ◽  
Alain Farley ◽  
...  
Keyword(s):  
Dual Therapy ◽  
Success Rates ◽  
Open Label ◽  
Treatment Allocation ◽  
Ulcer Disease ◽  
Intention To Treat ◽  
Bismuth Citrate ◽  
The Difference ◽  
H Pylori

OBJECTIVE: To assessHelicobacter pylorieradication after one week dual ranitidine bismuth citrate-clarithromycin (RBC-C) or triple omeprazole, clarithromycin and amoxicillin (OCA) therapy.METHODS: In this multicentre Canadian trial,H pylori-positive patients with functional dyspepsia or inactive peptic ulcer disease were randomized to open-label treatment with RBC-C (ranitidine bismuth citrate 400 mg plus clarithromycin 500 mg) or OCA (omezaprole 20 mg, clarithromycin 500 mg and amoxicillin 1000 mg), given twice a day for seven days. Treatment allocation was randomly assigned.H pyloriinfection was confirmed by positive13C-urea breath test (13C-UBT).H pyloristatus was reassessed by UBT at least four and 12 weeks after treatment (negative: δ13CO2below 3.5 per mil). Intention-to-treat (ITT) eradication rates were determined for all patients with confirmedH pyloriinfection. Per protocol (PP) rate was determined for all patients treated with at least two evaluable follow-up visits.RESULTS: Three hundred five patients were included in the ITT and 222 in the PP analysis. The ITT eradication rates were 66% for RBC-C and 78% for OCA. The PP success rates were 84% for RBC-C and 96% for OCA. The difference for both ITT 12% (95% CI 2 to 22) and PP 12% (95% CI 4 to 19) were statistically significant, P=0.030 and P=0.007, respectively. Treatment was generally well tolerated.CONCLUSION: The eradication rate for the seven-day dual RBC-C regimen was lower than that for OCA.

H. pyloristimulates gastrin release from canine antral cells in primary culture

1998 ◽  
Vol 274 (6) ◽  
pp. G992-G996 ◽  
Author(s):  
Frank S. Lehmann ◽  
Neal Schiller ◽  
Timothy Cover ◽  
Ritchard Hatch ◽  
Rein Seensalu ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Subsequent Development ◽  
Surface Proteins ◽  
Gastrin Release ◽  
Soluble Factor ◽  
Ulcer Disease ◽  
G Cells ◽  
Gastrin Secretion ◽  
H Pylori ◽  
Stimulation Of

Patients chronically infected with Helicobacter pylori are known to have hypergastrinemia. Previous studies have demonstrated the stimulation of gastrin from isolated G cells by monocytes and cytokines. The aim of this study was to determine if H. pylori can directly stimulate gastrin secretion. The secretion of gastrin from canine G cells in 48-h primary cultures was investigated using either live H. pylori bacteria or various bacterial extracts from three well-characterized strains. Whole bacterial sonic extracts and water-extracted surface proteins, but not PBS extracts, from strains 43579 (CagA+/VacA+), 60190 (CagA+/VacA+), and 60190:v1 (CagA+/VacA−) significantly stimulated gastrin release. Controls demonstrated that gastrin stimulation by the sonic extracts was not due to a direct toxic effect on G cells. We conclude that H. pylori produces a soluble factor(s), which can directly stimulate gastrin release in enriched canine G cell cultures. This stimulatory effect may play an important role in the H. pylori-associated hypergastrinemia and subsequent development of peptic ulcer disease.

scholarly journals The Role of Interleukin-1Beta and Other Potential Genetic Markers as Indicators of Gastric Cancer Risk

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 8B-12B ◽  
Author(s):  
Esther Troost ◽  
Georgina L Hold ◽  
Malcolm G Smith ◽  
Wong-Ho Chow ◽  
Charles S Rbkin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Clinical Outcome ◽  
Genetic Factors ◽  
Interleukin 1 ◽  
Subsequent Development ◽  
Ulcer Disease ◽  
Increased Risk ◽  
Host Genetic ◽  
H Pylori ◽  
Host Genetic Factors

Helicobacter pyloriinfects half of the world’s population, and is associated with asymptomatic gastritis and also with more serious conditions such as peptic ulcer disease and gastric carcinoma. The clinical outcome is largely dependent on the severity and distribution of theH pylori-induced gastritis, but the pathogenesis remains poorly understood. Bacterial virulence factors and environmental influences contribute to the pathogenesis, but do not explain the divergent outcomes. There is emerging evidence that host genetic factors play a key role in determining the clinical outcome ofH pyloriinfection. In particular, proinflammatory genotypes of the interleukin-1 beta (IL-1β) gene are associated with an increased risk of gastric cancer and its precursors. The effects are most likely mediated through the induction of hypochlorhydria and severe corpus gastritis with the subsequent development of gastric atrophy. The roles of IL-1β and other host genetic factors in the pathogenesis ofH pylorirelated cancer are discussed in this article.

The effect of H pylori eradication on symptom relief in patients with functional dyspepsia

1995 ◽  
Vol 108 (4) ◽  
pp. A997
Author(s):  
MM Ozmen ◽  
RS Patankar ◽  
CD Johnson
Keyword(s):  
Functional Dyspepsia ◽  
Symptom Relief ◽  
H Pylori

scholarly journals Comparison of Salivary and Serum Enzyme Immunoassays for the Diagnosis ofHelicobacter pyloriInfection

1998 ◽  
Vol 9 (5) ◽  
pp. 277-280
Author(s):  
John M Embil ◽  
Shurjeel H Choudhri ◽  
Gerry Smart ◽  
Thomas Aldor ◽  
Norman M Pettigrew ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Negative Predictive Value ◽  
Predictive Value ◽  
Antibody Detection ◽  
Upper Gastrointestinal Endoscopy ◽  
Noninvasive Test ◽  
Ulcer Disease ◽  
Enzyme Immunoassays ◽  
H Pylori

Infection withHelicobacter pylorihas been established as an important risk factor for the development of peptic ulcer disease, gastritis and gastric cancer. The diagnosis ofH pyloriinfection can be established by invasive or noninvasive techniques. Two noninvasive enzyme immunoassays (EIAs) for antibody detection – HeliSal and Pylori Stat – were compared with histology. Both assays detect immunoglobulin (Ig) G directed against purifiedH pyloriantigen. The test populations consisted of 104 consecutive patients scheduled for upper gastrointestinal endoscopy. Of these patients, 97 (93%) had symptoms compatible with peptic ulcer disease. Saliva and serum were collected simultaneously at the time of endoscopy. Salivary EIA had a sensitivity of 66%, specificity of 67%, positive predictive value of 67% and negative predictive value of 66% compared with the serum EIA, where the results were 98%, 48%, 64% and 96%, respectively. Although the salivary EIA is an appealing noninvasive test, it was not a sensitive and specific assay. The serum EIA also lacked specificity, but was highly sensitive with a good negative predictive value. Although a negative serum EIA rules outH pyloriinfection, a positive result must be interpreted in the clinical context and confirmed with a more specific measure.

scholarly journals Rescue Therapy with Furazolidone in Patients with at Least Five Eradication Treatment Failures and Multi-Resistant H. pylori infection

Antibiotics ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1028
Author(s):  
Elena Resina ◽  
Javier P. Gisbert
Keyword(s):  
Adverse Effects ◽  
Rescue Therapy ◽  
Efficacy And Safety ◽  
Stool Antigen Test ◽  
Ulcer Disease ◽  
Intention To Treat ◽  
Rescue Treatment ◽  
Resistant Infection ◽  
Stool Antigen ◽  
H Pylori

Helicobacter pylori infection may persist after multiple eradication treatments. The aim of this study was to evaluate the efficacy and safety of a furazolidone-based rescue regimen in hyper-refractory patients. A unicentre, prospective study was designed. Patients in whom five or more treatments had consecutively failed were included. All patients had previously received bismuth and key antibiotics, such as amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and rifabutin, and had positive H. pylori culture, demonstrating resistance to clarithromycin, metronidazole, and levofloxacin. A quadruple regimen with furazolidone (200 mg), amoxicillin (1 g), bismuth (240 mg), and esomeprazole (40 mg) was prescribed twice a day for 14 days. Eradication was confirmed by the stool antigen test. Compliance was determined through questioning, and adverse effects using a questionnaire. Eight patients (mean age 56 years, 63% men, 38% peptic ulcer disease, 12% gastric cancer precursor lesions, and 50% functional dyspepsia) were included. Per-protocol and intention-to-treat eradication rates were 63%. Compliance was 100%. Adverse effects were reported in two (25%) patients, and all were mild. Even after five or more previous H. pylori eradication failures, and a multi-resistant infection, rescue treatment with furazolidone may be effective in approximately two-thirds of the cases, constituting a valid strategy after multiple previous eradication failures with key antibiotics such as clarithromycin, metronidazole, tetracycline, levofloxacin, and rifabutin.

scholarly journals A Comparison between 10-day and 12-day Concomitant Regimens for Helicobacter Pylori Eradication: A Randomized Clinical Trial

2020 ◽  
Vol 12 (2) ◽  
pp. 106-110
Author(s):  
Zohreh Bari ◽  
Hafez Fakheri ◽  
Tarang Taghvaei ◽  
Mohammad Yaghoobi
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Bacterial Infections ◽  
Good Alternative ◽  
Concomitant Therapy ◽  
Ulcer Disease ◽  
Intention To Treat ◽  
H Pylori ◽  
Cost Of Drugs

BACKGROUND Helicobacter pylori (H. pylori) infection is one of the most common bacterial infections worldwide, which is associated with peptic ulcer disease and gastric cancer. In this study, we compared the efficacy of 10-day versus 12-day concomitant therapy as the first-line treatment for H. pylori eradication in Iran. METHODS 218 patients with peptic ulcer disease and naïve H. pylori infection, were randomly divided into two groups to receive either 10-day or 12-day concomitant regimens, composed of pantoprazole 40 mg, amoxicillin 1000 mg, clarithromycin 500 mg, and metronidazole 500 mg, all given twice daily. Eight weeks after treatment, H. pylori eradication was assessed by 14C- urea breath test. The trial was registered in the Iranian Registry of Clinical Trials (code: IRCT20170521034070N2). RESULTS 212 patients completed the study. According to the intention to treat analysis, the eradication rates were 83.6% (95% CI: 76.6-90.5) and 88.8% (95% CI: 82.8-94.7) in 10-day and 12-day concomitant therapy groups, respectively (p = 0.24). Per-protocol eradication rates were 85.9% (95% CI: 79.3–92.4) and 92.6% (95% CI: 87.6–97.5), respectively (p = 0.19). The rates of severe side effects were not statistically different between the two groups (3.6% vs. 8.1%; p = 0.428). CONCLUSION 12-day concomitant therapy could achieve ideal eradication rates by both intention to treat and perprotocol analyses. In order to reduce the cost of drugs and the rate of adverse effects of therapy, among 10-day and 12day regimens, 12-day concomitant therapy seems to be a good alternative to 14-day concomitant therapy that has been suggested by international guidelines.

scholarly journals CanadianHelicobacter pyloriConsensus Conference Update: Infections in Adults

1999 ◽  
Vol 13 (3) ◽  
pp. 213-217 ◽  
Author(s):  
RH Hunt ◽  
CA Fallone ◽  
ABR Thomson ◽  
Canadian Helicobacter Study Group
Keyword(s):  
Breath Test ◽  
Consensus Conference ◽  
Urea Breath Test ◽  
Antibiotic Resistant ◽  
Ulcer Disease ◽  
Consensus Document ◽  
Bismuth Citrate ◽  
The Subject ◽  
H Pylori ◽  
Study Group Meeting

The first CanadianHelicobacter pyloriConsensus Conference took place in April 1997. The initial recommendations of the conference were published in early 1998. An update meeting was held in June 1998, and the present paper updates and complements the earlier recommendations. Key changes included the following: the recommendation for testing and treatingH pyloriinfection in patients with known peptic ulcer disease was extended to testing and treating patients with ulcer-like dyspepsia; it was decided that the urea breath test (not serology) should be used for routine diagnosis ofH pyloriinfection unless endoscopy is indicated for another reason; and recommended therapies were a twice daily, seven-day regimen of a proton pump inhibitor (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) or ranitidine bismuth citrate 400 mg, plus clarithromycin 500 mg and amoxicillin 1000 mg, or plus clarithromycin 500 or 250 mg and metronidazole 500 mg. The need was reiterated to have funding for readily accessible, accurate testing forH pyloriinfection with the urea breath test. It was strongly recommended that regional centres be established to monitor the prevalence of antibiotic-resistantH pyloriinfections. The initial consensus document referred to pediatric issues that were not addressed in this update but were the subject of a subsequent CanadianHelicobacterStudy Group meeting, and will be published later in 1999.

Vacuoles Induced in Mammalian Cells by Helicobacter Cytotoxin are Acidic Organelles

1990 ◽  
Vol 48 (3) ◽  
pp. 168-169
Author(s):  
M. H. Chestnut ◽  
C. E. Catrenich
Keyword(s):  
Acridine Orange ◽  
Mammalian Cells ◽  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Ulcer Disease ◽  
Gastroduodenal Disease ◽  
H Pylori

Helicobacter pylori is a non-invasive, Gram-negative spiral bacterium first identified in 1983, and subsequently implicated in the pathogenesis of gastroduodenal disease including gastritis and peptic ulcer disease. Cytotoxic activity, manifested by intracytoplasmic vacuolation of mammalian cells in vitro, was identified in 55% of H. pylori strains examined. The vacuoles increase in number and size during extended incubation, resulting in vacuolar and cellular degeneration after 24 h to 48 h. Vacuolation of gastric epithelial cells is also observed in vivo during infection by H. pylori. A high molecular weight, heat labile protein is believed to be responsible for vacuolation and to significantly contribute to the development of gastroduodenal disease in humans. The mechanism by which the cytotoxin exerts its effect is unknown, as is the intracellular origin of the vacuolar membrane and contents. Acridine orange is a membrane-permeant weak base that initially accumulates in low-pH compartments. We have used acridine orange accumulation in conjunction with confocal laser scanning microscopy of toxin-treated cells to begin probing the nature and origin of these vacuoles.

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