The control of gastric acid and Helicobacter pylori eradication (original) (raw)
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Alimentary Pharmacology & Therapeutics, 2007
Helicobacter pylori is uniquely adapted to survival in the strongly acidic gastric lumen. In vitro, both acid and certain acid suppressors affect bacterial growth. In vivo, there is little evidence that acid suppressors have any effect on bacterial survival. In contrast, decrease of acid secretion quickly leads to a spreading of the bacterial infection throughout the body and fundus of the stomach, which is accompanied by an increase of the associated gastritis.
Current indications for acid suppressants in Helicobacter pylori -negative ulcer disease
Bailliere X027 S Best Practice and Research in Clinical Gastroenterology, 2001
Although Helicobacter pylori infection remains the single most common cause of peptic ulcer, an increasing proportion of patients have H. pylori-negative ulcers. The proportion is higher in the USA ± and possibly Australia ± than elsewhere. Although the precise aetiology of these ulcers is often unknown, some are caused by the use of aspirin or non-steroidal anti-in¯ammatory drugs. In areas with a high prevalence of H. pylori-negative ulcers, the empirical treatment of H. pylori infection for newly diagnosed peptic ulcer disease should be discouraged. All such patients should have documentation of their H. pylori status before treatment. Patients with H. pylori-negative ulcers may have the more serious ulcer diathesis and are likely to require long-term management with acid-suppressing drugs. Proton pump inhibitors are likely to be the drugs of choice; patients may be relatively refractory to H 2-receptor antagonists. The optimal duration of treatment is unde®ned but might be lifelong. There are no prospective studies of the ecacy of surgery or mucosal-protective agents in the treatment of H. pylorinegative ulcers.
Triple Drug Therapy with Proton Pump Inhibitor a Better Option for Helicobacter Pylori Eradication
Medico-Legal Update, 2020
H.Pylori is a gram-negative micro organism residing in the stomach of human. It is a important cause of acidpeptic disorders. Bismuth based triple therapy,triple therapy regimens (Tripple PPI) and Quadruple therapyare the available treatment options to eradicate H. pylori. Controversy still presents regarding the superiorityof treatment modality and results of available studies are variable. Hence this study was undertaken toevaluate and compare the efficacy of triple PPI, Quadruple therapy, and bismuth-based triple therapy intreating acid peptic disorders and Helicobacter pylori eradication. Method: This study was a prospectiveinterventional. After the establishment of a clinical diagnosis of the acid peptic disorder, the patient wasposted for endoscopy. H. pylori status was determined by the rapid urease test and culture examination.All patients divided into three groups and offered three different medical treatments the first group receivedbismuth bases triple therapy, the second...
Proton Pump Inhibitors and Helicobacter pylori Gastritis: Friends or Foes?
Basic & Clinical Pharmacology & Toxicology, 2006
H. pylori gastritis and gastric acid closely interact. In H. pylori-positive patients, profound acid suppressive therapy induces a corpus-predominant pangastritis, which is associated with accelerated corpus gland loss and development of atrophic gastritis. Both corpus-predominant and atrophic gastritis have been associated with an increased risk of development of gastric cancer. H. pylori eradication leads to resolution of gastritis and may induce partial regression of pre-existent gland loss. H. pylori eradication does not aggravate GERD nor does it impair the efficacy of proton pump inhibitor maintenance therapy for this condition. This is the background of the advise within the European guidelines for the management of H. pylori infection to offer an H. pylori test and treat policy to patients who require proton pump inhibitor maintenance therapy for GERD. As such a policy fully reverses H. pylori pangastritis even in patients who have been treated for years with proton pump inhibitors, there is no need to eradicate H. pylori before the start of proton pump inhibitors. In fact, the somewhat slower initial response of H. pylori-negative GERD patients to proton pump inhibitor therapy and the fact that many GERD patients will only require short-term therapy suggests to first start the proton pump inhibitor, and only test and treat when maintenance therapy needs to be prescribed. Such considerations prevent the persistent presence of active corpus-predominant gastritis in proton pump inhibitor-treated reflux patients without impairing the clinical efficacy of treatment.
Helicobacter pylori survival in gastric mucosa by generation of a pH gradient
Biophysical Journal, 1997
Helicobacter pylori has been established as the major causative agent of human active gastritis and is an essential factor in peptic ulcer disease and gastric cancer. The mechanism that has been proposed for H. pylori to control its inhospitable microenvironment happens to coincide with the pH control technique developed by us. This technique was developed to separate an acidic environment from a basic environment for a sequential enzymatic reaction by the hydrolysis of urea within a thin layer of immobilized urease. In this paper, a mathematical model is presented to consider how H. pylori survives the gastric acidity. The computed results explain well the experimental data available involving H. pylori.
Helicobacter, 2015
BackgroundProton‐pump inhibitor (PPI) consumption does lead to false‐negative results of Helicobacter pylori diagnostic tests such as biopsy culture and rapid urease test (RUT).Materials and MethodsHelicobacter pylori isolates from 112 dyspeptic patients with (56.5%) or without (43.5%) PPI consumption were recruited for examining the negative effects of omeprazole (OMP), lansoprazole (LPZ), and pantoprazole (PAN) on H. pylori viability, morphology, and urease, in vitro. The effect of a sublethal concentration of OMP on bacterial features and their recovery after removal of OMP was also assessed.ResultsOf 112 culture‐positive gastric biopsies, 87.5% were RUT positive and 12.5% RUT negative. There was a significant correlation between negative RUT results and PPI consumption (p < .05). OMP (minimum inhibitory concentration, MIC 32 μg/mL) and LPZ (MIC 8 μg/mL) inhibited the growth of 78.6% of H. pylori isolates. OMP and LPZ inhibited urease of 90.3% of isolates between 0 and 40 minu...
Changing Patterns of Helicobacter pylori Gastritis in Long-Standing Acid Suppression
Helicobacter, 2000
Helicobacter pylori colonization and associated inflammation are influenced by local acid output. Infected subjects with acid-related diseases, such as gastroesophageal reflux disease (GERD) are likely to have an antral-predominant gastritis. We hypothesized that long-term acid suppression would result in relatively greater bacterial colonization in the corpus leading to diffuse or corpus-predominant gastritis and that this would be prevented by prior H. pylori eradication. Materials and Methods. To investigate this, we conducted a prospective, double-blind trial of the effect on gastric histology of 12-month maintenance treatment with omeprazole in H. pylori -positive GERD patients randomly assigned to either an eradication or omeprazole-alone regime. A control group of 20 H. pylori -negative GERD patients also received omeprazole throughout the study period. Biopsies taken at baseline and at 12 months were graded "blind" by a single observer according to the updated Sydney System. The 41 H. pylori -positive subjects with grade B or C esophagitis were randomly assigned (20 to omeprazole alone, 21 to erad-
Gut, 2010
Background and aims-Helicobacter pylori infection of gastric mucosa causes gastritis and transient hypochlorhydria, which may provoke emergence of a mucosal precancer phenotype; H pylori strains containing a cag pathogenicity island (PAI) augment cancer risk. Acid secretion is mediated by the catalytic α subunit of parietal cell H,K-ATPase (HKα). In AGS gastric epithelial cells, H pylori induces nuclear factor-κB (NF-κB) binding to and repression of transfected HKα promoter activity. This study sought to identify bacterial genes involved in HKα repression and to assess their impact on acid secretion.
Helicobacter pylori containing only cytoplasmic urease is susceptible to acid
Infection and immunity, 1998
Helicobacter pylori, an important etiologic agent in a variety of gastroduodenal diseases, produces large amounts of urease as an essential colonization factor. We have demonstrated previously that urease is located within the cytoplasm and on the surface of H. pylori both in vivo and in stationary-phase culture. The purpose of the present study was to assess the relative contributions of cytoplasmic and surface-localized urease to the ability of H. pylori to survive exposure to acid in the presence of urea. Toward this end, we compared the acid resistance in vitro of H. pylori cells which possessed only cytoplasmic urease to that of bacteria which possessed both cytoplasmic and surface-localized or extracellular urease. Bacteria with only cytoplasmic urease activity were generated by using freshly subcultured bacteria or by treating repeatedly subcultured H. pylori with flurofamide (1 microM), a potent, but poorly diffusible urease inhibitor. H. pylori with cytoplasmic and surface-...