Helicobacter pylori Infection and Upper Gastrointestinal Disorders (original) (raw)
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Helicobacter pylori colonizes and grows in human gastric epithelial tissue and mucus. Its presence is associated with gastritis and there is substantial evidence that it causes peptic and duodenal ulcers and chronic gastritis. Since 1994, H. pylori has been classified as carcinogenic to humans. Helicobacter pylorus infection is one of the most common bacterial infections world wide.Nearly 50% of the world's population is affected. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignancy and dyspeptic symptoms.4 Majority of H. pylori infected persons remain asymptomatic. Approximately 10-15% of the infected persons develop associated illnesses, 1 to 10% developing peptic ulcer disease, 0.1 to 3% developing gastric cancer and less than 0.01% developing gastric mucosaassociated lymphoid tissue (MALT) lymphoma.
Eradication of Helicobacter pylori for the prevention of peptic ulcer rebleeding
Alimentary Pharmacology & Therapeutics, 2008
Aim: To evaluate the effect of Helicobacter pylori eradication on ulcer bleeding recurrence in a prospective, long-term study including more than 400 patients. Methods: Patients with peptic ulcer bleeding were prospectively included. H. pylori infection was confirmed by rapid urease test, histology or 13 C-urea breath test. Several eradication regimens were used. Ranitidine 150 mg was administered daily until eradication was confirmed by breath test 8 weeks after completing eradication therapy. Patients with therapy failure received a second or third course of therapy. Patients with eradication success did not receive maintenance anti-ulcer therapy, and were controlled yearly with a repeated breath test. Results: Four hundred and twenty-two patients were followed up for at least 12 months, with a total of 906 patient-years of follow up. Mean age was 59 years, and 35% were previous nonsteroidal anti-inflammatory drug (NSAID) users. Sixty-nine percent had duodenal, 24% gastric, and 7% pyloric ulcer. Recurrence of bleeding was demonstrated in two patients at 1 year (incidence: 0.22% per patient-year of follow up), which occurred after NSAID use in both cases. Conclusion: Peptic ulcer rebleeding does not occur in patients with complicated ulcers after H. pylori eradication. Maintenance anti-ulcer (antisecretory) therapy is not necessary if eradication is achieved.
Current consensus on the diagnosis and treatment of H. pylori-associated gastroduodenal disease
The Keio Journal of Medicine, 2003
Helicobacter pylori (H. pylori) is a spiral shaped bacterium that resides in the stomach mucosa. Isolation of H. pylori from the stomach mucosa changed the erstwhile widely held belief that the stomach contains no bacteria and is actually sterile. Once H. pylori is safely ensconced in the mucus, it is able to neutralize the acid in the stomach by elaborating an enzyme called urease. Urease converts urea, of which there is an abundant supply in the stomach (derived from saliva and the gastric juice), into bicarbonate and ammonia, which are strong bases. These bases form a cloud of acid neutralizing chemicals in the vicinity of the organisms, protecting them from the acid in the stomach. This urea hydrolysis reaction is utilized for the diagnosis of H. pylori infection in the urea breath test (UBT) and the rapid urease test (RUT). In Japan, both invasive tests, such as bacterial culture, histopathology and RUT, and non-invasive tests such as UBT and serology are conducted for the diagnosis of H. pylori infection. For confirming the results of eradication therapy, UBT is considered to be the most sensitive and specific. In order to treat H. pylori infection, a new one-week triple therapy regimen (lansoprazole or omeprazole+amoxicillin+clarithromycin) has been approved for use in patients with peptic ulcer disease in Japan. As for H. pylori eradication in the case of other diseases in which the bacterium has been implicated (e.g., chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, non-ulcer dyspepsia, chronic urticaria, idiopathic thrombocytopenic purpura (ITP)), further basic and clinical investigation is required.
Background: The use of triple therapy regimen for Helicobacter pylori (H. pylori) eradication is a highly efficacious, gold standard regimen. In the current study we have evaluated the H. pylori eradication rate following a triple therapy regimen that include pantoprazole, clarithromycin, amoxycillin. Objectives: To evaluate the efficacy, safety and compliance of a triple therapy regimen with a PPI, amoxicillin and clarithromycin for the eradication of H. pylori. Materials and methods: A total of 140 patients diagnosed with dyspepsia and H. pylori infection as documented by the rapid urease test (RUT) were treated with the following triple therapy regimen: pantoprazole (40mg ,12h), amoxycillin (1000 mg/12h),clarithromycin (500mg/12h) for a two-week period.Our primary expected outcome was H. pylori eradication as established by a negative rapid urease test at least six weeks after the end of treatment. Results: 122 patients could complete the treatment and follow-up protocol. H. Pylori eradication rate was 83.6%. Triple therapy regimen had a similar effect in women (82.9%) and men (83.8%) for the eradication of H. pylori, which was not statistically significant. H. pylori eradication rates according to age groups were: 18-30 years (96%), 31-40 years (85.7%), 41-50 years (81.8%) and 51-60 years(76.7%) with metallic taste being the most common side effect. Conclusions:Two week triple therapy regimen consisting of pantoprazole, clarithromycin and amoxycillin is a simple and effective approach to the cure of H. pylori infection in patients with peptic ulcer disease. In those patients who took the drugs as prescribed the H. pylori cure rate was 83.6 %,.
Helicobacter pylori infection and peptic ulcer disease
Current Opinion in Gastroenterology, 1993
Nearly all peptic ulcers are caused by either Helicobacter pylori infection or the use of non-steroidal anti-inflammatory drugs (NSAIDs), which include aspirin. As H. pylori infection is becoming less prevalent in developed countries, NSAIDs are an increasingly important cause of ulceration, including ulcers complicated by gastrointestinal (GI) bleeding. Only about 15% of H. pylori-infected people develop an ulcer in their lifetime, with the risk determined by virulence of the H. pylori strain, host genetics and environment (particularly smoking). NSAID-induced ulcers are largely the result of suppression of gastroprotective cyclooxygenase (COX)-1. The presence and type of ulcers cannot be accurately predicted from symptoms, and the differential diagnosis is broad. Older dyspeptic patients and those with 'alarm' symptoms or signs require upper GI endoscopy to exclude upper GI cancer and make a diagnosis. Younger patients with simple dyspepsia are treated empirically with a course of proton pump inhibitors (PPIs) or an H. pylori 'test-and-treat' strategy. For H. pylori-associated ulcers, H. pylori eradication treatment induces healing and prevents relapse. NSAID ulcers are treated by NSAID withdrawal and a course of PPI; NSAID-naive users requiring continuing treatment who are positive for H. pylori need bacterial eradication, whereas others should be prescribed a concomitant PPI or selective COX-2 inhibitor. Treatment of functional dyspepsia is difficult and requires a multifactorial approach.
Alimentary Pharmacology and Therapeutics, 2002
Background: Guidelines on the management of Helicobacter pylori, which cover indications for management and treatment strategies, were produced in 2000. Aims: To update the guidelines at the European Helicobacter Study Group (EHSG) Third Maastricht Consensus Conference, with emphasis on the potential of H pylori eradication for the prevention of gastric cancer. Results: Eradication of H pylori infection is recommended in (a) patients with gastroduodenal diseases such as peptic ulcer disease and low grade gastric, mucosa associated lymphoid tissue (MALT) lymphoma; (b) patients with atrophic gastritis; (c) first degree relatives of patients with gastric cancer; (d) patients with unexplained iron deficiency anaemia; and (e) patients with chronic idiopathic thrombocytopenic purpura. Recurrent abdominal pain in children is not an indication for a ''test and treat'' strategy if other causes are excluded. Eradication of H pylori infection (a) does not cause gastro-oesophageal reflux disease (GORD) or exacerbate GORD, and (b) may prevent peptic ulcer in patients who are naïve users of non-steroidal antiinflammatory drugs (NSAIDs). H pylori eradication is less effective than proton pump inhibitor (PPI) treatment in preventing ulcer recurrence in long term NSAID users. In primary care a test and treat strategy using a noninvasive test is recommended in adult patients with persistent dyspepsia under the age of 45. The urea breath test, stool antigen tests, and serological kits with a high accuracy are non-invasive tests which should be used for the diagnosis of H pylori infection. Triple therapy using a PPI with clarithromycin and amoxicillin or metronidazole given twice daily remains the recommended first choice treatment. Bismuth-containing quadruple therapy, if available, is also a first choice treatment option. Rescue treatment should be based on antimicrobial susceptibility. Conclusion: The global burden of gastric cancer is considerable but varies geographically. Eradication of H pylori infection has the potential to reduce the risk of gastric cancer development.
The role of an aggressive factor in peptic ulcer disease (pud)
African Journal of Infectious Diseases, 2010
The stomach is the expanded part of the digestive tract between the esophagus and the small intestine. It acts as a reservoir and has chief function in enzymatic digestion. Several types of glands provide different types of secretions in the alimentary tract most of which act as lubricant and to protect the stomach mucosa from excoriation. The pathophysiology of peptic ulcer disease (PUD) is often described as an imbalance between aggressive factors and mucosal protective mechanisms. Helicobacter pylori, a gram-negative organism that has been identified as a potential causative agent in the pathogenesis of peptic ulcer disease, which is diagnosed by invasive or non-invasive methods. Three classes of drugs have been shown to have a direct effect on Helicobacter pylori: antibiotics, bismuth salts, and proton pump inhibitors. Because Helicobacter pylori is difficult to eradicate, most treatment regimes combine agents from two or even all three of these cases. In all of them, patients with active peptic disease should also receive a total of 6 weeks of acid suppression with an H 2 -receptor antagonist. The discovery of Helicobacter pylori as a gastrointestinal pathogen has had a profound effect on current concepts of the pathogenesis and treatment of peptic ulcer disease.