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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori is an important factor in the pathogenesis of chronic gastritis and gastroduodenal ulcer disease. However, the basic causal mechanisms of H pylori colonization on the gastric mucosa are still unclear. The authors evaluated the prevalence of H pylori colonization in 266 children who underwent upper gastrointestinal endoscopy during a 12-month period. The indications for endoscopy were follow-up of esophagitis related to gastroesophageal reflux (n = 17), suspicion of gastroesophageal reflux (n = 51), abdominal pain (n = 28), vomiting (n = 30), follow-up of esophageal atresia (n = 46) and duodenal atresia (n = 28), inflammatory bowel disease (n = 28), and miscellaneous (n = 38). The methods used to detect H pylori colonization were histology and the rapid urease test. H pylori colonization was demonstrated in 31 (11.6%) of the 266 patients. In two patient groups, a high prevalence of colonization was identified. In patients with an operated duodenal atresia, 36% (10 of 28) had H pylori on the gastric mucosa. The organism was demonstrated on the gastric mucosa in 47% (8 of 17) of the patients with gastroesophageal reflux-related esophagitis; five of the eight patients had neurological impairment. In the other patient groups, the prevalence of H pylori infection ranged from 2% to 14%. The present study suggests that, in children, the disturbed esophagogastroduodenal motility, which is commonly associated with gastroesophageal reflux and duodenal atresia, predisposes to H pylori infection.
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PMID:Does disordered upper gastrointestinal motility predispose to Helicobacter pylori colonization of the stomach in children? 807 8

Acid peptic disorders, including gastric ulcers, duodenal ulcers, and gastroesophageal reflux disease, are commonly occurring conditions with high direct and indirect costs. The pathogenesis of these disorders involves an imbalance between acid secretion and gastric mucosal defenses. Pharmacologic treatment of acid peptic disorders has focused on correcting this imbalance by either improving mucosal defenses with drugs such as sucralfate, bismuth, and prostaglandin analogs, neutralizing acid with antacids, or decreasing acid secretion with histamine2 (H2)-receptor antagonists, or, more recently, proton pump inhibitors. Proton pump inhibitors are more potent inhibitors of acid secretion than H2-receptor antagonists. In clinical comparisons, proton pump inhibitors were shown to be more effective in the treatment of acid peptic disorders than H2-receptor antagonists. Helicobacter pylori infection is a factor in 85% to 100% of duodenal ulcers and 70% to 90% of gastric ulcers; eradicating this organism results in a considerable decrease in the recurrence of ulcers. Current management of peptic ulcer disease includes the use of combination antisecretory and antibiotic therapy for acute treatment of H pylori-associated disease. Patient self-medication with over-the-counter products, including H2-receptor antagonists, may have an impact on the potential for reducing the recurrence of peptic ulcer disease in patients with H pylori infection. Patients with recurrent disease should be informed of the need to seek medical treatment through aggressive education at the point of sale for over-the-counter drugs.
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PMID:Pathogenesis and treatment of acid peptic disorders: comparison of proton pump inhibitors with other antiulcer agents. 885 51

Available evidence would suggest that Helicobacter pylori infection does not contribute to the pathogenesis of gastro-oesophageal reflux disease. The prevalence of H pylori infection in patients with reflux disease is no greater than that in control populations. There are some data suggesting that the organism has a protective role: patients with duodenal ulcers develop reflux disease after H pylori eradication, whereas in patients with oesophageal reflux those with H pylori infection have less severe reflux changes. There is also evidence indicating that the presence of H pylori augments the anti-secretory properties of both the H2 receptor antagonists and proton pump inhibitors (PPIs), suggesting that eradication therapy may not be beneficial. However, the considerable recent interest in the association between H pylori and reflux disease has largely been generated by studies outlining the interactions between H pylori infection and acid suppression in the long term. In H pylori positive patients, therapy with PPIs is associated with a proximal extension of the infection and its associated gastritis. In addition long term PPI therapy is reported to be associated with an accelerated development of atrophic gastritis, suggesting that H pylori should be diagnosed and treated. Although these latter findings in particular need confirmation, H pylori eradication therapy should be considered in this patient group, at least until there is evidence to the contrary.
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PMID:Different management for Helicobacter pylori positive and negative patients with gastro-oesophageal reflux disease? 976 33

An algorithmic approach to evaluation of dyspepsia or abdominal discomfort begins with differentiation between peptic ulcer disease and gastroesophageal reflux disease as well as recognition of alarm signs and symptoms for gastric cancer, which are indications for early endoscopy. In the absence of alarm symptoms, most patients should undergo noninvasive testing for H pylori infection with a serologic, urea breath, or stool antigen test. Factors to consider in selection of appropriate testing include reliability, specificity, sensitivity, cost, and local access and expertise. As a general rule, physicians should choose a test that has the best accuracy for the level of testing expertise available. The basic principle underlying testing for H pylori is that patients should not undergo testing unless the physician is willing to treat on the basis of a positive test result. In patients who receive treatment, confirmation of cure is important for preventing further morbidity and reducing risk of transmission of infection.
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PMID:Recognizing peptic ulcer disease. Keys to clinical and laboratory diagnosis. 1008 37

Heartburn is a common symptom affecting 21-44% of the adult population on a monthly basis. Oesophagitis is less common, affecting 2% of individuals. Epidemiological studies have shown that patients with gastro-oesophageal reflux disease (GORD) have similar incidence rates of Helicobacter pylori infection as do controls. Some groups have reported that there is a lower incidence, deducing that infection does not cause, and in some way confers protection against GORD. Additional supportive evidence is available from reports of GORD development following successful H pylori eradication. The mechanisms involved are complicated. Individuals with H pylori induced pangastritis and subsequent hypochlorhydria may be protected whereas those with an antral predominant gastritis, as in duodenal ulcer disease, with an increased acid output may be prone to development of GORD. Recent evidence has linked H pylori infection with the development of inflammation of the gastric cardia---carditis. Reports are available which show that carditis is a frequent finding in patients with GORD. The incidence of both cardia and oesophageal carcinoma is increasing. The relation between GORD, carditis, intestinal metaplasia, and cardia carcinoma is unclear. Intestinal metaplasia may result from multifocal atrophic gastritis, linked to H pylori infection or from GORD and the development of Barrett's oesophagus. Long term follow up studies will be required to assess the malignant potential of these histological entities and whether or not H pylori infection has an aetiological role.
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PMID:Gastro-oesophageal reflux disease and Helicobacter pylori: an intricate relation. 1045 30

Dyspepsia is a digestive syndrome distinct from (although frequently overlapping with) gastro-oesophageal reflux disease (GORD) and irritable bowel syndrome (IBS), which is characterised by various combinations of painful and non-painful symptoms arising from the epigastrium. Dyspepsia can be secondary to a variety of diseases, but in most instances it is idiopathic. Helicobacter pylori infection is responsible for the majority of peptic ulcers and of other diseases potentially associated with dyspepsia. Nevertheless, a causal role for H pylori infection in symptom occurrence has not been established. Experimental data indicate that H pylori eradication does not improve symptoms in the majority of dyspeptic patients. It has been proposed recently that H pylori negative patients should be managed according to their clinical presentation. Some reports suggest that taking into consideration the most relevant or "predominant" symptom may help to identify distinct subgroups among dyspeptic patients with different underlying pathophysiological abnormalities and different responses to treatment. Well designed and conducted prospective studies are needed to verify whether treatment of H pylori negative dyspeptic patients based on the predominant symptom actually is a cost effective approach.
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PMID:How should Helicobacter pylori negative patients be managed? 1045 34

Parietal cell protrusion (PCP), swelling and bulging of parietal cells, has been observed in the oxyntic mucosa of patients receiving omeprazole. The frequency of this event and the underlying mechanisms remain to be clarified. As such, it is unknown whether there is a relation with either serum gastrin or Helicobacter pylori infection, and whether PCP predisposes to the development of fundic gland cysts (FGC). We therefore investigated the development of PCP and FGC in gastroesophageal reflux disease (GERD) patients treated with omeprazole and correlated findings to duration of therapy, gastrin, and H pylori infection. In a randomized, double-blinded study, GERD patients were evaluated by endoscopy with biopsy sampling for histology and culture at baseline, and after 3 and 12 months' therapy with omeprazole 40 mg daily. H pylori-positive patients were randomized to additional eradication therapy or placebo antibiotics at baseline. All histological slides were scored blinded for time and outcome of culture for the presence of PCP and FGC. Fasting serum samples from all visits were used for gastrin measurements. The prevalence of PCP increased during omeprazole therapy from 18% at baseline to 79% and 86% at 3 and 12 months (P < .001, baseline v both 3 and 12 months). The prevalence of FGC increased from 8% to 17% and 35% (P < .05, baseline v 12 months). The prevalence of PCP and FGC did not differ among the H pylori-positive and H pylori-negative patients at baseline (PCP 16% v 20% and FGC 7% v 8%, respectively). Whereas H pylori eradication did not significantly affect development of PCP (P = .7), FGC developed significantly more often in the H pylori-eradicated patients when compared with persistent H pylori-positive patients (P < .05). PCP development was related to serum gastrin rise during therapy. In conclusion, PCP occurs in most patients within the first months of omeprazole treatment and is related to increased gastrin levels. FGC develops more gradually and is enhanced by H pylori eradication.
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PMID:Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment. 1115 Mar 84

Infection with Helicobacter pylori is accepted as the primary cause of peptic ulcer disease, and there is evidence to suggest its role in other gastrointestinal disorders. An estimated 20% to 40% of the Canadian population is infected with H pylori; however, clinically relevant disease is present in only approximately 10% to 20% of these individuals. Therefore, it is crucial to identify the diseases for which eradication of H pylori is beneficial to ensure that patients do not receive unnecessary treatment. In patients with ulcers induced by long term treatment with nonsteroidal anti-inflammatory drugs, preliminary results suggest that eradication of H pylori may reduce the risk of peptic ulcer bleeding. Furthermore, a benefit has been observed for the eradication of H pylori before patients commence therapy with a nonsteroidal anti-inflammatory drug. An association between the presence of H pylori and specific dyspeptic symptoms has yet to be established; however, there may be a subset of patients with functional dyspepsia who benefit from the eradication of H pylori. The relationship between gastroesophageal reflux disorder and H pylori infection remains unclear. In Canada, the recommended therapy for the eradication of H pylori is seven days of twice-daily treatment with a proton pump inhibitor, clarithromycin, and amoxicillin or metronidazole. Although the proton pump inhibitors are treated as a class for use in these regimens, there is suggestion that a faster onset of action may lead to a higher rate of eradication.
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PMID:Update on the role of H pylori infection in gastrointestinal disorders. 1133 27

In patients with diseases known to be associated with Helicobacter pylori infection, such as peptic ulcer, treatment of the underlying infection is the standard of care. However, in most major consensus management guidelines, including those published in Canada, widespread testing for H pylori infection is not recommended. This practice is not encouraged because of insufficient evidence of cost-benefit in gastric cancer prevention, the potential for increases in antibiotic resistance and the controversial hypothesis of potential negative effects of eradication in certain clinical entities. For example, there is insufficient evidence to recommend against eradicating H pylori discovered in a patient with symptoms of gastroesophageal reflux disease. The management guidelines designed specifically in Canada should, therefore, continue to be applied, with H pylori diagnosed and treated in appropriately selected patients.
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PMID:Risks and benefits of Helicobacter pylori eradication: current status. 1182 40

There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease-free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.
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PMID:Motion--Helicobacter pylori worsens GERD: arguments for the motion. 1236 15


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