Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Barrett esophagus is a metaplastic condition that affects the lower esophagus and is a complication of gastroesophageal reflux disease (GERD). Under normal circumstances, the reflux of gastric contents into the esophagus is prevented by a complex barrier at the esophagogastric junction. Dysfunction of the lower esophageal sphincter and the presence of a hiatal hernia lead to failure of this barrier. Esophageal mucosal damage results from the chronic exposure of the esophageal mucosa to gastroduodenal contents and the lack of an effective mucosal defense. This article is an overview of the dysfunction of the esophagogastric junction that leads to GERD. The role of the contents of the reflux and that of Helicobacter pylori infection in the pathogenesis of Barrett esophagus are also summarized.
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PMID:Pathogenesis of gastroesophageal reflux and Barrett esophagus. 1121 15

The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma have increased in recent years as the incidence of peptic ulcer disease and distal gastric cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. Although H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism in which H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.
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PMID:GERD and H. pylori: is there a link? 1121 51

The precise role of Helicobacter pylori infection in gastroesophageal reflux disease (GERD) is a matter of intense debate. Twenty-four-hour esophageal pH monitoring has a higher accuracy than endoscopy for the diagnosis of GERD, but the correlation between H. pylori infection and esophageal pH-metric parameters has almost never been assessed. Therefore, we evaluated the relationship between the infection and the presence of disturbances not only in endoscopy but also in 24-hour esophageal pH monitoring. One hundred consecutive patients undergoing 24-hour esophageal pH monitoring because of symptoms suggestive of GERD were included in the study. Esophageal manometry was carried out to study the position and the pressure of the lower esophageal sphincter (LES). Prevalence of H. pylori infection was evaluated by histology (hematoxylin and eosin stain) and rapid urease test. The mean age of the patients was 50 +/- 15 years; 50% were men and 56% had an abnormal pH-metry (DeMeester score more than 14.7). The prevalence of H. pylori in patients with abnormal pH-metry was 57% (95% CI, 42-70%) and was 52% (95% CI, 39-64%) in those with normal pH-metry (nonsignificant differences [NS]). In the multivariate analysis, H. pylori infection did not correlate with an abnormal pH-metry (odds ratio, 0.8; 95% CI, 0.4-1.8; NS). The proportion of cases with abnormal pH-metry among infected patients was 54% (95% CI, 41-66%) and was 59% (95% CI, 44-72%) among uninfected patients (NS). Mean values of pH-metric parameters (+/-SD), respectively for H. pylori-positive and -negative patients, were total score (30 +/- 33 vs. 36 +/- 38), number of reflux episodes (7 +/- 7 vs. 11 +/- 11), number of episodes more than 5 minutes (3.7 +/- 5 vs. 3.8 +/- 5), longest reflux episode (2.4 +/- 2 minutes vs. 3.1 +/- 3 minutes), and fraction time (%) with pH less than 4 (total, 6 +/- 7 vs. 6.8 +/- 8; upright, 3.9 +/- 4 vs. 4.5 +/- 5; supine, 7.4 +/- 12 vs. 7.2 +/- 10) (all findings were NS). Endoscopic findings, respectively for H. pylori-positive and -negative, were hiatus hernia (41% vs. 41%), endoscopic esophagitis (Savary-Miller) (54% vs. 46%), and Barrett's esophagus (15% vs. 11%) (all findings were NS). Finally, differences were not demonstrated in the pressure of the lower esophageal sphincter (12 +/- 8 mmHg vs. 14 +/- 12 mmHg) among H. pylori-positive and -negative patients. H. pylori infection is not associated with gastroesophageal reflux disease, as evaluated endoscopically and with 24-hour esophageal pH monitoring.
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PMID:Helicobacter pylori and gastroesophageal reflux disease: lack of influence of infection on twenty-four-hour esophageal pH monitoring and endoscopic findings. 1124 45

Helicobacter pylori infection, which is present in 30 - 60% of the population in developed countries and in more than 60% in developing countries, is established to be a major cause of gastritis, peptic ulcer disease and gastric cancer. Eradication therapy has been incorporated into clinical practice over the past 15 years. Treatment regimens include a 2 week bismuth-based triple therapy (a bismuth compound plus metronidazole, tetracycline or amoxycillin), a 1 week proton-pump inhibitor (PPI)-based triple therapy and a 1 week ranitidine bismuth citrate (RBC)-based triple therapy (a PPI or RBC plus any two of the three antibiotics, metronidazole, amoxycillin and clarithromycin). These regimens achieve eradication rates of >> 80%. H. pylori resistance to metronidazole and clarithromycin decreases the clinical efficacy of most regimens, despite the high eradication rates for resistant strains achieved by the RBC-triple therapy in some recent trials. The dose of antibiotics (especially clarithromycin) and the duration of treatment may also influence the eradication rate. Doctors' beliefs impact on clinical practice and, thus, influence the clinical application of eradication therapy. Whereas peptic ulcer disease and primary gastric low-grade B-cell mucosa-associated lymphoid tissue lymphoma (MALToma) have become established as definite indications for eradication therapy, there remain controversies surrounding non-ulcer dyspepsia, gastro-oesophageal reflux disease, atrophic gastritis, intestinal metaplasia, use of non-steroidal anti-inflammatory drugs (NSAIDs) and H. pylori-related extradigestive diseases.
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PMID:Helicobacter pylori infection--current treatment practice. 1133 84

The detection of chronic inflammation and intestinal metaplasia at the gastric side of a normal-appearing esophagogastric junction started active research on gastric cardia pathology. The main causes for this interest have been the increasing incidence of gastroesophageal reflux disease (GERD) and cardia adenocarcinoma. Many controversies still exist. It is even controversial whether noninflamed gastric cardia epithelium is a normal structure present at birth or an acquired lesion as a consequence of GERD. Similarly, the pathogenesis of chronic inflammation and intestinal metaplasia of gastric cardia are a matter of debate. Some researchers consider these lesions to be a consequence of Helicobacter pylori infection, whereas others think that chronic cardia inflammation and intestinal metaplasia are consequences of GERD. In this paper we review recent published studies in this field.
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PMID:Inflammation in the cardia. 1135 57

Helicobacter pylori infection is usually acquired during childhood, and evidence-based guidelines regarding diagnosis and treatment of infected children have been recently published. Diseases associated with H. pylori infection are gastritis, duodenal ulcers, mucosal-associated lymphoid-type (MALT) lymphoma, and gastric adenocarcinoma. The association of specific symptoms with H. pylori infection in children and adults (ie, recurrent abdominal pain and nonulcer dyspepsia) remains controversial. Additionally, the role of H. pylori in gastroesophageal reflux disease or in extra-gastrointestinal diseases (ie, coronary artery disease) lacks sufficient evidence to demonstrate causality. The diagnosis of H. pylori-associated diseases in children can reliably be made through gastroduodenal endoscopy with biopsies. Clinical trials are underway for the validation of noninvasive diagnostic tests for the H. pylori-infected child, and current guidelines recommend eradication therapy for infected children with duodenal and gastric ulcer, gastric lymphoma, and atrophic gastritis with intestinal metaplasia. The natural history of childhood H. pylori infection is poorly described. Moreover, rational approaches to the prevention and control of childhood H. pylori infection are critically needed, requiring characterization of the determinants for acquisition and persistence and the disease outcomes following eradication.
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PMID:New approaches to Helicobacter pylori infection in children. 1135 61

Anti-secretory drug use is common in patients with uninvestigated and functional dyspepsia, but the value of such agents has been controversial. Four large studies have evaluated the symptomatic outcome after a short course of acid inhibition in patients with uninvestigated dyspepsia presenting in primary care. All of these studies demonstrated a superior symptom response to proton pump inhibitor therapy compared with placebo and acid-alginates or H(2)-receptor antagonists. In patients with documented functional dyspepsia, 17 parallel group trials have evaluated an H(2)-receptor antagonist against placebo, with mixed results. A recent Cochrane review based on eight controlled trials concluded that there was a significant benefit of H(2)-blockers over placebo with a relative risk reduction of 30%, but as gastro-oesophageal reflux disease was not excluded, the conclusions are questionable. Six controlled studies have compared symptom relief after a short course of proton pump inhibitor therapy compared with placebo. Overall, there does appear to be a therapeutic gain with proton pump inhibitors over placebo, although how much of this is explained by undiagnosed gastro-oesophageal reflux disease remains unclear. There is conflicting evidence on the value of symptom subgrouping as a predictor of response to acid suppression. Overall, there is little convincing evidence that Helicobacter pylori infection influences the therapeutic outcome of acid-suppressant therapy. In conclusion, there appears to be a subgroup of patients with functional dyspepsia who will respond to acid suppression over and above placebo, but further work is required to characterize these responders.
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PMID:Current indications for acid suppressants in dyspepsia. 1140 34

Gastro-oesophageal reflux disease (GORD) affects a large group of patients and has a negative impact on quality of life. In addition, this disorder is associated with considerable long-term morbidity and mortality. In Western countries, between 10% and 30% of the population is affected by GORD. Symptoms of GORD include retrosternal burning and regurgitation, which are highly predictive of acid exposure to the oesophageal mucosa. However, erosions or ulcers in the oesophageal mucosa occur in fewer than 30% of patients with this disorder as assessed by current endoscopic techniques. Treatment of symptoms in this patient population is nonetheless of paramount importance. Current data indicate that the prevalence of GORD is increasing in the population as a whole. Although the exact reasons for this increase are unknown, changes in diet and lifestyle may play some role. Furthermore, a decreasing prevalence of Helicobacter pylori infection in the population, which is thought to exert some protection against GORD, may also be involved. Along with the increasing prevalence of GORD is an increase in GORD-related complications, including Barrett's oesophagus and oesophageal adenocarcinoma. Given the delay in onset of these GORD-associated complications, these findings are particularly alarming. As these trends continue, current techniques for the treatment of GORD will need to be refined and reevaluated in terms of quality-of-life issues, health care utilization, and cost-efficacy. Treatment of GORD in the future will require effective techniques to control symptoms, maintain remission, and prevent complications in the affected patient.
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PMID:Reflux disease: the disorder of the third millennium. 1143 May 9

Epidemiological and clinical studies that have reported on gastro-oesophageal reflux disease (GERD), Barrett's oesophagus, oesophageal adenocarcinoma and Helicobacter pylori infection in sub-Saharan Africa were reviewed. The data indicate that Barrett's oesophagus is rare and oesophageal adenocarcinoma uncommon in all regions of sub-Saharan Africa studied (South Africa, Ethiopia, Nigeria, Zimbabwe, Kenya and Uganda). Hiatus hernia is also uncommon. There are too few reports of GERD to allow comment. The overwhelming majority of oesophageal cancers are squamous cell type. H. pylori infection is ubiquitous with an overall prevalence of 61-100%. It is concluded that although urbanization has resulted in an increase of risk factors associated with GERD, which would be expected to lead to an increase in this disease among Africans, this increase has not happened. It is believed that the critical factor preventing GERD in black Africans is H. pylori infection, which is usually acquired in childhood, is lifelong and is probably protective for the oesophagus.
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PMID:The gastro-oesophageal reflux disease complex in sub-Saharan Africa. 1143 7

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pylori status, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.
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PMID:H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans. 1144 14


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