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)

Proton pump inhibitors (PPIs), such as omeprazole, lansoprazole, rabeprazole, esomeprazole, and pantoprazole, are metabolized by cytochrome P450 isoenzyme 2C19 (CYP2C19) in the liver. There are genetic differences that affect the activity of this enzyme. The genotypes of CYP2C19 are classified into three groups: homozygous extensive metabolizer (homEM), heterozygous extensive metabolizer (hetEM), and poor metabolizer (PM). The pharmacokinetics and pharmacodynamics of PPIs differ among the different CYP2C19 genotype groups. Plasma PPI and intragastric pH levels during PPI treatment are the lowest in the homEM group and the highest in the PM group. These CYP2C19 genotype-dependent differences in pharmacokinetics and pharmacodynamics of PPIs are reflected in the cure rates for gastroesophageal reflux disease and Helicobacter pylori infection with PPI-based therapies. The CYP2C19 genotyping test is a useful tool for deciding on the optimal treatment regimen using a PPI, including a dual (PPI plus antibiotic) or a triple (PPI plus two antibiotics) therapy.
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PMID:Pharmacogenomics of proton pump inhibitors. 1501 9

Esophagus is often unregarded, being considered only a pathway for the food. As our knowledge has been rising, esophageal diseases become more frequently diagnosed. Gastroesophageal junction represents the region of contact between two different types of epithelium. Exact delimitation of the border is often very difficult. Also the region of cardia has not been yet precisely defined. The important component of the refluxate, which can impair the esophageal mucosa, is the duodenal content. One of the elemental causes of the reflux disease is probably transient relaxation of the lower esophageal sphincter, which is triggered by the central nervous system. When inflammatory changes are present in cardia, gastric carditis is diagnosed. Histological changes in cardia are related to the presence of Helicobacter pylori infection and also to the gastroesophageal reflux disease. If the aetiology of Helicobacter pylori infection cannot be proved, non-helicobacter solitary carditis is diagnosed. Barrett's esophagus represents an acquired serious impairment of the esophageal mucosa. Barrett's esophagus diagnose depends on the existence of histological changes in the biopsy samples form esophageal mucosa. The most effective treatment of the Barrett's esophagus is the early and long-lasting curing of the esophagus reflux disease. The conservative curing is based on the long-term suppression of gastric acid production by antisecretorics (most effective are inhibitors of proton pump). Functional gastric disorders represent an important group with the most recent international classification done in 1999 (Roma II).
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PMID:[The esophagus: organic and functional disorders--findings in literature in recent years]. 1507 66

The relationship between Helicobacter pylori infection and gastroesophageal reflux disease (GERD) remains controversial. Over 20 studies presented at the 2003 Digestive Disease Week meeting examined the implications of H. pylori infection for GERD. Although the findings were not uniform, most of the studies presented indicated a negative association between the presence of H. pylori and the presence of GERD symptoms, signs, or complications. In addition, eradication of H. pylori infection was related to the emergence of GERD and its complications. However, most studies favored a role for H. pylori rather than GERD in the development of pathologic changes in the gastric cardia. Finally, a few studies suggested the intriguing possibility that the modulation of GERD by H. pylori could be through the effects of H. pylori eradication on weight gain.
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PMID:The implications of Helicobacter pylori infection for gastroesophageal reflux disease: studies presented at Digestive Disease Week 2003. 1512 83

At the gastric cardia, the molecular mechanisms of inflammation and metaplasia are incompletely understood. Thus, the aim of this study was to determine the expression of TFF1, TFF2 and TFF3 at this site and correlate these data with Helicobacter pylori infection or gastro-esophageal reflux disease (GERD). In 27 patients without intestinal metaplasia at the cardia, endoscopic biopsies were obtained for histology and RT-PCR. TFF1 and TFF2 were expressed in all cardia samples. TFF3 expression was significantly more frequent at the cardia (n = 15/24) than in the corpus (n = 2/26). TFF3 expression at the cardia was mainly observed in GERD patients, and there was a clear tendency towards higher interleukin-8 (IL-8) transcription levels; whereas TFF3 expression was not correlated with the H. pylori status or to tumor necrosis factor-alpha (TNF-alpha) expression. The expression of TFF3 at the cardia may represent an adaptation to GERD and precede the development of Barrett's esophagus.
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PMID:TFF3 expression at the esophagogastric junction is increased in gastro-esophageal reflux disease (GERD). 1517 71

Gastro-oesophageal reflux disease (GORD) and Helicobacter pylori infection are both common in Western countries. A recently published meta-analysis has shown an association between an absence of H. pylori infection and GORD symptoms. Infection with cagA-positive H. pylori strains is a causative factor for the development of duodenal ulcer and is a risk factor for gastric cancer. Data about a protective role of cagA-positive H. pylori strains against more severe reflux oesophagitis are documented in several studies, but questioned by some other studies. There is a need for further studies to clear the definite role of cagA-positive H. pylori strains in severe reflux oesophagitis and their possible effect on the development of Barrett's adenocarcinoma. The role of Helicobacter pylori in gastro-oesophageal reflux disease (GORD) is still discussed controversially. Different factors might be responsible for the remarkably heterogeneous results of previously performed studies (e.g. location, environmental factors and different virulence factors of H. pylori strains). A very recently published meta-analysis has shown a significant association between the absence of H. pylori infection and GORD symptoms, and a positive correlation between anti-H. pylori therapy and the occurrence of both de-novo and rebound/exacerbated GORD. The results of this meta-analysis are questioned by some authors because of single larger trials and geographical variations of the studies analysed. Data on the role of the cytotoxic-associated antigen (cagA)-positive H. pylori strains are contradictory. Several studies have provided evidence supporting the protecting role of cagA-positive H. pylori strains against GORD, but these results were not confirmed by all studies. A multitude of patients suffer from H. pylori infection and GORD, simultaneously. Therefore, further studies are needed to clearly answer the question whether infection with cagA-positive H. pylori strains, which bear a well-documented risk for gastric cancer and gastro-duodenal ulcer, is really helpful against more severe reflux oesophagitis and, in consequence, perhaps protective against Barrett's oesophagus and Barrett's adenocarcinoma.
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PMID:cagA-positive Helicobacter pylori strains and gastro-oesophageal reflux disease: still puzzling? 1520 76

The demographics of esophageal and gastric cancer have been changing dramatically in the United States over the past several decades. While incidence rates for esophageal squamous cell carcinoma and distal gastric carcinoma have been declining, the trends for adenocarcinoma of the esophagus and proximal stomach have been rising rapidly, particularly among white males. The incidence of these upper gastrointestinal (GI) malignancies varies widely based on geographic location, race, and socioeconomic status. The primary causes of squamous cell carcinoma of the esophagus are tobacco use and alcohol consumption, whereas the main risk factors for adenocarcinoma of the esophagus are gastroesophageal reflux disease and obesity. Dietary factors and Helicobacter pylori infection play an important role in the development of gastric cancer. Understanding the epidemiology and etiologies of esophageal and gastric carcinomas will lead to the development of interventions for screening and prevention in high-risk populations.
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PMID:Epidemiology of upper gastrointestinal malignancies. 1529 38

Premalignant esophagogastric (EG) lesions develop against a background of chronic inflammation, called a premalignant condition. For esophageal squamous cell cancer, causal factors include alcohol, tobacco, hot beverages, oral consumption of opioids, and probably infectious agents. For adenocarcinoma in the Barrett's esophagus (BE), gastroesophageal reflux disease (GERD) is the principal causal factor. At the EG junction, adenocarcinoma arises either from the esophagus or from the proximal stomach (cardia). In the distal stomach, chronic gastritis with atrophy is the premalignant condition related to Helicobacter pylori infection. A high intake of salt and low intake of antioxidants also play a role. The histopathology of EG premalignant lesions is now included in the groups low-grade and high-grade intraepithelial neoplasia (IEN) of the revised Vienna classification. Endoscopy is the gold standard for detection of the lesions at the preclinical stage and their appearance is described in subtypes of the type 0 of the Japanese classification, with a distinction between protruding and nonprotruding lesions. There is a priority for primary prevention of causal factors rather than for mass screening, which is justified only in Japan for the prevention of stomach cancer. The trend to early detection of premalignant lesions justifies the development of mini-invasive endoscopic procedures of treatment.
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PMID:Premalignant lesions of the esophagogastric mucosa. 1529 42

With widespread treatment of Helicobacter pylori infection, and that peptic ulcer diseases are no longer considered a chronic illness and are declining in most parts of the world, gastroesophageal reflux disease (GERD) predominates the upper gastrointestinal disease spectrum. GERD is a well-defined condition. More innovative research in GERD in recent years led us to new conceptual frameworks on pathogenesis and novel diagnostic tests. The proton pump inhibitor test has evolved to become the diagnostic test of choice for the investigation of patients with the disease spectrum of GERD. Multi-channel intraluminal impedance with pH sensor allows the detection of pH episodes irrespective of their pH values (acid and nonacid reflux). It is useful to measure gastroesophageal reflux in the postprandial period, and in patients with persistent symptoms while on therapy and those with atypical symptoms.
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PMID:Definition and diagnosis of gastroesophageal reflux disease. 1532 79

Inflammation of the gastric cardia ('carditis') is a histological diagnosis. It seems reasonable to transfer histological criteria of the updated Sydney classification from the distal stomach to the cardia as long as a special classification of inflammation of the esophagogastric junction is lacking. The two best characterized causes of carditis are Helicobacter pylori infection and gastroesophageal reflux disease (GERD). However, the causal contribution and interference of these two factors are highly controversial, as is the clinical relevance of carditis in terms of eliciting symptoms or conferring an increased cancer risk. Variability of studies on carditis is based on conflicting concepts of the normal anatomy of the esophagogastric junction. Cardia-type mucosa (CM) apparently exists at birth as a tiny circular area, and extends to a larger area in adulthood. This implies that cardia-type mucosa is largely metaplastic. Metaplastic CM may evolve in the lower esophagus as a consequence of GERD. It is a general phenomenon that H. pylori-induced gastritis also involves the gastric cardia, irrespective whether the cardia is lined by fundus-type mucosa or CM. The contribution of GERD to inflammation of CM in H. pylori-negative individuals is, however, highly controversial. Prevalence of carditis in GERD patients fluctuates between 10 and 97%. Hence, because of its high frequency and low specificity, carditis can currently not be considered as a clinical entity. The role of carditis for the increasing incidence of cancer of the esophagogastric junction requires careful studies that include accurate description of the area with adequate biopsy protocols.
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PMID:Carditis at the interface between GERD and Helicobacter pylori infection. 1538 52

It is estimated that by 2020, >16% of people in the United States will be > or =65 years of age and that nearly 20 million will be >85 years of age. Aging imparts a variety of physiologic changes in the oropharynx, esophagus, and stomach that increase the risk for esophageal and gastrointestinal disorders. Older individuals also tend to have a higher prevalence of comorbid factors, such as Helicobacter pylori infection, smoking, presence of other diseases, or use of medications (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs]) that increase their risk for acid-related disorders. Given these physiologic and comorbidity factors, the elderly are at higher risk for gastroesophageal reflux disease (GERD), pill-induced esophagitis, peptic ulcer disease, and complications related to the use of NSAIDs. Unfortunately, in the elderly patient with these disorders--even those with severe disease or complications--symptom presentation may be subtle or atypical, resulting in a delayed diagnosis. Endoscopy remains the "gold standard" for the identification of mucosal disease and should be performed in all patients with "new-onset" or persistent symptoms who are >45 years of age, as well as in individuals of any age who present with alarm symptoms, such as weight loss, vomiting, anemia, dysphagia, or evidence of gastrointestinal bleeding. In general, the treatment of older individuals with peptic ulcer or GERD and its complications is similar to that of younger individuals. Proton pump inhibitors are the mainstay of therapy for symptom relief, healing of erosive esophagitis, resolution of peptic ulceration, reduction of the risk for NSAID-induced mucosal damage, and prevention of disease recurrence.
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PMID:Aging, the gastrointestinal tract, and risk of acid-related disease. 1547 47


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