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)

Gastro-oesophageal reflux disease (GOR) and asthma are both common medical conditions that often co-exist. Studies using oesophageal manometry and 24 h ambulatory pH monitoring have shown that up to 80% of asthmatics have abnormal GOR. A number of mechanisms whereby GOR may trigger asthma have been proposed, and it is believed that acid reflux may stimulate vagal receptors in the lower oesophagus causing reflex bronchoconstriction. However, GOR may be worsened by asthma causing abnormal diaphragm mechanics and by its treatment. Formal evaluation of GOR should be considered a part of asthma assessment, particularly if asthmatic symptoms are precipitated by factors known to trigger GOR such as reclining, alcohol ingestion, and the use of theophylline. Twenty-four hour ambulatory intra-oesophageal pH monitoring remains the gold standard for the diagnosis of GOR. Medical therapy with anti-reflux medications, such as acid suppressive agents and prokinetic agents may improve both GOR and asthma control. In those who fail medical therapy, anti-reflux surgery may be warranted in some.
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PMID:Gastro-oesophageal reflux disease and asthma. 940 Jun 76

Currently available data indicate a clear and probably causal relationship between long-lasting gastroesophageal reflux disease, the development of long segments with specialized intestinal metaplasia in the distal esophagus and subsequent progression to adenocarcinoma. To a lesser degree, this also appears to be the case for short segments of specialized intestinal metaplasia in the distal esophagus. In contrast, epidemiological data and classic parameters for the diagnosis of gastroesophageal reflux disease do not currently support a causal role of gastroesophageal reflux in the pathogenesis of specialized intestinal metaplasia at the gastric cardia. Despite its high prevalence and malignant potential, many questions about the prevention and management of intestinal metaplasia in the distal esophagus remain unsolved. In patients with chronic gastroesophageal reflux, current modes of medical therapy do not appear to prevent the development of intestinal metaplasia, while effective anti-reflux surgery seems to have a protective effect. Formal studies with adequate follow-up are, however, still lacking. Neither acid-suppression therapy nor anti-reflux surgery, with or without mucosal ablation, can reliably prevent the malignant degeneration of established intestinal metaplasia of the esophagus. Close endoscopic surveillance with extensive biopsies, therefore, remains mandatory in such patients, irrespective of the treatment modality.
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PMID:The relationship between gastroesophageal reflux, intestinal metaplasia and adenocarcinoma of the esophagus. 1102 1

Rumination is a syndrome characterized by the effortless regurgitation of recently ingested food. It has been linked to severe medical and psychosocial conditions including malnutrition, aspiration pneumonia, and complete social withdrawal. Psychotherapy, the current treatment modality for rumination, may improve symptoms but requires significant motivation and is rarely curative. We hypothesized that a complete fundoplication would eliminate, or at least impair, the ability to regurgitate gastric contents through the esophagogastric junction. We performed a Nissen fundoplication in five patients with a classic history of rumination. In all cases, symptoms had been resistant to medical and psychiatric intervention prior to fundoplication. Formal preoperative testing included esophageal manometry, 24-hour pH monitoring, endoscopy, and upper gastrointestinal barium swallow studies. All patients reported their primary symptom to be effortless recurrent postprandial regurgitation for 1 to 2 hours after meals consistent with rumination. Four (80%) of the five patients had low resting lower esophageal sphincter pressures with evidence of gastroesophageal reflux disease on 24-hour pH monitoring. All patients reported complete cessation of ruminating behavior after Nissen fundoplication. We report, for the first time, complete elimination of rumination symptoms after a Nissen fundoplication. Although further trials are needed to confirm our results, we recommend considering a Nissen fundoplication for treatment of rumination refractory to behavioral and medical interventions.
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PMID:Effective treatment of rumination with Nissen fundoplication. 1212 34

Pantoprazole (Protonix) is an irreversible proton pump inhibitor (PPI) that reduces gastric acid secretion. In combination with two antimicrobial agents (most commonly metronidazole, clarithromycin or amoxicillin) for 6-14 days, pantoprazole 40 mg twice daily produced Helicobacter pylori eradication rates of 71-93.8% (intent-to-treat [ITT] or modified ITT analysis) in patients without known antibacterial resistance. Pantoprazole-containing triple therapy was at least as effective as omeprazole- and similar in efficacy to lansoprazole-containing triple therapy in large trials. In the treatment of moderate to severe gastro-oesophageal reflux disease (GORD), oral pantoprazole 40 mg/day was as effective as other PPIs (omeprazole, omeprazole multiple unit pellet system, lansoprazole and esomeprazole) and significantly more effective than histamine H(2)-antagonists. Pantoprazole 20 mg/day provided effective mucosal healing in patients with GORD and mild oesophagitis. Intravenous pantoprazole 40 mg/day can be used in patients who are unable to take oral medication. Oral pantoprazole 20-40 mg/day for up to 24 months prevented relapse in most patients with healed GORD. According to preliminary data, oral pantoprazole 20 or 40 mg/day was effective at healing and preventing non-steroidal anti-inflammatory drug (NSAID)-related ulcers, and intravenous pantoprazole was at least as effective as intravenous ranitidine in preventing ulcer rebleeding after endoscopic haemostasis. Oral or intravenous pantoprazole up to 240 mg/day maintained target acid output levels in most patients with hypersecretory conditions, including Zollinger-Ellison syndrome. Oral and intravenous pantoprazole appear to be well tolerated in patients with acid-related disorders in short- and long-term trials. Tolerability with oral pantoprazole was similar to that with other PPIs or histamine H(2)-antagonists in short-term trials. Formal drug interaction studies have not revealed any clinically significant interactions between pantoprazole and other agents. In conclusion, pantoprazole is an effective agent in the management of acid-related disorders. As a component of triple therapy for H. pylori eradication and as monotherapy for the healing of oesophagitis and maintenance of GORD, pantoprazole has shown similar efficacy to other PPIs and greater efficacy than histamine H(2)-antagonists. Limited data suggest that it is also effective in Zollinger-Ellison syndrome and in preventing ulcer rebleeding. Pantoprazole is well tolerated with minimal potential for drug interactions. The availability of pantoprazole as both oral and intravenous formulations provides flexibility when the oral route of administration is not appropriate. Thus, pantoprazole is a valuable alternative to other PPIs in the treatment of acid-related disorders.
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PMID:Pantoprazole: an update of its pharmacological properties and therapeutic use in the management of acid-related disorders. 1248 24