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)

OEsophageal manometry, acid perfusion test and recording of oesophageal pH after gastric filling with 300 ml HCI were carried out in 55 patients with at least one symptom of gastro-oesophageal reflux (GER). None of the patients complained of dysphagia or had a history of haemorrage, but 19 had oesophagitis on endoscopy. pH probe recordings showed evidence of GER in 72% of the patients, and acid perfusion was painful in 44%. The resting lower oesophageal sphincter pressure was below normal in 20%. Thirty-eight p. cent had peristaltic disorders associated with significantly decreased sphincter pressure. In this category of patients, oesophageal pH recordings constitute the best method for diagnosing GER. Apositive acid perfusion test indicates that the clinical symptoms are due to abnormal sensitivity of the mucosa to hydrogen ions. Manometry is useful for a study of motor disorders resulting from GER, but insufficient to determine whether or not GER is present.
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PMID:[Gastro-oesophageal reflux syndrome. Functional exploration of the oesophage in 55 patients (author's transl)]. 742 98

The role of acid and duodenogastric reflux (DGR) in the development of esophageal mucosal injury has been extensively investigated using both animal and human models. In this report, clinical and experimental data are reviewed. The mechanisms by which gastric and duodenal contents produce esophageal mucosal injury are also discussed. Acid and pepsin are unquestionably important in causing mucosal damage at low pH values in both animal and human models. Animal models suggest synergistic damaging potential for conjugated bile acids and HCI as well as that of unconjugated bile acids and trypsin in more neutral pH values. Human evidence for the involvement of bile and its constituents has been controversial; however, the advent of better technology to detect DGR is beginning to clarify the role of these constituents. The contribution of each methodology in clarifying the extent of involvement of DGR in esophageal mucosal injury is reviewed. Despite some conflicting results, preliminary human studies support the results from the animal data suggesting synergistic damaging effects for both bile and acid in esophageal mucosal injury. The implication of these studies in treating gastroesophageal reflux disease are discussed.
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PMID:Role of acid and duodenogastric reflux in esophageal mucosal injury: a review of animal and human studies. 853 82

The hypothesis that fat increases esophageal sensitivity to acid was tested in eight patients with gastroesophageal reflux disease and 11 healthy subjects. Protocol 1 included randomized intragastric infusions of saline or Lipofundin S 20% (306 kcal) on two separate days, followed after 30 and 90 min by an 8 ml/min intraesophageal infusion of 0.1 N HCl. The time to the onset of heartburn and the maximum heartburn score by visual analog scale during the acid infusion were similar after intragastric saline (2 min and 29.5 mm, medians) and fat (2 min and 20.5 mm). Protocol 2 included two 8 ml/min intraesophageal infusions of 0.2 N HCI diluted in an equal volume of saline or Lipofundin S 20% at a time interval of 10 min in randomized order. The time to the onset of heartburn and the maximum heartburn score were unaffected by the presence of fat in the esophageal infusate (2.5 min and 53 mm without vs 1.5 min and 49 mm with fat). We conclude that fat does not increase esophageal sensitivity to acid.
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PMID:Fat and esophageal sensitivity to acid. 1191 56

This study is the first to examine site-specific changes in mucosal antioxidants and expression and localization of heat shock proteins (HSPs) following the induction of subacute esophagitis and after recovery using an established animal model. Distal, middle, and proximal samples were excised from anesthetized opossums 24 hr after three consecutive days of 45-min perfusion with saline or 100 mmol/liter HCI, or seven days after acid in recovery animals. Compared to controls, acid-induced erosive esophagitis significantly increased glutathione peroxidase and HSP90 at all sites and HSP60 proximally. Reduced glutathione was significantly decreased distally, as was HSP72 at distal and middle sites. No changes in superoxide dismutase or catalase occurred. After recovery, superoxide dismutase, catalase, and HSP expression were not different from controls. Glutathione peroxidase and glutathione were significantly decreased distally. Similar differential stress responses may occur in patients with chronic gastroesophageal reflux and could be important in the pathogenesis of reflux esophagitis.
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PMID:Analysis of mucosal stress response in acid-induced esophagitis in opossum. 1218 45