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)

Although more extensive research is required to fully characterize the pathophysiology of the gastrointestinal symptoms in PD, much of the presently available data suggest that the primary PD process is the major factor in the etiology of gut dysfunction in this patient population. This may be mediated by both central and peripheral mechanisms. Involvement of the dorsal motor nucleus of the vagus might produce dysfunction of muscles controlling deglutition and esophageal motility, thereby leading to drooling, dysphagia, and gastroesophageal reflux. The presence of Lewy bodies, the primary neuropathologic finding in the CNS in PD, in the myenteric plexus of both the esophagus and colon suggests that the PD process may also affect the enteric nervous system and contribute to the development of esophageal dysmotility and constipation through this peripheral mechanism. Dopamine receptors have been identified in the lower esophageal sphincter and the esophageal body of animals. If similarly present in humans, involvement of this dopaminergic system could contribute to the development of dysphagia and nausea of PD. Constipation may reflect both peripheral involvement, indicated by Lewy bodies in the colonic myenteric plexus, leading to colonic inertia, and central mechanisms, leading to pelvic floor dysfunction.
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PMID:Gastrointestinal dysfunction in Parkinson's disease: frequency and pathophysiology. 845 Oct 18

In 11 children (mean age 44.2 months) with symptoms suggesting upper intestinal dysfunction (nonulcer dyspepsia), in nine children (mean age 27.3 months) with gastroesophageal reflux (GER) disease, and in seven controls (mean age 20.4 months) we investigated fasting [for 3 hr or until two migrating motor complexes (MMC) were observed] and fed (90 min) antroduodenal motility by means of perfused catheter system; furthermore, we measured both gastric emptying of a radiolabeled milk formula and fasting duodenogastric reflux during manometry by assessing bile salt concentration in gastric aspirates. No structural abnormalities of gastrointestinal tract and organic disorders were detected in the patients. In a high proportion of both groups of patients we found manometric abnormalities of interdigestive and fed motor patterns that were not seen in the controls: absence of antral phase III of MMC; significant decrease of antral and/or duodenal motor activity during fasting and/or fed periods; abnormal propagation or configuration of MMC phase III that was significantly shorter than in controls; bursts of sustained fasting and/or fed phasic duodenal activity, frequently uncoordinated with adjacent gut segments. When compared to controls, the mean intragastric concentration of bile salts during all MMC phases and the mean 1-hr percent gastric activity of the radiolabeled milk were significantly higher in the two groups of patients. We conclude that in a high proportion of children with nonulcer dyspepsia and of children with GER disease, gastrointestinal manometry may reveal significant irregularities of antral and duodenal motility, which are associated with increased duodenogastric reflux and delayed gastric emptying.
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PMID:Abnormalities of gastrointestinal motility in children with nonulcer dyspepsia and in children with gastroesophageal reflux disease. 186 98

Omeprazole, a benzimidazole compound which inhibits H+/K+ ATPase in the gut, is used in the treatment of gastroesophageal reflux disease. Clinical and experimental use of omeprazole has been associated with inhibition of the cytochrome P450-dependent metabolism of a few drugs both in vivo in man and in vitro in animals. In these experiments, in vivo administration of omeprazole to rats failed to inhibit the cytochrome P450-dependent metabolism of four prototypic drugs, testosterone or estradiol.
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PMID:Omeprazole and cytochrome P450-dependent hepatic metabolism: a comparison of endogenous and exogenous substrates in male rats. 194 96

Gastrointestinal complications associated with non-steroidal antiinflammatory drugs (NSAID) represent a frequent and expensive drug side effect. Recent publications have shown that the deleterious effect of NSAID is not limited to the gastroduodenal tract but can involve all segments of the gut. Epidemiological and clinical studies have demonstrated that 20-30% of patients under NSAID develop digestive symptoms. The relative risk of gastric ulceration is 5 times higher and this risk increases in older patients and in those with peptic ulcer history. Bleeding and perforated gastroduodenal ulcer occur more frequently in patients who received NSAID and mortality in these complications seems to be higher than in control groups. Curative and preventive treatments are effective in gastropathy associated with NSAID use, but the indications for prophylactic therapy need to be more precise in the future. The risk of oesophageal stenosis is increased in patients with gastroesophageal reflux taking NSAID. Diarrhea occurs in 5-30% of patients under NSAID. Intestinal perforation and hemorrhage are more frequent in anti-inflammatory drug takers than in control groups. Mild intestinal inflammation had been recently reported under NSAID, marked by ileal dysfunction, blood and protein loss and occasionally diaphragm-like small intestinal stricture. The pathogenesis of the inflammation is uncertain but seems to be related to an increase in mucosal permeability.
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PMID:[Digestive complications of non-steroidal anti-inflammatory drugs]. 205 38

In a series of 18 patients with angina pectoris, in whom treatment over at least 3 years with nitroderivatives and Ca-antagonists had become partially ineffective on chest pain, and in 18 patients with angina-like non-cardiac chest pain, the following examinations were carried out: upper gut x-ray and endoscopy, acid perfusion test, esophageal manometry, 24-hour esophageal pH monitoring associated with Holter recording. The presence or absence of coronary insufficiency was established by means of scintigraphic and ECG tests, Holter monitoring and coronary arteriography. In both groups the majority of patients had abnormal esophageal function, but in patients with angina pectoris treated for a long period of time the motility changes were prevalently reflux-related. With respect to the origin of chest pain, the esophagus was found to be the likely cause in 4 patients with angina pectoris, and the probable cause in another 10 of the same group; it was the likely cause in 7 patients without angina pectoris, and the probable cause in another 7 of the same group. As nitroderivatives and Ca-antagonists decrease the LES tone and the amplitude of esophageal pressure waves, long-term treatment with these drugs may be taken into account in the genesis of gastro-esophageal reflux and related changes, including esophageal pain.
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PMID:The esophagus as a possible cause of chest pain in patients with and without angina pectoris. 237 62

Two patients with attacks of choking caused by aspiration of gastric contents in the laryngotracheal tube are presented. One had such severe attacks of respiratory arrest, that tracheostomy was done. The common symptoms of gastro-oesophageal reflux such as pirosis, acid regurgitation, or retrosternal burning were absent in both patients and upper gut radiological and endoscopic examinations were negative. Histology of the oesophageal mucosa showed a deep chronic eosophagitis, and the 24-hour pH-monitoring of the upper oesophagus showed frequent gastro-oesophageal refluxes. Manometry showed hypotonic lower oesophageal sphincter with marked alterations of peristalsis. In the patient with tracheostomy a 24 pH monitoring of the hypolaryngeal zone showed decreased pH at the time of choking attacks. In the other patient further investigations showed that amyotrophic lateral sclerosis was the cause of the oesophageal motility disorder. An intense antireflux treatment abolished the respiratory attacks in both patients.
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PMID:Laryngospasm and reflex central apnoea caused by aspiration of refluxed gastric content in adults. 270 45

Fifty-two patients with reflux oesophagitis resistant to medical treatment were randomized at operation to receive either the Angelchik prosthesis or a fundoplication. All patients were assessed postoperatively by a physician unaware of the nature of the operation. Forty-two patients have been followed up for 1-2 years; ten patients for 3-9 months. Ninety-six per cent of the Angelchik patients had satisfactory or excellent results compared with 81 per cent with a fundoplication. There were no failures to control reflux with the Angelchik prosthesis whereas 6 patients (23 per cent) of the fundoplication group have persisting reflux. Operating times for insertion of the prosthesis averaged a little over half that recorded for fundoplication. Complication rates were similar. The results of the trial encourage the use of the prosthesis in patients with gastro-oesophageal reflux, where medical treatment has failed. The prosthesis should not be used if the gut is opened during operation either inadvertently or deliberately, as in making a suture line or anastomosis, because of the risk of sepsis.
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PMID:Randomized prospective trial of the Angelchik anti-reflux prosthesis. 638 12

Bile reflux may occur after a variety of reconstructive procedures in the gastro-intestinal tract and biliary system. The present paper deals with reflux into the duodenum, jejunum, stomach, oesophagus and into blind loops. The demonstration of reflux by 99mTc labelled IDA acid derivatives, and a possible quantitative approach, are discussed. The advantages of an isotope method are: 1. Direct demonstration of bile reflux without any intervention in the physiological process and with little trouble to the patient, 2. The ability to use the method for various reconstructive procedures and 3. The additional information obtained which may help in the differential diagnosis of blind loops, biliary obstructions, cholecystitis or liver metastases if there has been a gastrectomy for a malignant tumour. In combination with a second administration of a radio-isotope tracer, one may be able to demonstrate abnormalities in the motility of the stomach or gut, or pyloric stenosis or gastro-oesophageal reflux.
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PMID:[Scintigraphic image of bile reflux following gastric and intestinal surgery]. 640 29

Some patients undergoing ambulatory oesophageal pH monitoring to investigate symptoms suggestive of gastro-oesophageal reflux disease (GORD) are found to have oesophageal acid exposure within the physiological range but show a close correlation between their symptoms and individual reflux episodes. It is suggested that these patients might exhibit enhanced oesophageal sensation, akin to the heightened perception of both physiological and provocative stimuli in the gut that has been described in patients with functional gastrointestinal disorders. This study tested the hypothesis by measuring the sensory thresholds for oesophageal balloon distension and discomfort in 20 patients with symptoms of GORD, in whom ambulatory pH monitoring had shown normal acid exposure times, but in whom the symptom index for reflux events was 50% or greater, and compared these with 15 healthy volunteer controls, and with control groups with confirmed excess reflux. The study group showed lower thresholds both for initial perception of oesophageal distension, and for discomfort, compared with healthy controls (median ml (range)); 7.5 (2-19) v 12 (6-30) (p = 0.002) and 10 (5-20) v 16 (8-30) (p < 0.0001), respectively. Sensory thresholds in the study group were also significantly lower than in patients with excess reflux, and than patients with Barrett's oesophagus, who also exhibited significantly higher sensory thresholds than healthy controls. No differences in sensory thresholds for somatic nerve stimulation were found between the study group and health controls. The results show a spectrum of visceral sensitivity in GORD, with enhanced oesophageal sensation in patients with symptomatic but not excess gastro-oesophageal reflux, suggesting that their symptoms result from a heightened perception of normal reflux events.
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PMID:Lowered oesophageal sensory thresholds in patients with symptomatic but not excess gastro-oesophageal reflux: evidence for a spectrum of visceral sensitivity in GORD. 767 84

Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.
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PMID:Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis. 792 44


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