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)

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

Peptic ulcer disease and gastric cancer of the antrum and body have been declining in the 20th century. In contrast, a new group of diseases are increasingly rapidly in Western countries: gastroesophageal reflux disease, Barrett's esophagus, and adenocarcinoma of the distal esophagus. Recent studies suggest this phenomenon may be related to the simultaneous fall in the prevalence of Helicobacter pylori (H. pylori) colonization, especially by the virulent cagA + strains. H. pylori infection with the cagA+ strain is potentially protective against the spectrum of gastroesophageal reflux disease because it lowers intragastric acidity as the result of a pangastritis, frequently with multifocal gastric atrophy and possibly increased intragastric ammonia production. Assuming that some types of H. pylori strains are protective, our entire approach to the worldwide elimination of this organism, sometimes indiscriminately, will need critical reevaluation.
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PMID:Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad. 1052 Aug 76

Two problems can be identified as possible long term negative consequences of HP eradication: diminished efficacy of acid-lowering drugs, and an accelerated development of GERD. It was shown that omeprazole produces a greater decrease in gastric acidity in subjects with H. pylori infection than in those who are H. pylori negative, and that omeprazole produces a smaller decrease in gastric acidity after cure of H. pylori. This effect persisted for at least one year after HP eradication. It is not limited to omeprazole, but can also be seen with the H2 receptor antagonist ranitidine. At least one proven mechanism involved in this phenomenon is the disappearance of the alkalinizing effect of ammonia, generated from urea by HP's urease, after eradication of the bacteria; other mechanisms may also be involved. HP eradication may therefore potentially hamper acid inhibitory treatment. It is unknown to what extent this is clinically relevant. Although one study did not observe a relation between H. pylori status and efficacy of omeprazole maintenance therapy for GERD, it cannot be excluded that some patients may need more potent or higher doses of acid-lowering medication after HP eradication. Three studies suggest that duodenal ulcer patients who were successfully treated with H. pylori eradication therapy, may be at increased risk to develop GERD. Labenz's study finds that the incidence of GERD may be double 3 years after eradication. The life-table analysis suggested that cure of the infection was associated with an increased risk of reflux oesophagitis during the first year after treatment, whereas later the incidence of reflux oesophagitis was similar in both groups. Patients who developed reflux oesophagitis after the cure had a more severe body gastritis before cure, gained weight more frequently after cure, and were predominantly men. There are no data on the fate of the oesophagus after HP eradication in patients with reflux oesophagitis. The data thus strongly suggest that there is a risk for developing reflux oesophagitis after HP eradication in patients with duodenal ulcer. It is unknown whether HP eradication in patients without duodenal ulcer also increases the risk for developing reflux oesophagitis.
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PMID:Adverse events of HP eradication: long-term negative consequences of HP eradication. 979 71

Numerous factors are important in the pathophysiology of gastroesophageal reflux disease (GERD). The anti-reflux barrier consists of the lower esophageal sphincter (LES) and crural portion of the diaphragm. Absolute LES pressure less than 6 mmHg is required for gastroesophageal reflux (GER), but this is more frequently associated with increased episodes of transient relaxation than persistently low LES pressure. The vast majority of patients with complicated GERD have a hiatal hernia, because the gastric excursion into the chest displaces the LES segment of the distal esophagus above the crural diaphragm, promoting a pinch-cock effect that impairs acid clearance. Clearance of refluxed acid from the esophagus is dependent on gravity, peristalsis and saliva (pH > 6) to neutralize residual acid. Ineffective peristalsis, characterized by low amplitude contractions and dysmotility, represents the major impairment to normal acid clearance. Despite our great attention to these areas, gastric factors may be the most amenable abnormalities to treatment in GERD. Delayed gastric emptying is present in 10-15% of GERD patients, but more subtle postprandial abnormalities may contribute to gastric distension and transient LES relaxation. Although reflux patients are infrequently hypersecretors of acid, studies find acid combined with pepsin to be the most injurious agents to the esophageal mucosa. Recent studies also show increased amounts of bile acids in the refluxate of GERD patients, especially those with Barrett's esophagus. The influence of gastric colonization by Helicobacter pylori is just now being understood. Exciting studies suggest that H. pylori colonization, especially with the more virulent cagA-positive strains, may be protective against severe esophagitis and Barrett's esophagus. Increased intragastric ammonia production and pangastritis with gastric atrophy and intestinal metaplasia, both promoting hypoacidity, are the most likely mechanisms. Conversely, eradication of H. pylori may aggravate GER in some susceptible subjects.
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PMID:Do we know the cause of reflux disease? 1044 6

The relationship between gastro-oesophageal reflux disease (GERD) and Helicobacter pylori is unclear. Recent data indicate that H. pylori probably exerts a protective effect against GERD. In recent years, the interaction between H. pylori, proton pump inhibitors and GERD has been widely studied. Currently available proton pump inhibitors produce significantly higher intragastric pH in H. pylori-positive patients than in those who are H. pylori negative, and this phenomenon may be clinically relevant. The mechanisms responsible for this difference in efficacy are not fully understood, although there are two major theories. Ammonia, produced by H. pylori, is able to neutralize gastric acid, and thus apparently increase the effect of acid suppressive agents (the 'ammonia theory'). The other theory is that decrease in acid output is due to the development of corpus gastritis during treatment with a proton pump inhibitor (the 'gastritis theory'). Treatment strategies to overcome this lowered sensitivity to acid suppression are to increase the frequency/dose of a proton pump inhibitor or to add an H2-receptor antagonist in the evening-but both have pharmaco-economic implications. An agent that could provide adequate pH control regardless of H. pylori status would be highly beneficial in the treatment of GERD, and may also lower treatment costs.
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PMID:Review article: the clinical influence of Helicobacter pylori in effective acid suppression-implications for the treatment of gastro-oesophageal reflux disease. 1093 Aug 91

For a long time heartburn was not considered a symptom for serious illness. By now, however, it is accepted that the incidence of secondary carcinoma of the esophagus caused by chronic GERD has increased dramatically since the nineteen-seventies. Mechanisms leading to GERD are complex and its incidence is not necessarily pathological. However pathological reflux in the lower esophagus (pH lower than 4 in 6 % of 24 hours), caused by decreased sphinctertonus, impaired peristalsis and clearance of the esophagus, may lead to complications. Helicobacter pylori may play a key role in GERD. There is strong evidence for a protective effect of Hp-infection in the development of GERD. In pangastritis, caused by Hp-infection, gastric acid production is inhibited resulting in a reduction of stomach-acid-concentration. This may be caused by either the chronic infection itself and the resulting atrophy of the stomach-mucosa, by the ammonia-producing HP-bacteria, or an increase in acid re-absorbtion of gastric epithelium. Laryngopharyngeal reflux (LPR) often results in atypical manifestations with oral, pharyngeal, laryngeal, and pulmonary disorders. Laryngopharyngeal reflux is known to contribute to posterior acid laryngitis and laryngeal contact ulceration or granuloma formation, laryngeal cancer, chronic hoarseness, pharyngitis, asthma, pneumonia, nocturnal choking, and dental diseases. Today, PPI are the medication of choice in both acute and long-term (prophylactic) therapy of GERD. The so called "step-up-strategy" of medication is no longer recommended. Here, patients were first treated with antacids, then prokinetics followed by H2-blockers and finally low-dose PPI. Only in the case of persisting symptoms medication was further increased to high-dose PPI therapy. In the past this increase in medication lead to a prolonged healing process and consequently to higher medication costs. Studies have shown that a "step-down"-therapy, beginning with high dose PPI, is highly preferable, since it is much more effective. Depending on the degree of the symptoms, however, medication may also be applied "on-demand". The BfArM has approved this kind of medication application only for Esomeprazol (Nexium mups 20 mg).
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PMID:[Gastroesophageal reflux -- a common illness?]. 1262 41

Five isonitrogenous diets (1-5) with 40% protein using oilcakes as protein sources were formulated and fed to Cirrhinus mrigala fingerlings maintained both under laboratory and field conditions. Water soaking of oilcakes for 24 h before incorporation in the diets helped in the reduction of antinutrient factors (phytase and tannins). Live weight gain in fish fingerlings fed on a diet containing groundnut oilcake (GNOC) was significantly (P < 0.05) enhanced in comparison to the other dietary treatments when examined at the end of a feeding schedule. Laboratory studies have further revealed that APD, PER, GPR and GER values were significantly (P < 0.05) enhanced, while those of feed conversion ratio were significantly (P < 0.05) reduced in fish fed on diet 1 containing GNOC. An analysis of water samples collected at two hourly interval from the aquaria revealed low levels of total ammonia (N-NH4+) excretion and reactive phosphate (O-PO4) production in fish fed on diet 1. Proximate carcass composition also revealed high accumulation of protein, fat, energy and phosphorus in fingerlings fed on a diet containing GNOC. Even in field studies a significant (P < 0.05) increase in mean fish weight gain and specific growth rate (SGR% d(-1)) was observed in fingerlings fed on diet 1, followed by canola (2), sunflower (3), mustard oilcake (4) and sesame (5). Water and sediment quality characteristics also correlated well with fish growth.
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PMID:Oilcakes as protein sources in supplementary diets for the growth of Cirrhinus mrigala (Ham.) fingerlings: laboratory and field studies. 1268 72

We systematically reviewed the literature on gastroesophageal reflux disease (GERD) related to Helicobacter pylori therapy, and classified the GERD according to various aspects. Preexisting GERD is active GERD before H. pylori therapy, and a substantial proportion of the GERD patients improve after successful H. pylori therapy. If the GERD does not persist or recur after cessation of acid-suppressive therapy combined with H. pylori therapy, it may have been cured (cured GERD). If it recurs, it may have been masked by acid-suppressive therapy and unmasked with cessation of the therapy (pharmacologically masked and unmasked GERD). Newly developed GERD after successful H. pylori therapy is a kind of unmasked GERD arising after cure of infection (de novo unmasked GERD). The possible mechanism of the improvement of cured GERD is normalized hyperacidity associated with an improved cytokine-somatostatin-gastrin system followed by normalized G-cell activity and parietal cell mass. Preexisting GERD is not a reason to avoid eradication therapy. De novo unmasked GERD develops in a substantial proportion of patients with cured infection. The possible mechanism is increased acid exposure in the esophagus due to gastric acid increase, which is caused by a loss of neutralizing effect by ammonia, normalized cytokine-acid suppression and improvement of corpus atrophy. De novo unmasked GERD is important because GERD is recurrent and may induce adenocarcinoma of the esophagus. However, it is expected that cure of infection lowers gastric cancer incidence. Eradication therapy is recommended irrespective of the possibility that de novo unmasked GERD may have a slight increase of the risk of esophageal adenocarcinoma.
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PMID:Active and inactive gastroesophageal reflux diseases related to Helicobacter pylori therapy. 1295 Jun

Laryngopharyngeal or gastroesophageal reflux is associated with laryngeal airway hyperreactivity (LAH), but neither the cause-effect relationship nor the underlying mechanism has been elucidated. Here we established a rat model with enhanced laryngeal reflex reactivity induced by laryngeal acid-pepsin insult and investigated the neural and hydroxyl radical (*OH) mechanisms involved. The laryngeal segments of 103 anesthetized rats were functionally isolated while animals breathed spontaneously. Ammonia vapor was delivered into the laryngeal segment to measure laryngeal reflex reactivity. We found that the laryngeal pH 5-pepsin treatment doubled the reflex apneic response to ammonia, whereas laryngeal pH 7.4-pepsin, pH 2-pepsin, and pH 5-denatured pepsin treatment had no effect. Histological examination revealed limited laryngeal inflammation and epithelial damage after pH 5-pepsin treatment and more severe damage after pH 2-pepsin treatment. In rats that had received the laryngeal pH 5-pepsin treatment, the apneic response to ammonia was abolished by either denervation or perineural capsaicin treatment (PCT; a procedure that selectively blocks capsaicin-sensitive afferent fibers) of the superior laryngeal nerves, but was unaffected by perineural sham treatment. LAH was prevented by laryngeal application of either dimethylthiourea (DMTU; a *OH scavenger) or deferoxamine (DEF; an antioxidant for *OH), but was unaltered by the DMTU vehicle or iron-saturated DEF (ineffective DEF). LAH reappeared after recovery from PCT, DMTU, or DEF treatment. We conclude that 1) laryngeal insult by pepsin at a weakly acidic pH, but not at acidic pH, can produce LAH; and 2) LAH is probably mediated through sensitization of the capsaicin-sensitive laryngeal afferent fibers by a *OH mechanism.
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PMID:Neural and hydroxyl radical mechanisms underlying laryngeal airway hyperreactivity induced by laryngeal acid-pepsin insult in anesthetized rats. 1678 36

Urea-nitrogen recycling to the gastrointestinal tract (GIT), N metabolism, and urea transporter-B (UT-B) mRNA abundance in ruminal epithelium were evaluated in partially defaunated (PDFAUN) and faunated (FAUN) growing lambs fed 2 levels (10%, low, or 15%, high) of dietary CP (DM basis). Four Suffolk ram lambs (43.9 +/- 1.4 kg initial BW) were used in a 4 x 4 Latin square design with 27-d periods. Sunflower oil was fed (6%; DM basis) as an anti-protozoal agent. Nitrogen balance was measured from d 22 to 26, with concurrent measurement of urea-N kinetics using continuous intrajugular infusions of [(15)N(15)N]-urea. Feeding sunflower oil decreased (P < 0.01) total ruminal protozoa by 88%, and this was associated with a decrease (P < 0.01) in ruminal ammonia-N concentrations. Endogenous production of urea-N (UER; 26.1 vs. 34.6 g/d) and urea-N loss in urine (UUE; 10.1 vs. 15.7 g/d) were less (P < 0.01), and urea-N entering the GIT (GER; 16.0 vs. 18.9 g/d) tended to be less (P = 0.06) in PDFAUN as compared with FAUN lambs. However, as a proportion of UER, GER was greater (P < 0.01) and the proportion of recycled urea-N that was utilized for anabolism (i.e., UUA) tended to be greater (P = 0.09) in PDFAUN lambs. Partial defaunation increased (P < 0.01) microbial N supply. The UER, GER, and UUE were greater (P < 0.01) in lambs fed the high diet. However, as a proportion of UER, GER and its anabolic use were greater (P < 0.01) in lambs fed the low diet. The expression of UT-B mRNA in PDFAUN lambs was numerically greater (by 20%; P = 0.15) compared with FAUN lambs. In summary, results indicate that part of the mechanism for improved N utilization in defaunated ruminants is an increase in the proportion of endogenous urea-N output that is recycled to the GIT, thus potentially providing additional N for microbial growth.
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PMID:Effects of partial ruminal defaunation on urea-nitrogen recycling, nitrogen metabolism, and microbial nitrogen supply in growing lambs fed low or high dietary crude protein concentrations. 1996 67


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