Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraluminal pH in the lower esophagus has been recorded during a 3-hr period following a ligh meal and a consecutive 12-hr nocturnal period in 20 patients with typical symptoms and radiological evidence of gastroesophageal reflux and in 10 patients without such signs of reflux. Evidence of acid reflux was obtained in 3 of the patients without reflux during the postcibal period but in only one during the 12-hr nocturnal period. In contrast all except one of the 20 patients who had evidence of reflux showed spells of high acidity both in the postcibal and nocturnal periods. There was no clear correlation between the frequency of paf high acidity in the nocturnal period. Those patients with endoscopic evidence of severe esophagitis showed a significantly longer duration of high esophageal acidity in the nocturnal period. We conclude that nocturnal exposure of the esophageal mucosa to acid is a major factor in the causation of reflux esophagitis.
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PMID:Esophageal intraluminal pH recording in the assessment of gastroesophageal reflux and its consequences. 1 83

We examined 66 patients with pain of possible esophageal origin for sensitivity to intraesophageal infusions of coffee, orange juice, spicy tomato drink, or HCl of varying concentrations as an addendum to their acid infusion (Bernstein) tests. Compared to Berstein-negative subjects, acid-sensitive patients were sensitive to infusion of coffee (P less than 0.01), orange juice (P less than 0.001), and tomato drink (P less than 0.001). Patients were largely insensitive to HCl solutions with a titratable acidity of 1 mEq per liter or less, less than the least acidic food solution tested. However, Berstein-positive patients were still highly sensitive to infusions of coffee, orange juice, and tomato drink adjusted to pH 7 (P less than 0.001). Patients were unable to differentiate symptoms caused by acid or food infusions, and solutions did not differ in the duration of infusion needed either to cause symptoms or to relieve them by saline. We conclude that the pain of esophagitis is nonspecific and can be precipitated by variety of seemingly unrelated substances.
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PMID:Food sensitivity in reflux esophagitis. 2 14

The mucous membrane of the oesophagus of 6 pigs was experimentally damaged with hydrochloric acid to create changes similar to reflux oesophagitis. The passage of contrast medium through the oesophagus of the pigs was observed by using spot radiography and pressure measurements. Acid contrast medium caused spasms and nonperistaltic pressure waves during the act of swallowing. Conventional contrast medium traversed the oesophagus normally and the swallowing complex was normal. On the basis of this experimental model it is concluded that the acidity of a bolus is of fundamental importance in the aetiology of spasms in oesophagitis.
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PMID:Effect of acid on the motility of the oesophagus of the pig with experimentally induced oesophagitis. 59 48

It is assessed that heartburn with associated oesophagitis is experienced by 45% to 70% of pregnant women. Posture is the most constant associated factor; bile regurgitation through the pylorus is likely to be important in its aetiology but gastric acidity is not. Treatment with alkalis or dilute hydrochloric acid affords some relief in 95% of cases and patient acceptability is the most important factor in choice of preparation. Hiatus hernia is likely to be present in severe cases and rupture of the oseophagus has been reported. Early delivery may be advisable in the interest of the mother.
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PMID:Heartburn in pregnancy. 75 Feb 49

The operations of Nissen, Hill, and Belsey are adequate in controlling esophaegeal reflux in the majority of patients. In a small percentage however, objective and subjective evidence of esophagitis persists in spite of repeated operations to restore lower esophageal sphincter competency. These failures are then usually treated by operative procedures of great magnitude involving organ interposition. Repeated antireflux operations directed to the gastroesophageal area may in some instances result in impairment of blood supply with an increased risk of both esophageal and gastric fistulae. In the past many observers have felt that reflux esophagitis resulted solely from the effects of acid-pepsin secretions bathing the distal esophagus. Recently experimental and clinical data have indicated the importance of duodenal contents in the etiology and perpetuation of reflux esophagitis. During a recent two year period, 6 patients with persistent reflux esophagitis uncontrolled by repeated antireflux procedures have been seen on our service. These 6 patients, underwent 12 unsuccessful antireflux operations elsewhere. Three of the 6 patients had also been subjected to vagotomy-antrectomy for a coexisting duodenal ulcer. A marked lowering of gastric acidity took place but esophageal reflux and esophagitis persisted. These three patients were treated on our service by takedown of the Billroth I anastomosis, closure of the duodenal stump and diversion of the duodenal contents into a Roux-en-Y limb. Three other patients who had undergone unsuccessful antireflux procedures alone were subjected to antral resection, Roux-en-Y diversion and transthoracid vagotomy. This simplified appraoch to the treatment of persistent esophageal reflux uncontrolled by repeated antireflux procedures has given satisfactory results. The operation should be considered when technical considerations preclude further surgical attempts to perform another effective antireflux operation. Total duodenal diversion should, however, not be considered as the primary operation for the patient suffering from reflux esophagitis. However, in circumstances discussed above this direct approach appears preferable to major resectional procedures.
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PMID:Total duodenal diversion for treatment of reflux esophagitis uncontrolled by repeated antireflux procedures. 97 51

The combination of a histamine H2-receptor antagonist and a muscarinic receptor antagonist has been reported to result in greater suppression of intragastric acidity than either agent alone. The present randomized, double-blind, multicentre trial compared the effects of the oral combination of 150 mg ranitidine b.d. plus 50 mg pirenzepine b.d. with 150 mg ranitidine b.d. plus placebo pirenzepine b.d. in the treatment of patients with reflux oesophagitis. All 157 patients had symptoms of gastro-oesophageal reflux with endoscopically confirmed oesophageal erosions (Savary and Miller grades I-III). After four weeks of treatment, healing rates were 32/75 (43%) in the combined treatment group and 34/76 (45%) in the group receiving ranitidine alone. After eight weeks, the cumulative healing rates had increased to 48/72 (67%) and 51/75 (68%), respectively. More patients receiving ranitidine plus pirenzepine had complete relief of day- and night-time heartburn after four weeks compared with those receiving ranitidine alone (day: 59% vs. 38%, P = 0.02; night: 69% vs. 52%, P = 0.04). After eight weeks, symptom relief was comparable in both groups. Clinical adverse effects were reported by nine patients receiving ranitidine and by 19 patients receiving the combination. It is concluded that combining ranitidine with pirenzepine does not aid the healing of reflux oesophagitis but does improve symptom relief at four weeks.
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PMID:The effect of combined therapy with ranitidine and pirenzepine in the treatment of reflux oesophagitis. 142 Jul 52

Esophageal pH-metry is the test of choice for diagnosing gastroesophageal reflux. However, although it allows acid refluxes to be distinguished, it is of limited value for identifying alkaline or mixed (acid mixed with alkaline material) refluxes. To evaluate the ability of dual pH-metry to identify alkaline or mixed refluxes, the gastric acidity and gastroesophageal reflux pattern were evaluated simultaneously in 64 patients with mild-moderate esophagitis, in 28 patients with severe or complicated esophagitis, and in 20 healthy subjects. A dual esophageal gastric pH-probe allowed three different types of esophageal reflux to be distinguished: (a) acid refluxes, defined as a drop in esophageal pH to values less than 4 together with a gastric pH less than 4; (b) mixed refluxes, defined as a drop in esophageal pH from baseline to values greater than 4 associated with rises in gastric pH to greater than 4 values; (c) alkaline refluxes, defined as a rise in esophageal pH to greater than 7 associated with a simultaneous increase in gastric pH to greater than 4. Gastric acidity was more significantly reduced in patients with severe or complicated esophagitis than it was in healthy subjects (P less than 0.01). The reflux pattern in both mild-moderate and severe esophagitis was characterized by mainly acid refluxes and a marked increase in the time the esophagus mucosa was exposed to acid (P less than 0.001). Pure alkaline refluxes were rare (less than 1%) in both healthy subjects and esophagitis patients. The number of mixed refluxes was considerably higher in severe esophagitis patients than it was in either mild-moderate esophagitis patients or controls (P less than 0.05). The finding of mixed refluxes in severe or complicated esophagitis suggests that biliary acids and/or pancreatic enzymes are involved in the pathogenesis of severe forms of esophagitis.
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PMID:Gastric acidity and gastroesophageal reflux patterns in patients with esophagitis. 844 Apr 52

Reduction of daytime as well as nighttime acidity is important in the healing of duodenal ulceration and reflux oesophagitis. The importance of the time of dosing of potent, long-acting H2 blockers for optimal suppression of intragastric acidity is unknown. The efficacy of different oral dosage regimens of SKF-94482, a new, competitive and long-acting H2-receptor antagonist, in reducing daytime and nighttime intragastric acidity was studied with 24-h pH-monitoring in 3 double-blind, randomized, crossover trials in 45 fed, healthy subjects. In study A 200 mg, 400 mg, or 600 mg SKF-94482 or placebo was given at 0830 h for 6 days. In study B the above doses were taken at 1830 h. In study C 200 mg or 300 mg of SKF-94482 or placebo was given at 0830 and 1830 h for 6 days. SKF-94482, 400 mg, was the most effective dose, and twice daily dosing was of no additional pharmacodynamic benefit. When 400 mg SKF-94482 was given at 0830 h, the median 24-h, day (0800-1800 h) and night (1800-0800 h) pH (interquartile range) were 2.6 (2.2-3.2), 2.3 (2.1-3.8), and 2.6 (1.8-3.6), respectively. When the time of dosing was 1830 h with 400 mg SKF-94482, median 24-h, day and night pH were 3.4 (2.5-4.0), 3.4 (3.1-4.3), and 3.7 (2.8-5.9), respectively. Early-evening dosing of this long-acting H2 antagonist resulted in substantially greater suppression of intragastric acidity than morning dosing.
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PMID:Is the time of dosing of a potent long-acting H2-receptor antagonist critical? Twenty-four-hour pH measurements with SKF-94482. 167 50

The human stomach has a normal circadian rhythm of intragastric acidity characterized by increasing acidity during the day and peaks in the early hours of the morning. Eating causes a transient decrease of intragastric acidity. Acid appears to be the permissive factor in peptic ulcer disease and to be responsible for symptoms; the patient with duodenal ulcer may secrete too much acid. Pharmacological control of gastric acid secretion will speed ulcer healing. Modern regimens, which typically use a bedtime dose of an H2-receptor antagonist, produce a pulse of decreased acidity. Intragastric acidity is decreased during the night and early morning, leaving a normal profile of acidity during the day and early evening. Higher or more frequent doses of an antisecretory agent can produce a more profound decrease of 24-h intragastric acidity. Theoretical problems associated with a sustained or profound decrease of 24-h intragastric acidity include the threat of enteric infection and infestation, potential bacterial overgrowth with possible N-nitrosamine formation, and drug-induced hypergastrinaemia. In light of these potential problems, for the management of simple peptic ulceration, it appears sensible to use the minimum intervention required. Bedtime H2-receptor blockade is one such regimen. The more potent antisecretory regimens can be used for difficult clinical problems such as the Zollinger-Ellison syndrome, intractable duodenal ulceration, and severe oesophagitis.
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PMID:Degrees of acid suppression and ulcer healing: dosage considerations. 188 35

Omeprazole is a specific inhibitor of H+,K(+)-ATPase or 'proton pump' in parietal cells. This enzyme is responsible for the final step in the process of acid secretion; omeprazole blocks acid secretion in response to all stimuli. Single doses produce dose-dependent inhibition with increasing effect over the first few days, reaching a maximum after about 5 days. Doses of omeprazole 20mg daily or greater are able to virtually abolish intragastric acidity in most individuals, although lower doses have a much more variable effect. Omeprazole causes a dose-dependent increase in gastrin levels. Omeprazole must be protected from intragastric acid when given orally, and is therefore administered as encapsulated enteric-coated granules. Absorption can be erratic but is generally rapid, and initially the drug is widely distributed. It is highly protein-bound and extensively metabolised. Its elimination half-life is about 1h but its pharmacological effect lasts much longer, since it is preferentially concentrated in parietal cells where it forms a covalent linkage with H+,K(+)-ATPase, which it irreversibly inhibits. Omeprazole binds to hepatic cytochrome P450 and inhibits oxidative metabolism of some drugs, the most important being phenytoin. Omeprazole has produced short term healing rates superior to the histamine H2-receptor antagonists in duodenal ulcer, gastric ulcer and reflux oesophagitis. It has also been shown to be highly effective in healing ulcers which have failed to respond to H2-receptor antagonists, and has been extremely valuable in treating patients with Zollinger-Ellison syndrome.
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PMID:Clinical pharmacology of omeprazole. 202 1


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