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)

The purpose of this study was to explore the efficacy of lansoprazole, a proton pump inhibitor, in reducing the acidity and volume of gastric aspirate in children immediately following the induction of anaesthesia. One hundred healthy in-patients aged 3-11 yr undergoing elective surgery were randomly allocated to four groups (n = 25 each): lansoprazole-lansoprazole, placebo-placebo, placebo-lansoprazole, and lansoprazole-placebo. For each treatment regimen, the first medication was administered at 9:00 pm on the night before surgery and the second at 5:30 am on the morning of the day of surgery (three hours preoperatively). The dose of lansoprazole was 30 mg (approximately 1.4 mg.kg-1 mean). Children were offered 10 ml.kg-1 apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. Lansoprazole increased gastric fluid pH and decreased gastric fluid volume regardless of whether it was administered before or after placebo. Two consecutive doses of lansoprazole was the most effective means of increasing the pH and reducing the volume of gastric aspirate; in this group, there were no subjects with gastric aspirate volume > 0.4 ml.kg-1 and pH < 2.5. Oral lansoprazole, at least 30 mg, given on the night before surgery or on the morning of surgery will improve the gastric environment at the time of induction of paediatric anaesthesia. The most effective regimen was two doses (at bedtime and on the morning) of lansoprazole.
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PMID:Lansoprazole reduces preoperative gastric fluid acidity and volume in children. 762 22

Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic drugs had only modest inhibitory effects on acid secretion, many side effects, and uncertain efficacy. Controlled trials using antacids demonstrated the value of reducing gastric acidity for healing duodenal ulcer. The discovery of histamine-2 (H2) receptor antagonists in the 1970s and the introduction of H+,K(+)-ATPase inhibitors in the 1980s made reduction of acid secretion the first-choice modality for healing and preventing recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from the stomach. However, antibiotic eradication of Hp can be difficult, often requiring simultaneous administration of a drug that suppresses acid secretion. Therefore, H2 and proton pump inhibitors continue to play a role in the management of duodenal and gastric ulcers associated with Hp and also play a primary role in the therapy of other acid-related disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gastrinoma (Zollinger-Ellison syndrome) and other acid hypersecretory states.
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PMID:Suppression of acid secretion in peptic ulcer disease. 767 7

High values (800-6000 parts per billion) of nitric oxide (NO) in expelled air from the stomach were shown in humans by chemiluminescence technique. These NO values were more than 100 times higher than those found in orally exhaled air. Intragastric NO production is probably non-enzymatic, requiring an acidic environment, as NO in expelled air was reduced by 95% after pretreatment with the proton pump inhibitor omeprazole. Furthermore, large amounts of NO were formed in vitro from lettuce and saliva when placed in hydrogen chloride (pH < 2). In conclusion, large amounts of NO are formed intragastrically in humans and this source of NO may be of importance for the integrity of the gastric mucosa in health and disease. Measurements of NO in expelled air might be of value as a non-invasive method for estimation of gastric acidity.
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PMID:Intragastric nitric oxide production in humans: measurements in expelled air. 782 69

Ambulatory 24-hour pH monitoring was conducted in 11 patients with H2-blocker resistant reflux esophagitis to compare the effects of standard doses of H2-blocker (famotidine 20mg twice daily) and proton pump inhibitor (omeprazole 20mg once daily) on the inhibition of intraesophageal acidity. Mean intraesophageal pH during PPI treatment was significantly higher than that during H2-blocker treatment. Proportion of abnormal intra-esophageal acidity in 24hr (%time pH < 4) during PPI treatment was significantly less than that during H2-blocker treatment (11.7 +/- 3.1% vs 31.6 +/- 4.8%). The difference of the effect was more apparent in day time (upright time) than in night time (supine time). Thus PPI is superior to H2-blocker in treatment for refractory reflux esophagitis, but proportion of abnormal intra-esophageal acidity in 24hr (%time pH < 4) could be normalized only in 4 out of 11 patients even by standard dose PPI treatment. Effects of not only long-term maintenance therapy but also high dose therapy with PPI should be examined in future studies.
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PMID:[Comparison of the effects between standard doses of H2-blocker (famotidine 20mg b.d.) and proton pump inhibitor (omeprazole 20mg o.d.) in the treatment of refractory reflux esophagitis by ambulatory 24-hr intra-gastroesophageal pH monitoring]. 783 83

Gastric acid is of central importance in the pathogenesis of duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Pharmacological reduction of acid secretion is, therefore, the mainstay of current treatment, but the optimal degree of acid suppression remains incompletely understood. This paper considers the ideal ways of assessing and reporting the pharmacological effectiveness of acid-inhibiting drugs and relating such data to clinical efficacy. Twenty-four-hour intragastric pH measurements are widely used for this purpose, although this technique cannot measure secretion quantitatively. Data on suppression of 24-hr intragastric acidity for groups of subjects have been successfully correlated with healing rates for duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Three primary determinants of healing have been derived from antisecretory data. These are the degree of suppression of acidity, the duration of suppression of acidity, and the duration of treatment. The order of importance of these determinants varies depending on the disease. Data on 24-hr intragastric acidity should be accompanied whenever possible by data on 24-hr plasma gastrin levels, as the relationship between suppression of acidity and a rise in gastrin varies widely between individuals. It is not possible to predict the plasma gastrin level from the intragastric pH or any other measurement of intragastric acidity. Comparative data sets in groups of subjects may provide useful information. Proton pump inhibitors produce a greater and longer-lasting degree of suppression of acidity than conventional doses of H2-receptor antagonists. For this reason, they are more effective in healing duodenal ulcer and gastric ulcer. However, in view of the importance of duration of treatment, healing rates with the H2-receptor antagonists approach those obtained with proton pump inhibitors if treatment is continued for a longer time. In gastroesophageal reflux disease in particular, although the optimal degree of acid suppression is not yet defined, the consistently superior performance of proton pump inhibitors demonstrates that increased suppression of acidity is clinically beneficial.
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PMID:Optimizing acid suppression for treatment of acid-related diseases. 785 82

Despite the fact that reflux esophagitis is a multifactorial disease, inhibition of gastric acid secretion is the mainstay of medical treatment, both for moderate and severe cases. Antisecretory agents lower the acidity of the refluxate, thus decreasing its aggressive effect, which favors the mucosal healing process. The greater the acid inhibition, the greater will be the mucosal repair. This is the reason for a therapeutic gain for H2-receptor antagonists over anticholinergics and antacids, and for proton pump inhibitors over H2-receptor antagonists. The most recently developed proton pump inhibitor, lansoprazole, at doses of 15, 30, or 60 mg/day for 4 and 8 weeks of treatment, has proven to be significantly more effective than placebo (one multicenter study involving 292 patients) or ranitidine (three multicenter studies involving 653 patients) in terms of mucosal healing and symptom relief. In two comparative trials with omeprazole 20 mg vs lansoprazole 30 mg (in a total of 349 evaluable patients) healing rates were found to be similar, but in one trial the relief of heartburn proved to be significantly more pronounced in patients receiving lansoprazole who also used fewer antacids. The frequency of adverse events was comparable in the two treatment groups. Reflux esophagitis is a chronic condition and after stopping antisecretory treatment, including lansoprazole, most patients relapse in terms of symptoms and endoscopical lesions, which suggests the need for long-term treatment. However, a strategy for long-term control of reflux esophagitis remains to be defined (lower daily dose, alternate-day standard dose, or concomitant prokinetic drugs?). The safety of proton pump inhibitors given for prolonged periods also needs to be more thoroughly evaluated.
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PMID:Treatment of gastroesophageal (acid) reflux with lansoprazole: an overview. 791

The present strategies for the management of peptic ulceration are well tolerated and clinically effective. Histamine H2-receptor antagonists can be used for mild to moderate disease, and proton pump inhibitors are of particular benefit for patients with severe peptic ulceration and the Zollinger-Ellison syndrome. However, none of these treatments provides protection against recurrent ulceration, except when taken as long-term continuous treatment. Long-term exposure to pharmacological agents raises problems of safety, particularly relating to a lack of intragastric acidity. In addition, the accelerated development of atrophic gastritis in patients receiving omeprazole requires investigation and assessment. It is unlikely that there will be any major development in the area of control of gastric acid secretion, except perhaps the introduction of specific immunization against gastrin. However, the clinical benefit of this strategy awaits assessment. The main area for development must be the introduction of convenient and effective regimens for the eradication of Helicobacter pylori infection. Existing regimens are either simpler and relatively ineffective, or too complicated for widespread application. Bearing in mind the long gestation period of any new drug, it seems likely that the only innovative drug that will be introduced for the management of peptic ulceration before the millennium will be ranitidine bismuth citrate, an antisecretory anti-H. pylori drug that will usually be used in combination with an antibiotic.
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PMID:Treatment of peptic ulcers from now to the millennium. 794 62

To test whether in RINm5F rat insulinoma cells luminal acidity and the activity of a vacuolar-type proton pump are involved in calcium sequestration by intracellular calcium stores sensitive to inositol 1,4,5-trisphosphate (InsP3) we examined the effects of various proton-conducting ionophores and ammonium chloride, and of bafilomycin, a specific inhibitor of vacuolar proton pumps, on this parameter. Bafilomycin in concentrations up to 1 microM did not affect calcium sequestration by nonmitochondrial, InsP3-sensitive stores at all; 50 microM carbonylcyanide m-chlorophenylhydrazone, 50 microM monensin and 30 mM NH4Cl, which are diverse ways to dissipate transmembrane pH gradients, did not inhibit calcium sequestration. This argues against signficant involvement of internal acidity and vacuolar proton pumps in calcium sequestration by InsP3-sensitive stores in RINm5F cells. The proton-potassium-exchanging ionophore nigericin (20-100 microM), however, inhibited calcium sequestration by nonmitochondrial and InsP3-sensitive stores. This effect was dependent on the presence of potassium and could be reversed by inclusion of carbonylcyanide m-chlorophenylhydrazone or acetate in the incubation medium. Thus, the inhibitory effect of nigericin appears to be based on proton extrusion coupled to potassium influx across the membrane of calcium stores in RINm5F cells, creating an internal alkalinization of these stores. The effect of nigericin implies the continuous maintenance of an outside-to-inside potassium concentration gradient by nonmitochondrial calcium stores in RINm5F cells. This feature will be of potential interest in the identification of InsP3-sensitive calcium-storing organelles.
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PMID:An investigation on the role of vacuolar-type proton pumps and luminal acidity in calcium sequestration by nonmitochondrial and inositol-1,4,5-trisphosphate-sensitive intracellular calcium stores in clonal insulin-secreting cells. 802 97

The 24-hour intragastric pH monitoring was conducted in patients with gastric ulcers treated with an H2 blocker, and the pathophysiological conditions and the treatment of intractable gastric ulcers were studied from the aspect of degree of intragastric acidity. During the administration of a standard dose of an H2 blocker, there was no difference of intragastric acidity at night between intractable gastric ulcers and tractable gastric ulcers. However, intragastric acidity was significantly higher during the day in the intractable gastric ulcers. The pH 3 holding time rate during the day in all intractable gastric ulcer patients was less than 45%; however, in the tractable gastric ulcer patients it was more than 45% during the day. In treating intractable gastric ulcers, if combined administration of synthetic prostaglandin E2 having a suppressing action of gastric acid secretion was performed or if the drug was changed to a proton pump inhibitor, a rise in intragastric pH was observed and earlier cure was obtained. That is to say, intractable gastric ulcers are characterized by inadequate suppression of gastric acid during the day, and it is surmised that if gastric acid can be adequately suppressed not only during the night but also during the day, no matter which drug or administration method is used, it will be effective against intractable gastric ulcers.
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PMID:[A clinical study of pathophysiology and treatment of intractable gastric ulcers based on 24-hour intragastric pH monitoring]. 809 80

Effect of omeprazole, a gastric proton pump inhibitor, on gastric secretion during anesthesia and surgery was evaluated in 39 elective surgical patients ranged in age from 18 to 69 years. These patients were divided into two groups according to their age either of 40 years and under or over. The patients of both groups underwent orthopedic, ophthalmic, ENT, plastic, oral or non-abdominal surgery under neuroleptanesthesia, enflurane anesthesia or total intravenous anesthesia with droperidol, fentanyl and ketamine. They all were administered omeprazole 20 mg orally at 21:00 the night before surgery and again at 7:00 on the morning of surgery. The volume and acidity of gastric juice were measured at anesthetic induction and emergence from anesthesia. The volume and pH of the gastric juice in patients of 40 years and under in age averaged to 9.8 +/- 3.2 (mean +/- SE) ml, 2.45 +/- 0.56 at the anesthetic induction and 9.3 +/- 4.1 ml, 4.66 +/- 0.60 at the emergence from anesthesia respectively. The mean volume and pH of the gastric juice in patients over 40 years of age were 5.0 +/- 1.7 ml, 4.68 +/- 0.56 at the anesthetic induction and 9.9 +/- 2.4 ml, 5.76 +/- 0.36 at the emergence from anesthesia respectively. Significant decrease in the volume and acidity of gastric juice was observed in the patients of both groups except that the average of intragastric pH of the patients under 40 years of age was below 2.50 at the induction of anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A gastric proton pump inhibitor as preanesthetic medication]. 818 82


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