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 gastric antisecretory effects of two dose levels of pirenzepine given at night were investigated in a group of healthy male volunteers. Compared with placebo, three days of treatment with pirenzepine 100 mg nocte or 150 mg nocte inhibited mean nocturnal intragastric acidity by 54% and 53%, respectively (p less than 0.01). The volume of gastric juice secreted was reduced by 47% and 52% (p less than 0.005), by 100 mg and 150 mg nocte, respectively. Each dose suppressed mean gastric acid output by 67% (p less than 0.001). Pepsin output was not significantly altered. There were no differences in effect between the two dose levels studied, but side-effects such as dry mouth were only seen with the higher dose. Pirenzepine 100 mg is the optimum dose which can conveniently be given at night. This will limit side-effects, and may be a useful treatment for patients with duodenal ulcer.
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PMID:Single nocturnal doses of pirenzepine effectively inhibit overnight gastric secretion. 286 23

Anticholinergic agents are most often divided into tertiary and quaternary ammonium compounds. Tertiary ammonium agents are fully and rapidly absorbed. Quaternary ammonium agents are slowly and incompletely absorbed, but do not cross the blood-brain barrier, or do so to a very limited degree, and have a very low rate of central nervous system side-effects. There are probably subclasses of cholinergic receptors, and anticholinergic agents have different affinities for these. Anticholinergics can decrease the basal acid secretion as well as secretion stimulated by histamine, pentagastrin, insulin or food. Combined therapy with antacids and anticholinergics will give a more long-lasting decrease in acidity than with either drug alone. The reported controlled studies with anticholinergic agents suggest that they can induce healing of duodenal ulcer to the same degree as cimetidine but at the cost of more frequent side-effects. Except for the studies on pirenzepine there are, however, too few studies in which anticholinergics have been compared with histamine H2-receptor antagonists; thus the place of anticholinergics in the treatment of an active duodenal ulcer is not clear. In doses of not less than 100 mg daily, pirenzepine is a candidate-drug for the short-term treatment of duodenal ulcer. At these doses, side-effects of dry mouth and visual disturbance are, however, rather frequent, and more serious side-effects such as urinary retention do also occur. More studies with both the conventional anticholinergics and pirenzepine, with emphasis not only on the desired effects but also on side-effects, are needed before anticholinergics can be taken into consideration as alternatives to histamine H2-receptor antagonists for healing and maintenance treatment. There is some evidence that long-term treatment with anticholinergic agents can decrease recurrences and complications of peptic ulcer disease. Even if there are some encouraging reports on the combination of anticholinergics and antacids, we need more such studies with lower doses of antacids and lower doses of anticholinergics before this combination therapy can be regarded as an equally good alternative to histamine H2-receptor antagonists for ulcer healing and symptom relief.
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PMID:Antacids and anticholinergics in the treatment of duodenal ulcer. 608 86

The pharmacology, pharmacokinetics, clinical studies, adverse reactions, and dosage of sucralfate (Carafate, Marion Laboratories), a unique drug for peptic-ulcer disease, are reviewed. Sucralfate exerts its antiulcer effect by binding with proteinacious material, neutralizing local acidity without affecting gastric pH, and forming a protective barrier at the ulcer site. It also inhibits the diffusion of hydrogen ion, inhibits the action of pepsin, and adsorbs bile salts. Approximately 3-5% of an orally administered dose of sucralfate is absorbed; more than 90% of the dose is excreted unchanged in the feces. Sucralfate remains at the site of gastric ulcers for up to six hours. In the treatment of duodenal ulcers, sucralfate is more effective than placebo and comparable with cimetidine and intensive antacid therapy. Healing rates for gastric ulcers are less impressive but are comparable with those produced by cimetidine and antacids. Additive or synergistic effects of sucralfate with cimetidine or intensive antacid therapy have not been studied. Sucralfate has few side effects because it is not absorbed; most frequently reported are constipation (3-4%), xerostomia (1%), and skin eruptions (0.6%). No drug-drug interactions have been reported. The recommended dose of sucralfate is 1 g four times a day one hour before meals and at bedtime. Sucralfate is a unique antiulcer drug that compares favorably with cimetidine and antacid therapy in terms of safety and efficacy. Sucralfate is FDA-approved for short-term (up to eight weeks) treatment of duodenal ulcers.
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PMID:Sucralfate--alternative therapy for peptic-ulcer disease. 676 89

Amifostine (Ethyol), an inorganic thiophosphate, is a selective broad-spectrum cytoprotector of normal tissues that provides cytoprotection against ionizing radiation and chemotherapeutic agents, thus preserving the efficacy of radiotherapy and chemotherapy. This review summarizes the preclinical data and clinical experience with amifostine, and provides insight into future clinical directions. Amifostine, an inactive pro-drug, is transformed to an active thiol after dephosphorylation by alkaline phosphatase found in the normal endothelium. The absence of alkaline phosphatase in the tumoral endothelium and stromal components, and the hypovascularity and acidity of the tumor environment, may explain its cytoprotective selectivity. The cytoprotective mechanism of amifostine is complicated, involving free radical scavenging, DNA protection and repair acceleration, and induction of cellular hypoxia. Intravenous administration of amifostine 740-900 mg/m(2) before chemotherapy and 250-350 mg/m(2) before each radiotherapy fraction are widely used regimens. The US Food and Drug Administration has approved the use of amifostine as a cytoprotector for cisplatin chemotherapy and for radiation-induced xerostomia. Ongoing trials are being conducted to determine the efficacy of amifostine in reducing radiation-induced mucositis and other toxicities. Novel schedules and routes of administration are under investigation, and may further simplify the use of amifostine and considerably broaden its applications.
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PMID:Amifostine in clinical oncology: current use and future applications. 1198 63

In humans, the association between mouth dryness and thirst has been examined in a variety of contexts. Typically, drinking behavior produces a concomitant reduction in unpleasant dry mouth sensations. Evidence is reviewed for a mechanism that influences the termination of drinking behavior by metering this change. Drinking behavior causes a progressive increase in parotid saliva flow. Thus, one possibility is that satiety results from a decrease in the reward associated with mouth wetting during a drinking episode. Beverages can differ in their satiating ability. This variability may be related to their mouth-wetting characteristic, and may be reflected in a shift in their acceptability when the mouth becomes dry. Physically drying the mouth appears to increase the acceptability of beverages that are either cold or acidic. It may be significant that two important determinants of mouth wetting are temperature and acidity. Cold or acidic beverages are also likely to be regarded as 'thirst-quenching.' Thus, shifts in acceptability, 'thirst quenching' and satiety may all be related to the mouth-wetting properties of a beverage. The extent to which this coincidence is meaningful warrants further investigation. However, if a common underlying process exists, then this may help to elucidate reasons for voluntary dehydration and aberrant drinking behavior in the elderly.
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PMID:Effects of mouth dryness on drinking behavior and beverage acceptability. 1211 79

After several decades of preclinical and clinical research, the first approved radioprotective drug, amifostine, is being used in clinical practice. Amifostine has been shown to specifically protect normal tissues from damage caused by radiation and chemotherapy. An inactive prodrug, amifostine is converted to an active thiol by dephosphorylation by alkaline phosphatase in the normal endothelium. The hypovascularity and acidity of the tumor environment and the differential expression of alkaline phosphatase in normal and neoplastic tissues contribute to its cytoprotective selectivity. The cytoprotective mechanism of amifostine is complicated, involving free-radical scavenging, DNA protection and repair acceleration, and induction of cellular hypoxia. The U.S. Food and Drug Administration has approved the i.v. use of amifostine to reduce the cumulative renal toxicity associated with repeated administration of cisplatin in patients with advanced ovarian cancer and to reduce the incidence of moderate to severe xerostomia in patients undergoing postoperative radiation treatment for head and neck cancer, where the radiation port includes a substantial portion of the parotid glands. Nonetheless, amifostine has potential applications in many other oncologic settings. Novel schedules and routes of administration are under investigation and may further simplify the use of amifostine, reduce any undesired effects, and considerably broaden its applications. This review summarizes the clinical experience with amifostine and provides insight into future clinical directions.
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PMID:Amifostine: the first selective-target and broad-spectrum radioprotector. 1760 63

Patients with xerostomia, or dry mouth, resulting from various causes, are at higher risk for developing caries because of a loss of saliva and its benefits. A loss of saliva increases the acidity of the mouth, which affects many factors that contribute to the development of caries, such as proliferation of acid-producing bacteria, inability to buffer the acid produced by bacteria or from ingested foods, loss of minerals from tooth surfaces and inability to replenish the lost minerals, and loss of lubrication. Currently, a number of new products that can substitute for these functions of saliva or induce production of saliva are available in Canada. Some of these products are reviewed and a protocol for caries prevention in this high-risk population is proposed.
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PMID:Caries prevention for patients with dry mouth. 2177 75

Acidic or EDTA-containing oral hygiene products and acidic medicines have the potential to soften dental hard tissues. The low pH of oral care products increases the chemical stability of some fluoride compounds and favours the incorporation of fluoride ions in the lattice of hydroxyapatite and the precipitation of calcium fluoride on the tooth surface. This layer has some protective effect against an erosive attack. However, when the pH is too low or when no fluoride is present these protecting effects are replaced by direct softening of the tooth surface. Oral dryness can occur as a consequence of medication such as tranquilizers, antihistamines, antiemetics and antiparkinsonian medicaments or of salivary gland dysfunction. Above all, patients should be aware of the potential demineralization effects of oral hygiene products with low pH. Acetyl salicylic acid taken regularly in the form of multiple chewable tablets or in the form of headache powder, as well as chewing hydrochloric acids tablets for the treatment of stomach disorders, can cause erosion. There is most probably no direct association between asthmatic drugs and erosion on the population level. Consumers and health professionals should be aware of the potential of tooth damage not only by oral hygiene products and salivary substitutes but also by chewable and effervescent tablets. Several paediatric medications show a direct erosive potential in vitro. Clinical proof of the occurrence of erosion after use of these medicaments is still lacking. However, regular and prolonged use of these medicaments might bear the risk of causing erosion. Additionally, it can be assumed that patients suffering from xerostomia should be aware of the potential effects of oral hygiene products with low pH and high titratable acidity.
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PMID:Oral hygiene products, medications and drugs - hidden aetiological factors for dental erosion. 2499 64