Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Acid aspiration syndrome of induction of anesthesia is a life-threatening complication whose severity is affected by both pH and volume of the aspirated gastric juice. We compared the effects of two proton pump inhibitors (PPIs), lansoprazole and omeprazole, and an H2 blocker, ranitidine, on gastric secretion in a prospective, randomized, double-blind fashion in 200 adult patients of ASA physical status I undergoing elective surgery. The patients were divided into eight groups (n = 25 each) according to their premedication. The patients received lansoprazole-lansoprazole (Group L-L), lansoprazole-placebo (Group L-P), placebo-lansoprazole (Group P-L), omeprazole-omeprazole (Group O-O), omeprazole-placebo (Group O-P), placebo-omeprazole (Group P-O), placebo-ranitidine (Group P-R), or placebo-placebo (Group P-P), as the first and second medications. The dose of the study drug was 30 mg for lansoprazole, 150 mg for ranitidine, and 80 mg for omeprazole. The first medication was administered orally at 9:00 PM on the night before surgery and the second at 5:30 AM in the morning on the day of the surgery. Each patient fasted overnight and took the drug with 20 mL of water. After tracheal intubation, gastric fluid was aspirated via an orogastric tube and the volume and pH of the aspirate were measured. The pH of the aspirated gastric fluid was higher in Groups P-R, L-L, P-L, O-O, and O-P than in Group P-P (P < 0.05). The volume of the gastric contents was similar in Groups P-0 and P-P, and the other groups had smaller gastric volume than Group P-P (P < 0.05). Gastric fluid from patients in Group P-R was the least acidic (pH 6.1 +/- 1.2) and had the least volume (0.09 +/- 0.06 mL/kg). Group L-L was comparable with Group P-R in both pH and volume, whereas Groups P-L and O-O were similar to Group P-R only in volume. The proportion of patients at risk according to the traditional criteria (pH < 2.5 and volume 0.4 mL/kg) was significantly lower in Groups L-L (0%), P-L (4%), O-O (4%), and P-R (0%) than in Group P-P (48%) (P < 0.05). We concluded that two consecutive doses of lansoprazole or a morning dose of ranitidine seemed to be the most effective preanesthetic medication for reducing gastric acidity and volume.
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PMID:A comparison of lansoprazole, omeprazole, and ranitidine for reducing preoperative gastric secretion in adult patients undergoing elective surgery. 861 6

This study examines whether acidic, vacuolar-type, proton-pump-carrying organelles of insulin-secreting cells (clonal endocrine pancreatic cell line INS-1) function as rapidly exchanging, inositol 1,4,5-trisphosphate-sensitive calcium stores. Calcium uptake into calcium stores will be modulated by the proton concentration within the stores, since calcium pumps in general appear to mediate a countertransport of calcium with protons. We therefore tested for sensitivity of calcium sequestration by nonmitochondrial stores (inhibition of mitochondrial calcium uptake by 2 microM ruthenium red) in saponin-permeabilized cells to proton-conducting ionophores and proton pump inhibition, using this as a marker for involvement of acidic organelles. Calcium sequestration was partially inhibited by the protonophores nigericin (10-50 microM) and carbonylcyanide m-chlorophenylhydrazone (CCCP; 20-50 microM), as well as by inclusion of 30 mM NH4Cl. Bafilomycin A1, a potent and selective inhibitor of vacuolar-type proton pumps, alone (1 - 500 nM) had no effect on calcium sequestration. however, it induced an inhibitory effect in the presence of nigericin or CCCP, even at low concentrations (5 microM) of these ionophores, lacking itself an inhibitory action on calcium sequestration. Bafilomycin A1 then was already maximally active at a concentration as low as 10 nM. Corres ponding to inhibition of total nonmitochondrial calcium sequestration, filling of inositol 1,4,5-trisphosphate-sensitive stores was decreased or even abolished by the protonophores alone or the protonophores combined with bafilomycin A1. We conclude that vacuolar-type proton pumps are present in at least a part of nonmitochondrial and inositol 1,4,5-trisphosphate-sensitive calcium stores in INS-1 cells. This assigns these stores to organelles such as secretory granules, the trans Golgi network, or endosomes. Luminal acidity of these stores will stimulate calcium sequestration by providing more protons for countertransport of calcium by calcium pumps. High concentrations of protonophores may be required for inhibitory effects because otherwise the proton pumps may be able to compensate sufficiently for ionophore-mediated proton loss. The lack of effect of bafilomycin A1 without protonophores may be due to a sufficient luminal buffering capacity or to preceding inhibition of the pump by an inside-positive transmembrane potential.
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PMID:Evidence for vacuolar-type proton pumps in nonmitochondrial and inositol 1,4,5-trisphosphate-sensitive calcium stores of insulin-secreting cells. 866 73

Endosomal proteases have been implicated in the degradation of internalized regulatory peptides involved in the control of metabolic pathways and in the processing of intracellular antigens for cytolytic immune responses. Processing in the endocytic vesicles is regulated by changes in endosomal acidity due to the presence of an ATP-dependent proton pump which modulates protease activity, protein unfolding and receptor-ligand interactions. A limited number of proteases appear to reside in endosomes which do not contain the full complement of active proteases capable of completely degrading all internalized polypeptides. Retention of some acid hydrolases in endosomes is apparently related to their association with undefined endosomal membrane receptors. The limited number of proteases and the pH gradient from neutral to acidic (pH 7 to 5) within endosomes make possible a selective and controlled processing environment in comparison to lysosomes. The full set of endo- and exopeptidases that break down proteins to amino acids are active later in the pathway in lysosomes.
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PMID:Endosomal proteolysis of internalized proteins. 868 6

The role of endogenous acid was evaluated in a rat model of gastric epithelial damage induced by local ischemia-reperfusion (IR). Because no gross lesion was induced in this model, the damage was quantified by measuring the blood-to-lumen [51Cr]EDTA clearance. A proton pump inhibitor (omeprazole) or an H2-receptor antagonist (T-593) was used to suppress luminal acidity from pH 5 to pH 6.3-7.0. Both drugs significantly attenuated the increase in clearance induced by IR, indicating an important role for endogenous acid. A second series of experiments was performed to confirm whether the change in pH from around 5 to 7 was sufficient to reduce IR-induced gastric mucosal damage. Phosphate-buffered saline was perfused into the gastric lumen to neutralize the endogenous luminal acid. Although the luminal acid was completely neutralized, no reduction in clearance was observed. These data indicate that endogenous luminal acid does not play an important role in gastric injury induced by local IR stress and that a proton pump inhibitor or H2-receptor antagonist may suppress IR injury by a mechanism other than reducing luminal acidity, i.e., reducing consumption of ATP needed for acid secretion, thereby improving gastric mucosal energy metabolism.
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PMID:Role of endogenous acid in gastric mucosal injury induced by local ischemia-reperfusion in the rat. 877 1

Amoxicillin is one of the most active antimicrobials against Helicobacter pylori in vitro, with a minimum inhibitory concentration (MIC) of < or = 0.01-0.1 mg/l. Thus far, neither primary nor secondary resistant strains have been found. Amoxicillin, which has a bactericidal effect on H. pylori, but is less inhibitory in the stationary growth phase and against cell-adherent or slowly growing H. pylori, probably has both topical and systemic activity. It is fairly acid stable and is less affected by gastric acidity than macrolides. Nevertheless, its activity in vivo is considerably enhanced when it is given concomitantly with proton pump inhibitors. Several amoxicillin-containing treatment regimes have yielded H. pylori eradication rates of > or = 90%. Of particular interest are 1-week treatment regimens containing amoxicillin + clarithromycin + omeprazole, or amoxicillin + metronidazole + omeprazole, as well as a 1-h topical therapy developed in Japan.
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PMID:Amoxicillin for the treatment of Helicobacter pylori infection. 895 18

H. pylori causes inflammatory lesions of the stomach and duodenum. At the present time eradication is essentially recommended in case of gastric or duodenal ulcer. The choice of the appropriate drug depends on the characteristics of the H. pylori infection, the localization deep in the gastric mucosa, the physico-chemical properties of the gastric medium, especially the acidity which deactivates antibiotics, slow bacterial growth and the germ's sensitivity to antibiotics. Anti-infectious treatment is now based on a three-drug regimen combining an antisecretory drug (proton pump inhibitor or H2 receptor antagonist) and two antibiotics: clarithromycin associated with amoxicillin or an imidazol derivative (metronidazol or tinidazol) or tetracycline. Two antibiotics (clarithromycin, amoxicillin) as well as three anti-secretory agents (lansoprazole, omeprazole, ranitidine) have been authorized in France for three-drug regimens of 1 or 2 weeks leading to approximately 90% eradication. Special attention should be placed on the risk of resistance to antibiotics (macrolids and imidazol derivatives) and patient compliance required for successful eradication of H. pylori. Other therapeutic schemes are under assessment and a vaccine is being prepared. Eradication of H. pylori has totally changed the treatment of gastric and duodenal ulcers, eliminating the need for long-term treatment and avoiding complications.
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PMID:[The treatment of Helicobacter pylori infection]. 903 12

GERD is a common disorder. Symptoms of reflux, such as heartburn, are due to a combination of factors: relaxation of the lower esophageal sphincter, hypersecretion of gastric acid, and resulting burning of the esophageal mucosa. Symptoms are usually classified as classic, atypical, or complicated. Treatment approaches include dietary and lifestyle changes, reduction of acidity with use of H2 receptor antagonists, and reduction of acid secretion with use of proton pump inhibitors. Patient motivation is an important factor in the management of gastroesophageal reflux. In rare instances, patients do not respond to medical treatment and are candidates for antireflux surgery.
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PMID:Gastroesophageal reflux disease: gaining control over heartburn. 904 34

Suppression of gastric acid secretion is widely used and logical for the treatment of acid-related diseases. Healing of duodenal ulcer, gastric ulcer and gastroesophageal reflux disease is correlated significantly with the degree and the duration of suppression of intragastric acidity over 24 hours and with the length of the treatment. To date, proton pump inhibitors are the most effective agents among the currently available antisecretory drugs in offering the highest healing rate and fastest resolution of symptoms. Combinations of an antisecretory drug with one or more antimicrobial agents accelerate healing of peptic ulcers.
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PMID:pH, healing rate and symptom relief in acid-related diseases. 911 48

Gastro-oesophageal reflux disease (GORD) is a very common disorder of upper gastro-intestinal motility, differing widely in severity and prognosis. Medical therapy of GORD has involved antacids, alginates, prokinetic agents and antisecretory compounds, primarily H2 receptor antagonists and proton pump inhibitors. Knowledge of the pharmacokinetics of these compounds is important, to optimise the therapeutic benefit in each patient. GORD patients are often elderly and pharmacokinetics are move variable in this group. Furthermore, they often suffer from other diseases needing medical therapy and may need a combination of drugs to heal reflux oesophagitis and relieve reflux symptoms. The ideal therapy for GORD will have linear pharmacokinetics, a relatively long plasma half-life (t1/2), a duration of action allowing once daily administration, and a stable effect independent of interactions with food, antacids and other drugs. Over-the-counter antacids and alginates are widely used, buy may affect absorption of H2 receptor antagonists like cimetidine and ranitidine. Aluminium-containing antacids may, over time, cause toxicity in patients with renal insufficiency. In the treatment of GORD, cisapride presents important advantages over earlier prokinetic compounds, with a longer plasma t1/2, low penetration of the blood-brain barrier and fewer adverse effects. The group of H2 receptor antagonists is still the most frequently use therapy for GORD. Linear pharmacokinetics make dose adjustments easy and safe. In individual patients, suppression of gastric secretion is related to the area under the plasma concentration-time curve (AUC), but there is wide interindividual variation in the effect of the same oral dose. Only with frequent administration and high doses will acid suppression approximate that of proton pump inhibitors. Tolerance, with loss of effect over time, however, is most pronounced in this situation. H2 receptor antagonists seem well suited for on-demand treatment of reflux symptoms, due to the rapid onset of effect and a decrease likelihood of the development of tolerance. Effervescent formulations provide more rapid absorption and almost immediate clinical effect. Cimetidine, however, causes interference with the metabolism of several other drugs in common use. In elderly patients elimination is delayed and in patients with renal insufficiency, dose reductions of all H2 receptor antagonists are recommended. The most effective medical therapy for any severity of GORD, particularly in severe oesophagitis, are the proton pump inhibitors. The substituted benzimidazoles (omeprazole, lansoprazole and pantoprazole), are prodrugs which once trapped and activated in the acid milieu of the gastric glands potently suppress gastric secretion of acid and pepsin. Their long duration of action, more related to the slow turnover of parietal cell H(+)-K+ ATPase molecules, allows once daily administration in most patients. Interindividual variation in bioavailability sometimes calls for higher doses or twice daily administration. Acid suppression is closely related to the AUC. Omeprazole is prone to interaction with the metabolism of other drugs, some of which may e be clinically important. Lansoprazole seems to have an earlier onset of action than omeprazole, ascribed to higher bioavailability during the first days of treatment. Proton pump inhibitors have a slow onset of action, which makes them unsuited for on-demand therapy. Clinical practice in GORD calls for the use of not one but several substances, according to the severity and symptom pattern of the patient. Pharmacokinetic optimisation in the treatment of GORD is a question of selecting the most suitable substances and administration schemes within each group. Cisapride is superior to other prokinetics in terms of longer plasma t1/2 and less toxicity. Amongst H2 receptor antagonists, the more long-acting compounds, ranitidine and famotidine, will improve acidity control througho
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PMID:Pharmacokinetic optimisation in the treatment of gastro-oesophageal reflux disease. 911 86

Gastro-oesophageal reflux disease (GERD) is primarily due to incompetence of the lower oesophageal sphincter (LOS) and crural diaphragm, with transient LOS relaxation frequently accounting for daytime reflux. In the absence of drugs that adequately correct the motility defects of GERD, treatment is directed towards decreasing gastric acidity. Oesophageal healing is related to control of 24-h intragastric acidity, the degree of acid suppression and duration of treatment. H2-receptor antagonists are generally less effective in GERD than in peptic ulcer disease. While providing symptomatic relief in non-erosive GERD, they are often ineffective in healing erosive oesophagitis. Proton pump inhibitors provide more rapid and complete healing and symptom resolution. They are superior to H2-receptor antagonists in the long-term management of erosive oesophagitis and in reducing recurrence of oesophageal stricture following mechanical dilatation. In Barrett's oesophagus, high-dose proton pump inhibitors in combination with laser/photodynamic ablation therapy can produce metaplastic regression, although this does not preclude future emergence of adenocarcinoma. Surgical morbidity and mortality rates in GERD generally remain higher than those associated with long-term pharmacotherapy. However, direct comparisons between laparascopic anti-reflux surgery and proton pump inhibitor maintenance therapy remain to be performed. Although there is no evidence that H. pylori infection worsens the severity of oesophagitis or that H. pylori is carcinogenic in the metaplastic oesophageal mucosa. It has been suggested that H. pylori-positive patients requiring long-term proton pump inhibitor therapy receive bacterial eradication therapy to reduce the risk of developing atrophic gastritis.
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PMID:Review article: current practice and future perspectives in the management of gastro-oesophageal reflux disease. 930 72


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