Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pepsin 1, the ulcer-associated pepsin, occurred significantly more frequently in the gastric juice of those patients with duodenal ulcer who did not secrete A, B, or H antigens into gastric juice than in those secreting these antigens. This observation may explain the increased proportion of such non-secretors among patients with duodenal ulceration. In patients with gastric ulcer and non-ulcer dyspepsia, and in a miscellaneous group of patients, there was no association of pepsin 1 secretion with secretor status, suggesting that the association noted in duodenal ulceration is an indirect rather than a direct one. No increase of pepsin 1 occurred in group O patients with peptic ulcer, so that the increased proportion of such patients in peptic ulcer does not arise from differences in pepsin 1 secretion.
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PMID:Hereditary aspects of duodenal ulceration: pepsin 1 secretion in relation to ABO blood groups and ABH secretor status. 11 57

The effect of a pepsin-inhibiting pentapeptide, pepstatin, upon the peptic activity and gastric acidity was investigated in 9 men with ulcer dyspepsia and a high acid output. Subtotal inhibition of peptic activity was obtained, basally as well as after broth stimulation, as early as 15 minutes after the method of administration, and the inhibition remained almost unchanged during the 60 minutes of the experimental period. The acidity was not affected by pepstatin. No side-effects occurred. The results confirm preliminary reports on the pepsin-inhibitory activity of the drug. It is concluded that pepstatin ought to be investigated with regard to its clinical effect upon peptic ulcer.
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PMID:Effect of a pepsin-inhibitory pentapeptide upon the peptic activity and acidity of gastric secretion. 78 87

The quantification of mucus glycoproteins (GPs) faces paramount difficulties in terms of methods and interpretation. Mucus glycoprotein erosion, however, might be quantified in gastric juice by measurement of GP-bound sialic acid. Basal sialic acid content was low in normal healthy subjects (N) and in nonulcer dyspepsia (NUD) patients. They were five to six times higher in duodenal ulcer (DU), or more in Zollinger-Ellison patients. Pentagastrin stimulation induced a five- to sixfold rise in N and NUD patients although it did not affect DU patient sialic acid contents. Relationships between sialic acid content and pepsin output in DU indicate that pepsin exerts a variable mucolytic activity depending on disease evolution. In addition to pepsin, duodenogastric reflux exerts a potent mucolytic effect. Therapeutically, highly selective vagotomy without recurrent ulcer markedly reduced mucus erosion. The reduction of mucus erosion by protective drugs has been observed in some cases but in other cases sialic acid measurement did not allow to verify a protective effect. Adherent mucus analysis by high-performance liquid chromatography (HPLC) should allow one to appreciate GP fractions qualitatively. Combination of both methods should allow further determination of the mucus protective role, simultaneously investigating the adherent mucus quality and eroded GPs.
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PMID:Assessment of mucus glycoprotein erosion by measurement of sialic acid in gastric secretions: pathophysiologic and therapeutic aspects. 194 Jan 93

The heterogeneity of muscarinic receptors has been well supported by differential characteristics between pirenzepine and atropine both in receptor binding and in whole tissue pharmacology studies. Under these conditions pirenzepine has been classified as a selective receptor antagonist with high affinity for M1 receptors. The antisecretory properties of pirenzepine on gastric acid and pepsin secretion may be attributed to the antagonistic activity of the drug on muscarinic M1 receptors of gastric intramural plexuses, whereas the effect on parietal muscarinic M2 receptors seems of less importance. Additional inhibitory mechanisms on gastric secretion may be represented by pirenzepine-induced increase in somatostatin release from gastrointestinal system. Significant cytoprotective properties of pirenzepine have been observed on a variety of experimentally induced peptic ulcerations. This protective activity may be due to pirenzepine-induced increase in gastric mucosal blood flow as well as to the increase in gastric transmural electric potential difference. In accordance with this pharmacodynamic profile of pirenzepine, numerous clinical studies have revealed its efficacy in the treatment of both duodenal and gastric ulcerations. In addition to this, the clinical usefulness of the drug has been demonstrated in Zollinger-Ellison syndrome, in stress ulceration, in acute gastrointestinal bleeding as well as in gastritis, duodenitis and non-ulcer dyspepsia. In most of the studies pirenzepine has been found to be well tolerated with a low incidence of antimuscarinic effects which may occur at salivary, ocular, cardiac and urinary sites. The clinical use of pirenzepine alone or in association with H2 blockers is recommended in the treatment of peptic ulcer patients, in the case of acute gastrointestinal haemorrhage and in patients non responders to H2 antagonists.
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PMID:[A selective antimuscarinic agent: pirenzepine. Review of its pharmacologic and clinical properties]. 257 37

'Acid-related disorders' is a term used to describe a whole range of conditions from the Zollinger-Ellison syndrome, where acid is entirely responsible for the problems, to aerophagia and motility-type non-ulcer dyspepsia, where acid plays little if any role in the dyspeptic symptoms. Careful evaluation of the patient's symptoms is required to establish the basis for the dyspepsia and from that, careful selection can be made for any investigations that might be needed. These symptoms are the basis for advising on the most effective management--but as many doctors and patients erroneously attribute dyspepsia solely to acid, it is all too easy for inappropriate treatment to be offered. Acid is not the only cause of dyspeptic symptoms. Dyspepsia is a very common complaint with many causes. Acid and pepsin are often held responsible for these symptoms, by both the medical profession and the lay public. The term, 'acid-related disorders' is used to embrace this wide variety of conditions in which acid may play a part. However, in spite of current folklore, it is a spectrum of conditions ranging from situations where acid is crucial to conditions where acid may play little part.
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PMID:Acid-related disorders: what are they? 324 3

Cigarette smoking has been linked with duodenal ulcer disease although the mechanism of this association is unclear. This study assessed basal gastric secretory response to acute smoking of smokers with an active duodenal ulcer; in addition the possible effects of chronic smoking on gastric secretory capacity, as expressed by pentagastrin stimulated gastric acid secretion and fasting serum pepsinogen I (PG I) concentrations, were investigated in patients with active duodenal ulcer, or non-ulcer dyspepsia. In 10 smokers with duodenal ulcer smoking four cigarettes during 40 minutes did not influence basal gastric secretion of acid and pepsin, or serum PG I and gastrin concentrations. In 136 patients with duodenal ulcer and 90 controls with non-ulcer dyspepsia, pentagastrin stimulated acid secretion and fasting serum PG I concentrations were significantly higher among habitual heavy smokers than among non-smokers. These findings suggest that in heavy smokers with duodenal ulcer acid- and pepsin-secreting cell function is not affected by acute cigarette smoking. By contrast, chronic cigarette smoking seems to be associated either with an increase of parietal- and chief-cell mass, or with an enhancement of their secretory capacity.
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PMID:Cigarette smoking, gastric acid secretion, and serum pepsinogen I concentrations in duodenal ulcer patients. 393 54

In the first communication (3), we reported on the conception, the composition, and the efficacy of the polyvalent oral vaccine from 6 strains of salmonellae, 2 strains of shigellae, and 4 strains of dyspepsia coli. The inactivation took place at 100 degrees C/3 min. The question going to be answered in this communication was as follows: Does the immunogenicity of the vaccine decreased during the gastrointestinal passage under influence of acid and enzymes? We allowed the vaccine to react with simulated gastric juice and/or pepsin at pH = 3 and 37 C/60 min on the one hand and with simulated intestinal juice and/or pancreatin at pH = 7 and 37 degrees C/180 min on the other hand either individually or in combination. The vaccinal preparations produced this way were examined for their immunogenicity in the mouse protection test. The mice were orally immunized with the aid of a probang for ten times (total dose = 3.75 x 10(10) germs) and intraperitoneally infected with the virulent enteropathogenic strain of E. coli 2,380 being contained in the twelvefold vaccine on the 10. day after the last oral vaccination. In the main test, 70.4% of 351 non-vaccinated control animals died. 277 mice were immunized with the vaccine having been treated in the strongest way (gastric juice + pepsin + intestinal juice + pancreatin); 4.0% of those died which is an index of efficacy of 94.3. The mice immunized with untreated vaccine served as positive controls and were protected in the same way; 3.1% of 255 mice died (index of efficacy = 95.6). The results show that the simulated gastro-intestinal passage did not have a negative influence upon the immunogenicity of the polyvalent vaccine.
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PMID:[An oral enteritis-vaccine composed of twelve heat inactivated Enterobacteriaceae. 2. Communication: the immunogenicity after treatment with simulated gastric and intestinal juice proved in an active mouse protection test (author's transl)]. 678 80

Patients with dyspepsia were asked to volunteer for two gastric secretion tests preceded by a single intravenous injection of pirenzepine 10 mg in the one and 0.9% saline in the other (in random order). In each test gastric secretion was aspirated continuously. 0.9% saline was infused intravenously for 30 minutes followed by insulin 0.15 micrograms/kg-h for 90 minutes, saline for 30 minutes and finally pentagastrin for 90 minutes in doses of either 6, 1, 0.5 or 0.25 micrograms/kg-h. Gastric samples were analysed for volume, pH, titratable acidity and pepsin. Basal outputs of acid and pepsin were not altered by pirenzepine. Insulin-stimulated acid output was significantly reduced (p less than 0.05) from a mean of 32.7 to 22.6 mmol/h (-31%). The mean percentage reduction was 16%. Acid and pepsin outputs after pentagastrin 0.25-6 micrograms/kg-h were not significantly altered by this dose of pirenzepine.
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PMID:Influence of intravenous pirenzepine on gastric acid and pepsin in man. 678 94

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1

We have investigated the effects of methanolic and alcoholic extracts from Amomi Semen on gastric secretion, as well as gastrointestinal propulsion or the prokinetic activities. The methanolic extract from Amomi Semen dose dependently decreased the volume output, acid output, and pepsin output in rat's gastric juice with increasing pH value, while the alcoholic extract had no influence on basal gastric acid secretion. Furthermore, the alcoholic extract improved the L-dopa to induce a delay of gastrointestinal transit in mice, while the methanolic extract did not improve it. However, both extracts had no influence on gastrointestinal transit in intact mice. These results suggest that Amomi Semen has an inhibitory effect on gastric acid secretion and that it has effects as the gastrointestinal prokinetics rather than propulsion. The present study pharmacologically elucidates a belief that Amomi Semen has been used in Chinese medicine for the treatment of gastrointestinal dyspepsia, which includes hyperchlorhydria, stomachache, abdominal distention, anorexia, gastric atony, etc.
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PMID:Evaluation of the pharmacological activity of extracts from amomi semen on the gastrointestinal tracts. 1090 82


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