Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A modification of Berstad's spectrophotometric method was tested and proved capable of detecting pepsin concentrations in mucosal perendoscopic biopsy homogenates. The relationship between this parameter and pepsin in gastric juice and pepsinogen group I in serum and in biopsy homogenates was analyzed. From the biochemical point of view, the assay was found sufficiently accurate. Mucosal pepsinogen group I, but not mucosal pepsin, concentration was found higher in gastric and duodenal ulcer patients than in controls. Patients with corpus-fundic gastric ulcer showed significantly lower mucosal pepsin and mucosal pepsinogen group (PG) I. Aging and smoking did not influence either parameter but male duodenal ulcer subjects presented higher mucosal pepsinogen group I concentration. The lack of any relationship between serum and mucosal PG I and between pepsin in gastric juice and in mucosa raises a question, at least in methodological terms, about the validity of using serum pepsinogen group I and pepsin as indicators of peptic output.
 ...
PMID:Pepsin concentration in gastroduodenal biopsy homogenates in chronic ulcer disease. 831 12

Gastric ulceration is a complex, multifaceted, pluricausal illness. The pathophysiology of gastric ulcer disease continues to be unclear. The mainstay for pharamacological management of gastric ulceration exists in reduction or neutralization of gastric acid secretion through administration of histamine H2 receptor blockers such as cimetidine and ranitidine. Recent studies show however that the majority of patients experiencing gastric injury exhibit normal or below normal levels of HC1 and pepsin secretion which leaves question to the effectiveness of acid reduction therapy. A viable alternative to H2 receptor blockade is to prevent mucosal injury by maintaining the integrity of the mucosal barrier through administration of prostaglandin analogues. This cytoprotection may reduce gastric damage while maintaining normal acid secretion. Our purpose is to review prostaglandins as a potential therapeutic treatment of gastric and duodenal injury and explore the role of prostaglandins as natural physiological defense mechanisms against gastroduodenal mucosal damage. We also discuss several gastric mucosal damaging agents such as nonsteriodal anti-inflammatory drugs, alcohol, and stress along with comparisons of effectiveness between prostaglandin analogues and H2 receptor blockers in reparation and prevention of injury caused by these agents.
 ...
PMID:Prostaglandins: viable therapy in gastric ulceration. 844 26

The peptic ulcer (PU) is characterized by definite gastric cyto-secretory profiles. In case of duodenal ulcer (DU) and pre-pyloric gastric ulcer (PPGU), there is a prevalence of hyperparietalism with hyperchloridria, while in ulcer with body-fundic localization (BFGU) normo-hypoparietalism with normo-hypochloridria prevails. As well, the total peptic activity follows a superimposable course: it increases in cases of DU and PPGU, while it remains in the normal range in case of BFGU. With reference to the qualitative variations of pepsin, in course of PU the amount of pepsin 1 increases significantly. Such pepsin has a powerful proteolytic action even at high pH: which explains the possible onset of PU even in hypochloridria conditions. Helicobacter pylori (HP) has revolutionized the pathogenetic approach towards the gastric pathology: in 75% of cases there are alterations of the mucosae superficial profile, micropapillary changes, erosions, vacuolations with cellular degeneration. In 90% of cases is present chronic active inflammation in correspondence of the glandular neck of the gastric epithelium. In 70% of cases of BFGU there are qualitative alterations of the superficial epithelium. The gastric anatomic-functional behaviour, however, has an autonomous course and it is not influenced by the presence of infection. It results, therefore, that the bacterium is an important cofactor in PU pathogenesis by means of a direct cytotoxic-enzymatic action, without influencing a secretory behaviour which, in PU, is substantially conditioned by the genetic characteristics of the patient.
 ...
PMID:[Aggressive factors in the physiopathology of peptic ulcer. Recent findings]. 876 56

Gastric juice acidity was examined in 131 patients with gastric ulcer. In 31 (23.7%) patients it appeared to be high, in 57 (43.5%)-normal, in 42 (32.8%)-low. In 28.6% cases the pepsin concentration was high, in 26.5%-normal, in 44.9% - low. In elder patients, patients with cardial ulcer, plural and combined ulcers, big size ulcers, long-term ulcer anamnesis the rate of low acidity increases. Among patients with unsatisfactory results of conservative treatment 15.8% had high acidity and 38.7% low acidity. Low acidity is an unfavorable prognostic factor.
 ...
PMID:[Gastric juice acidity in gastric ulcer]. 896 51

The action of Codonopsis pilosula extract in 5 animal models of gastric ulcer was investigated. It was found that the extract had higher efficacy on gastric ulcer induced by stress, acetic acid and sodium hydroxide and little significant effect on ulcers induced by pyloroligature and indomethacin. The C. pilosula extract was also capable of reducing gastric acid pepsin secretion. It is possible that inhibition of gastrointestinal movement and propulsion is one of the mechanisms underlying the antiulcer action of C. pilosula extract.
 ...
PMID:Investigations on the protective action of Condonopsis pilosula (Dangshen) extract on experimentally-induced gastric ulcer in rats. 906 93

The 24 patients with gastric ulcer were treated ranitidine (2 x 150 mg daily) or nocloprost (2 x 200 micrograms daily). The effects of these drugs on the gastric juice components were measured. We evaluated hydrochloric acid, total protein, pepsin and some carbohydrates components secretion. We showed, that ranitidine decreased significantly total protein, fucose, N-acetylneuraminic acid and hexoses contents in the gastric juice in the basal secretion; the same tendency was observed in the pentagastrin-stimulated secretion. The similar direction of the changes, but weakly expressed was confirmed in the patients treated with nocloprost. It has been shown, that ranitidine modified the gastric mucin components content, what can suggest diminished degradation of mucus directly adhering to the gastric mucosa.
 ...
PMID:Effects of ranitidine or nocloprost on the selected gastric juice components in the patients with the gastric ulcer. 958 90

1. Polyriboinosinic-polyribocytidylic acid (Poly I:Poly C), an interferon inducer was studied for its effect on gastric ulceration in rats. Polyriboinosinic-polyribocytidylic acid (1, 2 and 4 mg/kg, i.m.) showed a dose-dependent inhibition of gastric ulcers induced by aspirin, cold restraint stress and pylorus ligation (Shay's model). Protective dose (PD50) +/- SEM values of Poly I:Poly C on these models of ulcers were 1.9 +/- 0.2, 2.3 +/- 0.4 and 2.8 +/- 0.4 (mg/kg, i.m.) respectively. 2. Polyriboinosinic-polyribocytidylic acid (10-60 micrograms) produced dose-dependent inhibition of gastric proton pump (H+/K(+)-ATPase) activity in the gastric parietal microsomal fraction. The concentration of Poly I:Poly C causing a 50% inhibition (IC50) +/- SEM was found to be 17.6 +/- 1.2 micrograms. 3. Polyriboinosinic-polyribocytidylic acid caused a significant decrease in free and total acid and pepsin and an increase in mucin content in Shay (pylorus-ligated) rat. 4. Polyriboinosinic-polyribocytidylic acid did not exert a significant influence on isolated tissue preparations for anti-cholinergic (acetylcholine-induced contraction of guinea-pig ileum) and H2-anti-histaminic (histamine-induced contraction of rat uterus and guinea-pig auricle) activities. 5. Thus, the present study indicates that Poly I:Poly C may possess anti-gastric ulcer activity as a result of inhibition of the gastric proton pump.
 ...
PMID:Interferon-inducer polyriboinosinic-polyribocytidylic acid: a potent anti-gastric ulcer agent and inhibitor of the gastric proton pump in rats. 967 29

Lansoprazole is the new proton pump inhibitor, decreasing the volume of gastric acid secretions and inhibiting secretion of gastric acid and pepsin. Lansoprazole appears to be more effective in therapy of gastric ulcer and duodenal ulcer in comparison with H2-receptor antagonists and omeprasole. Reflux oesophagitis and Zollinger-Ellison syndrome are also healed by Lansoprazole. The best results in the treatment of patients with peptic ulcer, reflux oesophagitis and Zollinger-Ellison syndrome were occurred after a daily 30 mg dose of Lansoprazole. Treatment of patients with duodenal ulcer should be continued for 2 to 4 week and the case of gastric ulcer a well as reflux oesophagitis should be prolonged till 4 to 8 week. Lansoprazole is well tolerated, reported adverse effects are similar to the incidence observed in patients treated with other proton pump inhibitors.
 ...
PMID:[Lansoprazol ++ : a new proton pump inhibitor]. 977 Oct 21

The promising strategy of gastric ulcer healing with perorally administered epidermal growth factor (EGF) is so far strongly limited by the pepsinic degradation of this therapeutic polypeptide in the stomach. The incorporation of EGF in a bioadhesive polymer-pepsin inhibitor conjugate used as drug carrier matrix, however, might provide sufficient protection toward pepsinic degradation. The synthesis of appropriate pepsin inhibitors represents a prerequisite for the development of such polymer-inhibitor conjugates. The presented study demonstrates that modifications at the N-terminus of simplified analogues of pepstatin which can be synthesized in a simple and straight way result only in slight variations of the inhibitory activity. These analogues display only 10-fold reduced inhibitory activity, compared to pepstatin A, when bearing a greater N-terminal group like isovaleryl, Boc, or Cbz. Compounds which are substituted at the N-terminus by a shorter N-acyl group like propionyl or cyclopropylcarbonyl show further reduced activity (0.01, compared to pepstatin A). The presence of an amide or a urethane moiety at the N-terminus has no considerable effect on enzyme inhibition. Therefore, the N-terminus of these analogues is able to be modified forming a covalent bond to various bioadhesive polymers via a suitable functionality.
 ...
PMID:Simplified pepstatins: synthesis and evaluation of N-terminally modified analogues. 1035 12

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.
 ...
PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>