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

Many different experimental models for the induction of gastric ulcers have been reported in rats. Most of these experimental designs are often not reproducible and the interpretation of the results obtained is sometimes difficult. In the present study, three different models were found to give reliable and reproducible results, which could be repeated at any time of the year with different experimenters performing the procedure. To date, these methods are in our opinion, the best in designing gastric ulcer experiments and assessing the effect of pharmacological active substances. Two pharmacological active substances were investigated in the present study, pindolol, a beta-blocking agent with intrinsic sympathomimetic activity and salmon calcitonin, a hormone influencing calcium homeostasis in blood. Using all three different models no effect was seen after pindolol administration, while a strong inhibitory effect on the formation of gastric ulcers was observed after salmon calcitonin. Following ligation of the pylorus, the ulcer formation rate was significantly decreased from 80 to 33% with a significant fall in ulcer index from 2 to 0.42 and reduction of the ulcer areas from 6.6 to 0.58 mm2 (p less than 0.05). In addition, following phenylbutazone administration the appearance of gastric ulcers was diminished after salmon calcitonin from 1.4 to 0.43 and in ulcer area from 4.5 to 0.95 mm2 (p less than 0.01). These three ulcer models used in the present study were found to be very reliable as compared with other models reported in the literature and tested in our laboratory.
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PMID:The effect of pindolol and salmon calcitonin on experimental gastric ulcers in rats. 721 27

Omeprazole is an inhibitor of gastric H+,K(+)-ATPase. Although the major proton transport of osteoclast is mediated by a vacuolar-type H(+)-ATPase which is different from the gastric H+,K(+)-ATPase, in vitro studies have demonstrated that omeprazole inhibits bone resorption. In this study, the effect of omeprazole on bone resorption was evaluated in patients who had a history of gastric ulcer and were treated with maintenance doses of H2 blocker without any gastric complaints at the study time. H2-blocker administration was changed to omeprazole treatment in the study group and to no treatment in the control group. Urinary excretion of hydroxyproline and calcium decreased after omeprazole treatment in the study group. Serum intact PTH, alkaline phosphatase, osteocalcin, and tartrate-resistant acid phosphatase (TRAP) increased in this group. In the control group, there were not any changes in these parameters. The discrepancy between serum TRAP and urinary excretion of hydroxyproline and calcium in the study group was thought to be due to the suppression of bone resorption by omeprazole, which probably interfered the acidification at resorption lacunae and resulted in the inactivation of TRAP and other lysosomal enzymes. The results of our study suggest the possibility that the specific inhibitors of the osteoclastic proton pump (such as bafilomycins) will more effectively suppress bone resorption and be useful for the treatment of metabolic bone diseases with increased bone resorption.
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PMID:Effect of omeprazole, an inhibitor of H+,K(+)-ATPase, on bone resorption in humans. 810 18

Nocloprost, a 9 beta-chloro-16,16-dimethyl derivative of prostaglandin E2 (PGE2), belongs to the gastric cytoprotective agents that are used in the therapy of gastric ulcer. Since methylated derivatives of PGE2 are known to have proaggregatory effects the influence on platelets was studied. In platelet-rich citrated plasma, nocloprost (> 0.1 mumol/l) caused aggregation with a biphasic course at higher concentrations. Aggregation induced by nocloprost (1 mumol/l) corresponded to that induced by adenosine diphosphate (ADP) (5 mumol/l). Activation of platelets by nocloprost was accompanied by formation of thromboxane A2 and an increase in cytosolic calcium in Indo 1-loaded platelets. At 0.1 mumol/l it potentiated aggregation induced by low concentrations of ADP or adrenaline. The effect of nocloprost on platelets was blocked by iloprost, daltroban and indomethacin. PGE2, which was studied for comparison, at 0.1-1.0 mumol/l inhibited aggregation induced by 1 mumol/l nocloprost. The concentrations of nocloprost required for therapeutic use as antiulcer agent were lower by three orders of magnitude than those which induce human platelet aggregation.
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PMID:Activation of human blood platelets induced by nocloprost, a stable prostaglandin E2 derivative. 831 70

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.
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PMID:Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients. 844 8

Long-time oral intake of magnesium-silicate-containing drugs is thought to be a causative factor inducing silicate urolithiasis. Besides, magnesium seems to play an anti-urolithogenic part in the formation of calcium oxalate stones. We report a recurrent calcium oxalate former who had been treated with magnesium aluminometasilicate antacid for gastric ulcer for approximately 17 years. One of the fragments found during extracorporeal shock wave lithotripsy was identified as 100% silicate. Deposition of silica was also found on other fragments. A large dose of magnesium (given in a part of the drug) might have little influence on the formation of calcium oxalate.
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PMID:Pure silicate fragment in a recurrent stone former of calcium oxalate. 918 43

The phenomenon of the dual reciprocal regulation of succinate dependent 2H+/Ca2+ exchange was studied in heart and liver mitochondria of experimental animals (allogenic heart transplantation in rat; myocardium infarction in rabbits; pulmonary arteria coarctation in dogs) and in liver bioptates from patients with stomach ulcer. Under pathology two coupled but opposite changes (simultaneous activation and inhibition) in succinate dependent Ca2+ transport occur. The inhibition of Ca2+ transport was detected by its elimination with glutamate, being mostly pronounced after cycle of ADP phosphorylation added to suspension of mitochondria. The treatment of animal with 2-oxoglutarate abolished this inhibition. This was not observed in healthy animals. The described phenomenon can prevent hyperactivation of succinate oxidation under strong pathological (distress) influences.
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PMID:[Dual reciprocal regulation of the succinate oxidation system in heart and liver mitochondria in pathological conditions]. 963 17

Stress ulceration of the stomach in mice was investigated from the aspect of the calcium/calmodulin-dependent dopamine synthesizing system in the brain. Cold stress was induced in mice by restraining them at 4 degrees C. Serum and brain calcium levels were increased by cold stress, and an increased brain calcium level was found to enhance dopamine synthesis and a successively increased brain dopamine level induced gastric ulcer formation. Development of gastric ulcers elicited by cold stress was significantly decreased by i.p. pretreatment with EDTA (1 micromol/mouse, 1 h before restraint) or alpha-methyltyrosine (a tyrosine hydroxylase inhibitor, 100 mg/kg, 24 h before restraint), and was further significantly increased by pretreatment with CaCl2 (40 micromol/kg, 1 h before restraint). These findings suggest that the development of gastric ulcers in cold-stressed mice may be linked with the enhancement of calcium/calmodulin-dependent catecholamine synthesis in the brain.
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PMID:Gastric ulcer formation in cold-stressed mice related to a central calcium-dependent-dopamine synthesizing system. 967 76

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

Osteoporosis is a growing health problem in Asian women and it is expected that half of the world's hip fractures will occur in Asia in 50 years' time. As the use of hormonal replacement therapy (HRT) is extremely low in postmenopausal Asian women, nonhormonal agents will be more acceptable for the treatment and prevention of osteoporosis. The efficacy, tolerability, and acceptability of alendronate, an amino-bisphosphonate, for Asian women was evaluated in 70 osteoporotic southern Chinese women in a prospective, randomized, double-blind study. The subjects were randomized to receive either alendronate 10 mg daily or placebo, plus calcium supplementation 500 mg daily. The baseline L 1-4 and hip bone mineral density (BMD) were similar between both groups. At the end of 1 year, there was an increase of 5.8% in the lumbar spine BMD and 3.4% at the total hip with alendronate treatment when compared with baseline values (P < 0.001). Alendronate treatment for 1 year resulted in significant improvement in BMD at all sites measured when compared with placebo. There was also marked reduction in serum alkaline phosphatase (ALP) and urinary n-telopeptide (NTx) in the alendronate group when compared with the placebo group (ALP 25% versus 2%, NTx 75% versus 14%, both P < 0.005). The changes in ALP and NTx at 6 and 12 months correlated with the change in BMD at all sites measured at 1 year (P all <0.05). Alendronate was well tolerated and accepted, although two cases of gastric ulcer were reported. We conclude that alendronate is an effective and well-accepted agent for the treatment of osteoporosis in Asian women.
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PMID:The efficacy and tolerability of alendronate in postmenopausal osteoporotic Chinese women: a randomized placebo-controlled study. 1100 Mar 41

Once a peptic ulcer has developed, angiogenesis plays a critical role in its healing by enhancing the microcirculation in the healing site. Previous reports have shown that Helicobacter pylori infection delays the healing of chronic gastric ulcers. To elucidate the mechanism of delayed ulcer healing caused by H. pylori, we investigated the angiogenic phenotype and expression of receptors of angiogenic growth factors in vascular endothelial cells. After human umbilical vein endothelial cells (HUVECs) were treated with H. pylori water extract, angiogenic phenotype was determined by capillary tube formation and DNA synthesis assay. The expressions of the receptors of vascular endothelial growth factor and angiopoietin-1/-2 were assessed by reverse transcription-polymerase chain reaction and Western blot analysis in HUVECs and by double immunofluorescent staining in gastric mucosa. Angiogenic signaling in HUVECs was evaluated by using a quantitative intracellular calcium mobilization assay. H. pylori water extract significantly inhibited capillary tube formation and DNA synthesis and down-regulated the expressions of receptors of vascular endothelial growth factor and angiopoietin in HUVECs. H. pylori water extract suppressed vascular endothelial growth factor-induced intracellular calcium signaling in HUVECs. H. pylori may inhibit the expression of angiogenic growth factor receptors in vascular endothelial cells, which could explain, in part, the delayed healing of gastric ulcer by H. pylori.
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PMID:Helicobacter pylori down-regulates the receptors of vascular endothelial growth factor and angiopoietin in vascular endothelial cells: implications in the impairment of gastric ulcer healing. 1525 99


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