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)

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.
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PMID:[Gastric juice acidity in gastric ulcer]. 896 51

The study included 736 probands with ulcer disease and 110 healthy subjects as well as all their relatives up to a third-degree of relation (n = 21889). All subjects underwent a thorough genealogical analysis, blood group, PTC and dermatoglyphic studies were performed on the whole contingent. Using extensive genealogical, genetico-mathematical and multifactorial analysis we studied the manifestations of anticipation, the influence of hereditary predisposition on gastric secretion and acidity under conditions of maximum pentagastrin stimulation as well as the disease inheritance pattern. The results of our comprehensive studies suggest that type I gastric ulcer according to H. Johnson, unlike type II and type III, is not genetically determined. On the other hand, type II and type III gastric ulcer do not differ substantially from duodenal ulcer and should therefore be categorised as belonging to this form of the disease. On this basis we propose a new classification system which accepts the existence of two ulcer diseases: gastric ulcer disease, and ulcer disease of the pyloroduodenal region.
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PMID:The ulcer disease: an updated classification system. 897 52

The effect of cromakalim, a potassium-channel opener, was studied on pylorus ligation-induced, aspirin-induced and water-immersion plus restraint stress-induced gastric ulcers in rats and on histamine-induced duodenal ulcer in guinea-pigs. Pretreatment with cromakalim (50-500 micrograms kg-1, p.o.) resulted in a significant reduction in the incidence of gastric and duodenal ulceration in each model. The anti-ulcer activity of cromakalim was comparable with that of cimetidine. Cromakalim at 100, 250 and 500 micrograms kg-1 caused a reduction in the volume of the gastric content in pylorus-ligated rats, and a dose of 250 micrograms kg-1 resulted in a significant reduction in total acidity (28.81 +/- 11.73 mEq L-1, P < 0.02) in the pylorus ligation model. A significant reduction in total acid output was observed at doses of 250 micrograms kg-1 (84.27 +/- 22.33 mEqH+, P < 0.02) and 500 micrograms kg-1 (120.17 +/- 24.49 mEqH+, P < 0.01) in pylorus-ligated rats. A significant reduction in the ulcer index in pylorus-ligated rats was observed at all cromakalim doses: 50 micrograms kg-1 (0.23 +/- 0.09, P < 0.05), 100 micrograms kg-1 (0.15 +/- 0.09, P < 0.02), 250 micrograms kg-1 (0.12 +/- 0.05, P < 0.01) and 500 micrograms kg-1 (0.14 +/- 0.03, P < 0.02). A significant reduction in the ulcer index of aspirin-treated rats was also observed at all cromakalim dose levels: 50 micrograms kg-1 (0.39 +/- 0.03, P < 0.01), 100 micrograms kg-1 (0.28 +/- 0.06, P < 0.01), 250 micrograms kg-1 (0.22 +/- 0.04, P < 0.001) and 500 micrograms kg-1 (0.28 +/- 0.03, P < 0.01). In the water-immersion plus restraint stress-induced gastric ulcer model, cromakalim significantly reduced gastric ulceration at all the dose levels: 50 micrograms kg-1 (28.2 +/- 2.12, P < 0.001), 100 micrograms kg-1 (20.24 +/- 1.71, P < 0.01), 250 micrograms kg-1 (19.95 +/- 1.46, P < 0.001) and 500 micrograms kg-1 (21.61 +/- 3.00, P < 0.001) but there was no consistent reduction of gastric bleeding. In addition to gastric ulcers, duodenal lesions were also reduced by pretreatment with cromakalim at all dose levels: 50 micrograms kg-1 (97.87 +/- 20.03 mm2, P < 0.02), 100 micrograms kg-1 (70.72 +/- 12.82 mm2, P < 0.02), 250 micrograms kg-1 (48.32 +/- 8.42 mm2, P < 0.01) and 500 micrograms kg-1 (55.50 +/- 12.50 mm2, P < 0.01). Cromakalim at a dose of 100 micrograms kg-1 also reduced total acidity (99.36 +/- 9.12 mEqL-1, P < 0.02) and total acid output (172.22 +/- 45.33 mEq of H+, P < 0.05) in this model. These findings demonstrate the anti-ulcer activity of cromakalim in different experimental models and suggest its potential use in ulcer therapy.
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PMID:Anti-ulcer activity of cromakalim (BRL 34915), a potassium-channel opener, against experimentally induced gastric and duodenal ulcers in rats and guinea-pigs. 905 94

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

Clinico-statistical evaluation of reparative process in 332 gastric ulcer and 294 duodenal ulcer patients revealed factors of objective value to its course. In order of significance the factors rank as follows: area of ulcer, localization, combination with certain mucosal erosions, total fasting acidity, free fasting hydrochloric acid, basal gastric secretion, cardial function, duodenogastric reflux, sex, age, number of cigarettes smoked daily. When studying treatment effects on regeneration in ulcer patients in is necessary to take into consideration basal clinico-endoscopic parameters.
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PMID:[The course of the reparative process in patients with gastric and duodenal peptic ulcers (a clinico-statistical study)]. 913 99

Saliva contains several factors that protect the alimentary canal mucosa against acidity. We measured the secretory carbonic anhydrase (CA VI) levels in the saliva of patients with gastrointestinal disorders using a time-resolved immunofluorometric assay. The mean enzyme concentrations were found to be lower in patients with verified esophagitis, gastric ulcer, or duodenal ulcer than in control patients with nonacid peptic diseases. The biochemical data from the enzyme activity assays and western blots of the human gastric mucosa and gastric juice samples indicated that the swallowed CA VI probably retains its activity in the harsh environment of the gastric lumen. In the upper alimentary canal, CA VI may neutralize the acid by catalyzing the formation of carbon dioxide and water. The present findings suggest that drugs supplemented with CA VI may prove beneficial in treating acid-peptic diseases.
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PMID:Salivary carbonic anhydrase protects gastroesophageal mucosa from acid injury. 914 56

The biosynthesis of sulfated mucin in gastric tissue was investigated in cold-stress and indomethacin (CSI)-induced gastric ulcer models. To examine the synthesis of gastric sulfated mucin, [35S]H2SO4 (sulfate) incorporation into gastric mucin was measured. The treatment of CSI inhibited the incorporation of [35S]sulfate after 2 hr. The gastric acid hypersecretion or the formation of severe ulcer was observed at 1 or 4 hr after the CSI-treatment, respectively. Pibutidine hydrochloride (IT-066), a novel H2-receptor antagonist, (0.3 mg/kg, s.c.) inhibited the formation of ulcer and reversed the inhibition of mucin sulfation by the CSI-treatment, whereas atropine sulfate, a muscarinic receptor antagonist, (1.0 mg/kg, s.c.) did not inhibit the development of ulcer nor decrease in the mucin sulfation at 6 hr after the CSI-treatment. IT-066 inhibited the total acid output (T.A.O.) due to the reduction of the acidity in the gastric juice, whereas atropine inhibited the T.A.O. due to that of the volume. These results indicated that a different mode of action between IT-066 and atropine on gastric acid secretion influences their actions in the incorporation of [35S]sulfate and the formation of ulcer in the CSI-treated rat. Therefore, it is considered that the reduction of biosynthesis of gastric sulfated mucin following acid hypersecretion may be responsible for the formation of gastric ulcer.
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PMID:Effect of cold-stress and indomethacin on the biosynthesis of gastric sulfated mucin in rats. 946 26

The reverse transcription polymerase chain reaction (RT-PCR) was performed to detect genes of RNA viruses in the freshly biopsied gastric mucosa of seven patients with low gastric acidity. Although nucleoprotein genes of Sendai virus and hemmaglutinin genes of influenza virus A were not detected, nucleoprotein genes of influenza virus B were detected in samples from three of the seven patients. The first patient had had antrectomy and vagotomy for gastric ulcer, the second patient was receiving a histamine type 2 receptor blocker for gastritis, and the third patient was receiving a proton pump inhibitor for gastric ulcer. Virus isolation from gastric mucosa and from gargles was negative for all seven patients. These findings suggest that genes of influenza viruses may exist in the gastric mucosa of patients with low gastric acidity.
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PMID:Detection of genes of RNA viruses from freshly biopsied gastric mucosa by reverse transcription polymerase chain reaction. 960 41

Croton cajucara Benth. (Euphorbiaceae) is widely used in Amazonian folk medicine for the treatment of a wide range of gastrointestinal symptoms. The essential oil from its bark was investigated for acute toxicity in mice and for its ability to prevent the formation of ulceration of the gastric mucosa in different models of experimentally induced gastric ulcer in mice and rats. When previously administered orally at a dose of 100 mg kg(-1), the essential oil significantly reduced (P < 0.01) the gastric injury induced by hypothermic restraint stress (48%), indomethacin (47%), ethanol (86%) and pylorus ligature models (87%) in rats. In the HCl/ethanol-induced gastric ulcer model in mice, at oral doses of 100 and 200 mg kg(-1), the essential oil from C. cajucara significantly reduced (P < 0.01) the formation of gastric lesions by 52% and 67%, respectively, when compared with the control group. In rats submitted to pylorus ligature, the essential oil given orally increased the volume of gastric juice when compared with the control group (P < 0.01). When the essential oil (100 mg kg(-1)) was administered intraduodenally to mice, significant modifications were found in gastric parameters such as pH and total acid content after oil treatment. We observed significant changes (P < 0.01) in gastric juice parameters such as an increase in volume and a decrease in gastric acidity (pH and total acid content). The acute toxicologic effects of the essential oil from C. cajucara were assessed in mice. The LD50 values were 9.3 g kg(-1) by the oral route and 680 mg kg(-1) by the intraperitoneal route. The good yield of essential oil obtained from dried C. cajucara bark (1%) as well as its anti-ulcerogenic activity and low toxicity suggest that pharmacological studies of this substance as a potential new anti-ulcerogenic drug are warranted.
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PMID:Effects of an essential oil from the bark of Croton cajucara Benth. on experimental gastric ulcer models in rats and mice. 1034 36

The bark of Croton cajucara Benth, is used in Brazilian folk medicine as an infusion to treat gastrointestinal disorders. The aim of the present study was to assess the mechanisms involved in the antiulcerogenic activity of dehydrocrotonin (DHC), a diterpene isolated from C. cajucara bark. We studied the effects of DHC on pylorus ligature (Shay) in mice treated with the drug (100 mg/kg) by the intraduodenal route. DHC did not induce any alteration in gastric volume in Shay mice but modified the pH and total acid concentration of gastric juice. Incubation of gastric juice with DHC did not reduce gastric acidity compared to control. We also investigated the effects of DHC on the response to histamine of right atria isolated from guinea pigs and on the response to carbachol of stomach fundus strips from rats. The concentration-response curves for the chronotropic effect of histamine in guinea pig right atria were shifted to the right, with a significant decrease in the maximum response, in the presence of DHC. Similar results were obtained with DHC (30 microM) for the concentration-response curves to carbachol in the isolated rat stomach. The ability of DHC to increase PGE2 release from rat stomach mucous cells was also studied. We observed that DHC induced a significant increase in PGE2 production (60% compared to control). In addition, the effects of DHC on the healing of acetic acid-induced gastric ulcer in rats were evaluated 14 days after acid injection. Oral administration of DHC (100 mg/kg per day) for 14 consecutive days had no effect on gastric ulcer healing in rats. Thus, the protective effect of DHC on induced gastric lesions could be due to synergistic effects, e.g., an increase in PGE2 release and non-competitive antagonism of H2-receptors and of muscarinic receptors. Whereas the former result represents an increase in the protective factors, the latter one shows a decrease in the aggressive factors against the gastric mucosa.
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PMID:Antiulcerogenic mechanisms of dehydrocrotonin, a diterpene lactone obtained from Croton cajucara. 1036 37


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