Drugs online research references
Eur J Gastroenterol Hepatol. 1997 Jan;9(1):41-4.
Previous use of non-steroidal anti-inflammatory drugs and anticoagulants: the influence on clinical outcome of bleeding gastroduodenal ulcers.
Vreeburg EM, de Bruijne HW, Snel P, Bartelsman JW, Rauws EA, Tytgat GN.
Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
OBJECTIVE: To evaluate the relationship between prior non-steroidal anti-inflammatory drug (NSAID) or anticoagulant use and clinical outcome in bleeding gastric and duodenal ulcer patients. DESIGN: Prospective cohort-study. PARTICIPANTS: All patients (n = 132) admitted because of upper gastrointestinal bleeding during 3 months in the Amsterdam area. METHODS: We compared clinical outcome (blood transfusion, rebleeding, surgery and mortality) between ulcer patients who used NSAIDs or anticoagulants and patients who did not use these drugs before the bleeding-episode. RESULTS: Of the 132 patients admitted, 56 patients had gastric or duodenal ulcers. NSAIDs were used significantly more often before the bleeding episode in these ulcer patients than in the non-ulcer patients (n = 76), 21/56 (37.5%) vs. 15/76 (19.7%), respectively (P < 0.05), relative risk = 2.57, 95% confidence interval: 1.04-5.77). Stigmata of recent haemorrhage were found in 16/21 (76.2%) patients in the NSAID ulcer group, in 2/9 (22.2%) in the coumarin-ulcer patients, and in 12/24 (50%) in the no-medication ulcer group (not significant). Prior NSAID usage increased the in-hospital rebleeding rate from 16.7% to 42.9% (P = 0.05), leading to an increased need for surgical intervention from 16.7% to 42.9% (P = 0.05). In contrast prior usage of anticoagulants, which could be antagonized, did not affect the clinical outcome of the bleeding. Mortality was 9.5% in the NSAID group, 0% in the coumarin group, and 4.2% in the no-medication group. CONCLUSION: Prior use of NSAIDs increases the risk of rebleeding in bleeding ulcer patients, and leads to a higher need for urgent surgery. In contrast, prior anticoagulant therapy does not raise the rebleeding risk.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9031897&dopt=Abstract
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mb.kyoto-phu.ac.jp
BACKGROUND: Pantoprazole, 2-[(2-pyridylmethyl) sulphinyl] benzimidazole, is a new substituted benzimidazole that inhibits the parietal cell H+/K+-ATPase. METHODS: In the present study, the anti-secretory and anti-ulcer activities of pantoprazole were compared with those of omeprazole and lansoprazole in rats. RESULTS: Pantoprazole (0.3-3 mg/kg, p.o.) as well as omeprazole (1-10 mg/kg, p.o.) and lansoprazole (1-10 mg/kg, p.o.) dose-dependently decreased both basal acid secretion in pylorus-ligated rats and the stimulated acid secretion induced by mepirizole in acute fistula rats, and the effects of pantoprazole were more potent than those of omeprazole and lansoprazole, the ED50 values for the stimulated acid secretion being 0.8, 2.0 and 1.2 mg/kg, respectively. Neither of these drugs had any effect on duodenal HCO3- secretion. These pump inhibitors prevented the development of duodenal lesions in response to mepirizole in a dose-related manner, the ED50 values for pantoprazole, omeprazole and lansoprazole being 0.4, 2.0 and 1.3 mg/kg, respectively. Likewise, pantoprazole showed the healing promoting action on chronic duodenal ulcers induced by acetic acid, and this effect was also more potent when compared to omeprazole or lansoprazole. CONCLUSIONS: We conclude that pantoprazole exhibited both anti-ulcer and healing promoting effects on duodenal ulcers in rats, and the effects may be attributable to its potent anti-secretory action. Other pump inhibitors such as omeprazole and lansoprazole were almost equally effective as pantoprazole, yet this drug was most potent on the basis of ED50 values.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10197495&dopt=Abstract
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Jpn J Pharmacol. 1993 Nov;63(3):345-51.
Antisecretory effects of a novel and long-lasting histamine H2-receptor antagonist, YM-14471, in rats and dogs.
Yuki H, Kamato T, Nishida A, Fujihara A, Takeda M, Miyata K.
Neuroscience & Gastrointestinal Research Laboratories, Yamanouchi Pharmaceutical Co., Ltd., Ibaraki, Japan.
We investigated some properties of YM-14471 (2-2(-[2-(diaminomethyleneamino)thiazol-4-yl]methylthio)ethy l-5-[3- (diethylamino)propyl]-6-methyl-pyrimidine-4-one trihydrochloride), a new H2-receptor antagonist, in comparison with those of famotidine, cimetidine and omeprazole. In guinea pig atria, famotidine and cimetidine produced a competitive dose-dependent displacement of histamine-induced tachycardia. In contrast, low concentrations of YM-14471 showed competitive inhibition of tachycardia, whereas high concentrations were irreversible or slowly dissociable. In pylorus-ligated rats, intravenous YM-14471, famotidine and cimetidine dose-dependently inhibited basal gastric secretion with ED50 values of 0.04, 0.43 and 31.2 mg/kg, respectively. ED50 values for oral YM-14471, famotidine, cimetidine and omeprazole were 0.81, 0.42, 28.9 and 7.7 mg/kg when given at 1 hr before ligation, and 5.7, 26.7, 1639.5 and 18.6 mg/kg at 5 hr before ligation. In anesthetized dogs, intravenous YM-14471, famotidine, cimetidine and omeprazole also dose-dependently inhibited histamine (160 micrograms/kg.hr)-induced acid secretion with ED50 values of 13.7, 8.7, 333.3 and 65.3 micrograms/kg, respectively. In Heidenhain pouch dogs, YM-14471 inhibited histamine (40 micrograms/kg.hr)-induced acid secretion by both intravenous (0.02 mg/kg) and oral administration (0.3 mg/kg). Moreover, the inhibitory effect of YM-14471 was more prolonged than those of famotidine and cimetidine by either route, and it was as long as that of omeprazole dosed orally. These results suggest that YM-14471 is an irreversible or slowly dissociable H2-receptor antagonist, and has long antisecretory effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7906319&dopt=Abstract
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