Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D00446 (Sucralfate)
 278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the course of a prospective selective digestive decontamination (SDD) trial to prevent nosocomial pneumonia (NP) during mechanical ventilation (MV), we carried out serial cultures of gastric aspirate to assess the importance of gastric colonization for potential respiratory pathogens and its relationship to the simultaneous gastric pH, to whether the patients were receiving Sucralfate or Ranitidine and to the nutritional biochemical parameters. If NP developed, a bronchial sample was taken by fibreoptic bronchoscopy to determine the causal organisms and its relationship to the previous gastric isolated. Results show: 1) Increase in aerobic Gram negative bacilli colonization during hospitalization. 2) Direct relationship between colonization level and gastric pH. 3) Greater pH in ranitidine vs sucralfate group. 4) Low incidence of NP (11%), the majority of these (66%) being early. 5) No bacteriological correlation between gastric colonization and aetiological agents of NP. 6) Close relationship between pharyngeal colonization and causative germs of pulmonary infection (40%).
 ...
PMID:Role of selective digestive decontamination (SDD) in the prevention of nosocomial pneumonia (NP): is gastric decontamination necessary? 143 May 85

Non-steroidal anti-inflammatory drug (NSAID) use is associated with gastro-duodenal erosions and ulcers. Bleeding and perforation are reported complications in NSAID users. Therapeutic recommendations for NSAID-induced gastroduodenal injury are necessary because of our rapidly growing geriatric population, a steady increase in prescriptions for NSAIDs, and the widespread use of over-the-counter NSAIDs. Studies seem to indicate that there is no relationship between acute NSAID-induced mucosal injury and potential damage from chronic NSAID ingestion. Ranitidine (150 mg) b.d. effectively reduces the incidence of duodenal ulcer in NSAID users, but the same dose does not reduce the incidence of gastric ulcer. Misoprostol is effective in reducing the incidence of gastric ulcer in NSAID users, although confirmatory data on its effectiveness in preventing NSAID-induced duodenal ulcer are lacking. In addition to anti-ulcer therapy, treatment of NSAID-induced ulcers includes discontinuing the drug, reducing the dose, or switching to a less potent NSAID. Longer courses of anti-ulcer treatment may be required to achieve expected healing rates when NSAIDs are not discontinued. Results of treatment of NSAID-related ulcers with currently available anti-ulcer medications vary. Several studies have shown that 150 mg ranitidine b.d heals both gastric and duodenal NSAID-induced ulcers. Sucralfate has also been shown to heal NSAID-induced duodenal ulcers. Misoprostol treatment of NSAID-induced ulcers is not well documented, although there are placebo-controlled data that substantiate its benefit in gastric ulcer patients not taking NSAIDs.
 ...
PMID:Non-steroidal anti-inflammatory drug-induced gastroduodenal injury: therapeutic recommendations. 167 75

In a randomized trial involving 20 Italian centers, the effectiveness of 1 g sucralfate three times a day and 150 mg ranitidine twice a day in the treatment of chronic gastritis was assessed and compared. Five hundred outpatients with dyspeptic symptoms and endoscopic evidence of chronic nonerosive gastritis were randomly assigned to either treatment for a period of eight weeks. Endoscopic scores were determined at the beginning and at the end of the study. The severity of dyspeptic symptoms was assessed at Weeks 0, 2, 4, 6, and 8. Four hundred seventy-three patients completed the study. In 331 cases, biopsies were taken during endoscopy, and a histologic evaluation was also performed, according to Whitehead's criteria. Sucralfate was significantly more effective than ranitidine in inducing healing or improvement of both endoscopic (p less than 0.02) and histologic (p less than 0.001) features. At the end of the study, 77.6 percent of the patients in the sucralfate group and 79.4 percent in the ranitidine group were symptom free. Ranitidine was significantly more efficacious at releiving pain during the first four weeks of therapy. Mild side effects were reported by 4.9 percent of patients treated with sucralfate and by 3.6 percent of patients treated with ranitidine. Treatment was withdrawn in one patient treated with sucralfate because of nausea. In conclusion, sucralfate appears significantly superior to ranitidine in improving endoscopic and histologic aspects of chronic nonerosive gastritis. The symptomatic activity of the two drugs is similar, although more rapid relief is obtained with ranitidine.
 ...
PMID:Comparison of sucralfate and ranitidine in the treatment of chronic nonerosive gastritis. A randomized, multicenter trial. 266 May 57

In this prospective study for pharmacotherapy of non varicial upper gastrointestinal haemorrhage eight therapy groups were examined. The efficacy of the most important drugs for ulcus disease was considered. The drugs were used alone and in combination. The results indicated no favourable effect of one preparation (Cimetidine, Pirenzepine, Ranitidine). Significant benefit for the long time healing rate was noted among the combination therapies, especially with Sucralfate, which was not used alone.
 ...
PMID:[Conservative therapy of upper gastrointestinal hemorrhage (prospective, randomized, controlled)]. 387 31

The role of nonprotein sulfhydryls (NP-SH) in the protective effects of honey against absolute ethanol-induced gastric lesions was studied in rats. Sucralfate and ranitidine were used as known standard gastroprotective agents. Honey orally and drugs orally or subcutaneously were administered to 24 h fasted rats 30 or 90 min before oral administration of ethanol. Mucosal damage and the glandular NP-SH levels were measured 1 h after ethanol. Both honey and sucralfate dose-dependently afforded protection against gastric damage and reversed the changes in glandular NP-SH levels induced by ethanol. Ranitidine was ineffective in this model. Pretreatment with indomethacin (IND) did not alter the protective effects of honey or the NP-SH levels, but significantly reduced the protective effects of sucralfate. On the other hand, pretreatment with N-ethylmaleimide (NEM) significantly reduced the protective effects of both honey and sucralfate and lowered the NP-SH levels. Combined IND and NEM treatment caused a significant reduction of the protective effects of honey and the NP-SH levels, but the values were not significantly different from those obtained with NEM alone. In contrast, combined IND plus NEM treatment completely abolished the protective effects of sucralfate and significantly lowered the NP-SH levels. Although these results suggest the involvement of prostaglandins (PGs) -- sensitive process in the protective effects of sucralfate, but honey and sucralfate (partially) share a common mechanisms of action in mediating the gastroprotective effects through NP-SH sensitive processes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Natural honey exerts its protective effects against ethanol-induced gastric lesions in rats by preventing depletion of glandular nonprotein sulfhydryls. 764 50

The proton pump inhibitors omeprazole and lansoprazole and the histamine H2 receptor antagonists ranitidine and nizatidine were investigated for their effects on gastric transmucosal potential difference (PD) in the rat, in comparison with the gastroprotective compound sucralfate. Omeprazole (1-3 mg kg-1, i.v.) and lansoprazole (1-3 mg kg-1, i.v.) did not modify basal PD, but significantly reduced (by approx. 50-60%) the drop in PD caused by intragastric administration of acetylsalicylic acid (ASA, 60 mg kg-1). Ranitidine (3-100 mg kg-1, i.v.) and nizatidine (10-30 mg kg-1, i.v.) behaved similarly to proton pump inhibitors, being ineffective on basal PD, while significantly reducing the effect of ASA. The antisecretory compounds did not change basal pH values. Sucralfate (0.5-1.5 g kg-1 intragastrically) caused a slight increase (approx. 20%) of basal PD and a dose-dependent reduction of ASA-induced fall in PD, with a maximum effect (65% reduction) comparable to that caused by the antisecretory agents. These results showed that ASA-induced disruption of the mucosal barrier can be reduced to the same extent by various antiulcer drugs, irrespective of their effects on gastric acid secretion.
 ...
PMID:Effects of different antisecretory drugs on gastric potential difference in the rat: comparison with sucralfate. 999 Jun 56