Disease relevance of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• Oral sucralfate suspension for mucositis [1].
• Sucralfate bezoar [2].
• BACKGROUND & AIMS: The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear [3].
• Sucralfate appears useful for duodenal but not gastric ulcers [4].
• Sucralfate promotes the healing of peptic ulcers and, in large doses, increases gastric mucosal prostaglandins [5].

Psychiatry related information on (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• These results suggest that the 2 g b.i.d. dose of sucralfate in granule form is at least as effective as the conventional dose of 1 g q.i.d. in the treatment of active gastric ulcers and could lead to better patient compliance [6].
• At the base-case assumptions of 6% risk of developing stress-related hemorrhage and 50% risk-reduction due to prophylaxis, the cost of sucralfate was $1,144 per bleeding episode averted [7].
• After 2 years of follow-up, sucralfate was found to be superior to both placebo and antacid (P < 0.001) with regard to duration of pain, reduction of the healing period, response time to first treatment and duration of remission [8].
• Endoscopy showed symptomatic improvement in 67% of the patients treated with sucralfate and in 74% of the combination therapy group [9].
• Sucralfate dose-dependently decreased the clinical signs of enterocolitis (e.g., lethargy, diarrhea) as well as the number and area of ileal and colonic erosions and ulcers [10].

High impact information on (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• There are conflicting data on the effect of histamine H2-receptor antagonists and the cytoprotective agent sucralfate on rates of gastrointestinal bleeding, ventilator-associated pneumonia, and mortality [11].
• Clinically important gastrointestinal bleeding developed in 10 of 596 (1.7 percent) of the patients receiving ranitidine, as compared with 23 of 604 (3.8 percent) of those receiving sucralfate (relative risk, 0.44; 95 percent confidence interval, 0.21 to 0.92; P=0.02) [11].
• In the ranitidine group, 114 of 596 patients (19.1 percent) had ventilator-associated pneumonia, as compared with 98 of 604 (16.2 percent) in the sucralfate group (relative risk, 1.18; 95 percent confidence interval, 0.92 to 1.51; P=0.19) [11].
• H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily) [3].
• Sucralfate suppresses Helicobacter pylori infection and reduces gastric acid secretion by 50% in patients with duodenal ulcer [3].

Chemical compound and disease context of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• A unicenter, single-blind, randomized study was conducted on 283 patients with active duodenal ulcer to compare possible factors that may affect healing and relapse in patients treated with a potent antisecretory agent, cimetidine, or a site-protective and cytoprotective agent, sucralfate [12].
• Recurrent duodenal ulcers, treated with cimetidine, 400 mg, or ranitidine, 150 mg, once nightly, or with sucralfate, 1 g twice daily, can be prevented in approximately 75% of patients for up to 1 year [13].
• Misoprostol compared with sucralfate in the prevention of nonsteroidal anti-inflammatory drug-induced gastric ulcer. A randomized, controlled trial [14].
• Therefore, we investigated the possible effects of sucralfate, an aluminium hydroxide complex of sulfated sucrose used in the treatment of gastric ulcer, in preventing radiation-induced diarrhea and bowel discomfort in patients treated with curative intention for pelvic cancer with external radiotherapy [15].
• Effect of omeprazole and sucralfate on prepyloric gastric ulcer. A double blind comparative trial and one year follow up [16].

Biological context of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• When aspirin-induced lesions were prevented by sucralfate, the inhibition of gastric emptying was blocked during the fasting period and was attenuated following the water load [17].
• Although the action of sucralfate on ulcerated mucosa has been demonstrated, its effect on the histology, ultrastructure, and function of normal gastric mucosa is unknown [18].
• RESULTS: The frequency of defecation and stool consistency were significantly improved by sucralfate [15].
• Results in group 1 showed that neither ketoprofen bioavailability nor maximal plasma concentration and time to reach maximal concentration were affected by the administration of sucralfate [19].
• Three studies were conducted on three groups of 12 volunteers in order to determine the influence of food or sucralfate on the pharmacokinetics of naproxen and ketoprofen [19].

Anatomical context of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• At 15 min, 1 h, and 3 h after intragastric instillation of sucralfate, whitish incrustations of the drug were firmly adhering to the glandular mucosa [18].
• Does sucralfate affect the normal gastric mucosa? Histologic, ultrastructural, and functional assessment in the rat [18].
• Mucosal histology after sucralfate administration demonstrated the following: disruption and exfoliation of some of the surface epithelial cells, mucosal hyperemia, prominent release of mucus from the surface epithelial cells, and edema of lamina propria and submucosa [18].
• Mucosal protection by sucralfate and its components in acid-exposed rabbit esophagus [20].
• Sucralfate has been reported to protect the esophageal epithelium of the rabbit and cat against acid injury [20].

Associations of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran with other chemical compounds

• Several in vitro tests suggested that the clear sucrose sulfate solution, like the sucralfate gel, probably acts through a topical protectant effect, rather than through pepsin inactivation [21].
• These results indicate that sucralfate can protect against acid injury in esophagus and that this protection is mediated by (a) intraluminal pH buffering through its content of aluminum hydroxide and (b) enhancing mucosal defense against H+ entry and injury through its content of SOS [20].
• Animals were exposed for 1 h to either acid alone (HCl at pH 2), acid plus pepsin (0.8 mg/ml), or acid plus taurocholic acid (5 mM), as well as to the same injurious agents with the addition of 1 g of sucralfate [21].
• Nosocomial pneumonia was diagnosed in 6%, 12%, and 13% of controls, sucralfate recipients, and cimetidine recipients, respectively (sucralfate: relative risk, 2.0 [CI, 0.79 to 5.01], P = 0.14; cimetidine: relative risk, 2.2 [CI, 0.88 to 5.33], P = 0.09) [22].
• Ranitidine alone or combined with sucralfate did not prevent ethanol-induced histologic or functional changes in the mucosa [23].

Gene context of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• To explore the mechanisms of the effects of sucralfate on the stomach, we investigated the action of sucrose octasulfate (SOS), a constituent of sucralfate, on the function of canine gastric parietal cells and somatostatin cells and in the isolated perfused intact rat stomach [24].
• Recent studies highlight the capacity of sucralfate to bind basic fibroblast growth factor (bFGF) and deliver it in high concentration to the ulcer [25].
• Role of interleukin-4 in down-regulation of endothelin-1 during gastric ulcer healing: effect of sucralfate [26].
• Effect of chronic duodenal ulceration and its treatment with lanzoprazole or sucralfate on gastroduodenal mucosal protein turnover and TGF-alpha, bFGF, and EGF receptor expression in humans [27].
• The study was designed to determine the gastroprotective and ulcer healing efficacy of basic transforming growth factor (bFGF) and to assess whether this peptide contributes to the action of sucralfate on the rat stomach [28].

Analytical, diagnostic and therapeutic context of (2R,3R,4S,5R,6S)-3,4,5-trisulfoxy-2-(sulfoxymethyl)-6-[(2R,3S,4S,5R)-3,4,5-trisulfoxy-2-(sulfoxymethyl)tetrahydrofuran-2-yl]oxy-tetrahydropyran

• GRP-stimulated plasma gastrin concentrations, GRP-stimulated acid output, and basal acid output all decreased by approximately 50% during sucralfate therapy and returned to pretreatment levels after treatment was discontinued [3].
• Healing of the ulcer was documented 8 wk after vagotomy, antrectomy, gastrojejunostomy, and a course of sucralfate therapy [29].
• Eight chair-adapted rhesus monkeys received a subcutaneous injection of either 150 mg/kg of aspirin or vehicle in combination with either a therapeutic oral dose of sucralfate (50 mg/kg X day) or water [5].
• Protective effect of sucralfate against alcohol-induced gastric mucosal injury in the rat. Macroscopic, histologic, ultrastructural, and functional time sequence analysis [30].
• INTERVENTIONS: Patients who were expected to receive at least 3 months of NSAID therapy and who did not have a gastric ulcer at the time of the initial screening endoscopy were randomized to receive misoprostol, 200 micrograms four times a day, or sucralfate, 1 g four times a day [14].

References