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)

The mucous gel maintains a neutral microclimate at the epithelial cell surface, which may play a role in both the prevention of gastroduodenal injury and the provision of an environment essential for epithelial restitution and regeneration after injury. Enhancement of the components of the mucous barrier by sucralfate may explain its therapeutic efficacy for upper gastrointestinal tract protection, repair, and healing. We studied the effect of sucralfate and its major soluble component, sucrose octasulfate (SOS), on the synthesis and release of gastric mucin and surface active phospholipid, utilizing an isolated canine gastric mucous cells in culture. We correlated these results with the effect of the agents on mucin synthesis and secretion utilizing explants of canine fundus in vitro. Sucralfate and SOS significantly stimulated phospholipid secretion by isolated canine mucous cells in culture (123% and 112% of control, respectively). Indomethacin pretreatment significantly inhibited the effect of sucralfate, but not SOS, on the stimulation of phospholipid release. Administration of either sucralfate or SOS to the isolated canine mucous cells had no effect upon mucin synthesis or secretion using a sensitive immunoassay. Sucralfate and SOS did not stimulate mucin release in the canine explants; sucralfate significantly stimulated the synthesis of mucin, but only to 108% of that observed in untreated explants. No increase in PGE2 release was observed after sucralfate or SOS exposure to the isolated canine mucous cells. Our results suggest sucralfate affects the mucous barrier largely in a qualitative manner. No increase in mucin secretion or major effect on synthesis was noted, although a significant increase in surface active phospholipid release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of sucralfate on components of mucosal barrier produced by cultured canine epithelial cells in vitro. 147 34

This randomized, multiple cross-over pharmacokinetic study was undertaken to determine if food or sucralfate alter the bioavailability of the active S(+) enantiomer of ibuprofen. Eleven healthy adult male volunteers were given three single 600-mg doses of ibuprofen (separated by 1 week) administered either in a fasting state, after a standardized breakfast, or with sucralfate 1 g. The main outcome measures were area under the concentration (AUC), maximum peak plasma concentration (Cmax), and time to reach peak concentration (tmax) for total, S(+), and R(-) enantiomer serum ibuprofen levels, drawn up to 10 hours after dosing. The AUC for R(-) ibuprofen was significantly lower than S(+) ibuprofen in all three treatment groups. The treatments had no different effects on AUC for S(+), R(+), or total ibuprofen. There was no difference in the ratio of S(+):R(-) enantiomers across different treatment groups, but the intersubject variability was significant (P < .05). The S(+) ibuprofen Cmax was greater than the R(-) ibuprofen Cmax for all treatment groups (P < .05). Sucralfate reduced the peak concentration of both S(+) and R(-) enantiomers when compared with fasting (P < .05). There was a slight but nonsignificant increase in the mean time to achieve peak concentration of both S(+) and R(-) enantiomers. Neither food nor sucralfate has a significant effect on ibuprofen enantiomer pharmacokinetics, but interindividual variability contributes significantly to the variability of enantiomer bioavailability.
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PMID:The effect of food or sucralfate on the bioavailability of S(+) and R(-) enantiomers of ibuprofen. 148 49

Drugs used in the treatment of peptic ulcer disease may interact with the renal system in a variety of ways. Since many agents are eliminated by renal excretion, clearance of these agents may be reduced and half-life extended in the presence of renal insufficiency. The histamine H2-receptor antagonists may interfere with renal tubular excretion of creatinine and cationic drugs, resulting in elevated serum concentrations and reduced renal clearance. The prostaglandin E1 analogue misoprostol is used as a cytoprotective agent but has renal effects. The renal effects differ between systems studied. In the rat, misoprostol reduces cyclosporin-induced renal tubular toxicity, whereas in humans it has been shown to attenuate renal allograft rejection. Sucralfate is the aluminium salt of sucrose octasulfate. It permits the absorption of aluminium in amounts similar to aluminium-containing antacids, and toxicity has been demonstrated in the presence of renal insufficiency. Bismuth compounds are used increasingly to treat peptic ulcer disease, and bismuth toxicity has been described in association with renal insufficiency. Aluminium-, calcium- and magnesium-containing antacids are used as oral phosphate binders in patients with renal insufficiency in addition to their usual indications. Cation absorption and accumulation with all of these antacid preparations has been described and may lead to toxicity.
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PMID:Renal effects of peptic ulcer therapy. 152

Sucralfate and ranitidine were compared in the treatment of gastric ulcer (GU) in this multicenter randomized double-blind study. Sixty-four patients with endoscopically diagnosed GU initially included in the trial were randomly assigned to treatment with sucralfate, 2 g b.i.d. (morning and evening on an empty stomach), or ranitidine, 150 mg b.i.d. Nine patients were subsequently excluded for various reasons. The remaining 55 were examined endoscopically after 4 and, if unhealed, 8 weeks. At 4 weeks, 54.2% (13 of 24) of the sucralfate group had a healed ulcer, in comparison to 45.2% (14 of 31) of the ranitidine group (NS). At 8 weeks, cumulative healing rates were 87.5% (21 of 24) and 84% (26 of 31), respectively (NS). No differences were found in the healing effects of the drugs on smokers and nonsmokers or in side effects. These results suggest that both drugs are equally effective in the short-term treatment of GU.
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PMID:Sucralfate and ranitidine twice daily in the treatment of gastric ulcer. A multicenter randomized double-blind study. 155 14

Chronic microaspiration through a tracheal cuff is the main culprit in the penetration and colonization of the lower respiratory tract. A total of 145 patients intubated for more than 3 days were randomly assigned to a double nosocomial pneumonia (NP) prevention: 1--Prevention of aspiration by hourly subglottic secretion drainage (SSD) with a specific endotracheal tube (HI-LO Evac tube, Mallinckrodt); 2--Prevention of gastric colonization using either sucralfate or antacids. Four random groups were defined, similar in age and severity of illness. Subglottic secretion drainage treatment was associated with: a) a twice lower incidence of NP (no-SSD: 29.1%, SSD: 13%); b) a prolonged time of onset of NP (no-SSD: 8.3 +/- 5 days, SSD: 16.2 +/- 11 days); c) a decrease in the colonization rate from admission to end-point day in tracheal aspirates (no-SSD: +21.3%, SSD: +6.6%) and in subglottic secretions (no-SSD: +33.4%, SSD: +2.1%). Sucralfate was not associated with a significantly lower incidence of NP (antacids: 23.6%, sucralfate: 17.8%), but with a lower increase in the colonization rate in subglottic and gastric aspirates, from admission to end-point day.
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PMID:Prevention of nosocomial pneumonia in intubated patients: respective role of mechanical subglottic secretions drainage and stress ulcer prophylaxis. 157 42

Twelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s. for 1 month. Ulcers healed in 8 of the 12 patients without an alteration in the H. pylori-associated antral gastritis. Sucralfate produced a significant fall in basal acid output in all the patients, from a median of 4.8 (range 2.1-12.1) to 1.6 (0.4-8) mmol/h, P less than 0.01, whereas peak acid output was unchanged from 41 (21-59) before to 38 (24-55) mmol/h after treatment. Basal plasma gastrin concentrations and the meal-stimulated integrated gastrin response were not altered significantly by sucralfate: 8 (2-17) pmol/L and 732 (188-1045) pmol. min/L pre-treatment and 6 (2-17) pmol/L and 600 (140-1302) pmol. min/L post-treatment, respectively. The fall in basal acid output observed may contribute to prolonged duodenal ulcer remission after treatment with sucralfate.
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PMID:Sucralfate diminishes basal acid output without affecting gastrin, H. pylori or gastritis in duodenal ulcer patients. 160 44

Sucralfate, a basic aluminum salt of sucrose, was the first successful drug with a major cytoprotective mechanism of action. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. Sucralfate stimulates the synthesis and release of gastric mucosal prostaglandins as well as bicarbonate and the epidermal growth factor which stimulates healing. Sucralfate is the safest drug available today in the treatment of dyspeptic symptoms and compared to ranitidine and cimetidine it has the following characteristics. (2) The short-term healing of duodenal ulcers is the same for sucralfate, cimetidine and ranitidine. (3) Sucralfate-treated patients have a lower recurrence rate of duodenal ulceration after healing when compared with cimetidine and the recurrence rate is not connected with the presence or absence of Campylobacter pylori.
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PMID:Role of sucralfate in peptic disease. 161 11

We investigated the role of nitric oxide (NO) and prostaglandins (PG) in the prevention by sucralfate of ethanol-induced gastric damage and the decrease of gastric blood flow and compared them with those obtained with nocloprost, a potent locally acting gastroprotective agent. Sucralfate and nocloprost given intragastrically (i.g.) protected dose dependently the gastric mucosa against the damage by absolute ethanol and prevented the decrease in blood flow induced by ethanol. Pretreatment with NG-nitro-L-arginine (L-NNA), an inhibitor of NO synthase decreased dose dependently the protection and the maintenance of blood flow provided by sucralfate but not by nocloprost. This decrease of sucralfate protection was antagonized by L-arginine but not D-arginine. Pretreatment with indomethacin also reversed, in part, the protective and hyperemic effects of sucralfate but the combination of both indomethacin and L-NNA completely abolished these effects. We conclude that sucralfate activates both the NO and PG systems that cooperate in the gastroprotective action of this drug and that NO is not involved in the protection induced by a PGE2 analog.
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PMID:Role of nitric oxide and prostaglandins in sucralfate-induced gastroprotection. 161 13

The influence of sucralfate on the detection of occult blood in simulated gastric fluid by two screening tests was investigated. Two simulated gastric solutions (pH 1.2 and 4.1) containing sucralfate 2.5 or 10 mg/mL were spiked with fresh whole blood (hemoglobin concentration, 15.7 g/dL) to achieve a blood concentration of 1 or 5 microL/mL. Fifty-microliter samples were applied to separate Hemoccult and Gastroccult test slides, which were read by a blinded evaluator at 60, 120, and 180 seconds after the addition of developer. Any trace of blue in the test area was considered a positive result. Sucralfate-free simulated gastric fluid spiked with blood served as a positive control, and fluid with or without sucralfate and containing no blood served as a negative control. No false-positive or false-negative results were obtained with Gastroccult. Hemoccult yielded false-positive results in 3 of 20 determinations at 60 seconds for solution containing sucralfate 10 mg/mL (pH 1.2) and 13 of 20 determinations at 60 seconds for solution containing sucralfate 2.5 mg/mL (pH 1.2). All the results with Hemoccult were positive when the slides were read at 120 and 180 seconds. Also, all the results for the negative controls were positive at 120 seconds. Hemoccult did not produce any false-negative results. False-positive results occurred when Hemoccult was used to test simulated gastric fluid that had a low pH (1.2) and contained sucralfate. Gastroccult did not yield false-positive results.
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PMID:Influence of sucralfate on the detection of occult blood in simulated gastric fluid by two screening tests. 161 13

Prevention of respiratory tract infections is only possible when the pathogenesis is known. Three types of infection can be distinguished: primary endogenous infections, caused by pathogens carried in the throat at the commencement of mechanical ventilation, generally develop early and can only be prevented by intravenous antibiotics. Secondary endogeneous infections, caused by hospital-acquired pathogens, generally develop later and can be prevented by selective decontamination of the digestive tract (SDD). The GI-tract is decontaminated by oral nonabsorbable antibiotics and for oropharyngeal decontamination a sticky antibiotic ointment is used. To date 16 controlled SDD trials in intensive care have been fully published. In all except one study, the pneumonia rate decreased significantly from 40%-50% in controls to about 10% in SDD-treated patients. All studies showed a consistent reduction of ventilator days, ICU-stay and an improved outcome in SDD-treated patients. However, in only few studies did these differences reach statistical significance. Selection of resistant strains has not been observed during prolonged use of SDD. Sucralfate reduces the pneumonia rate compared to H2-blockers or antacids by not interfering with the gastric barrier. However, gastric colonization is reduced rather than eliminated and sucralfate has almost no effect on oropharyngeal or tracheal colonization. Whether sucralfate is significantly better than a placebo remains to be established. SDD is superior to sucralfate in preventing both colonization and infection.
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PMID:Prevention of pneumonia by selective decontamination of the digestive tract (SDD). 164 28


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