Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: KEGG:D00446 (Sucralfate)
278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sucralfate is an effective agent in reducing the incidence of upper GI tract (UGIT) stress bleeding and nosocomial pneumonia in critically ill patients. Many of these patients are not intubated and are at increased risk for aspiration of large volumes of UGIT contents containing sucralfate. The effects of aspirated sucralfate are unknown. To investigate this, large-volume aspiration (2 ml/kg) was simulated in freshly tracheostomized rats (n = 6, all experimental groups) using normal saline, particulate antacid, and sucralfate adjusted to pH 3.6 and 5.0. Four hours after aspiration, the rats were killed and their lungs were formalin-fixed. Significant increases in lung inflammation were seen by light microscopy in all experimental groups at pH 3.6. Antacid aspirated at pH 5.0 induced significant increases in airway as well as parenchymal inflammation. At pH 3.6, the antacid aspiration led to significant increases in lung edema and hemorrhage. Sucralfate aspiration produced significant increases in pulmonary hemorrhage at pH 5.0. Our microscopic findings are consistent with the acute pulmonary histopathologic changes known to occur after large-volume aspiration of particulate materials, including antacids. Additionally, we show that large-volume aspiration of sucralfate produced significant acute pneumonitis, including pulmonary hemorrhage. In view of the proven usefulness of sucralfate, further investigations are indicated to evaluate these experimental findings before extrapolating to critically ill patients.
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PMID:Acute histologic effects of simulated large-volume aspiration of sucralfate into the lungs of rats. 204 91

Sucralfate is the first drug to be shown to prevent ulceration in bile duct-ligated pigs. Usually such ulceration is uniformly fatal. Seven pigs in each of four groups in this study received only saline, or sucralfate (1 g every six hours), famotidine (40 mg per day), or misoprostol (200 micrograms every six hours). A Foley catheter was placed into a gastrectomy after bile duct ligation. Similar groups of sham-operated pigs were also prepared. After 48 hours, all saline-, famotidine-, or misoprostol-treated pigs showed severe macroscopic ulceration, whereas only two of those treated with sucralfate showed minimal macroscopic ulceration. Until now, only highly selective vagotomy has reduced ulceration caused by bile duct ligation. The present results suggest that acid inhibition is not the only important factor in healing bile duct ligation-induced peptic ulceration.
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PMID:Sucralfate in the prevention of porcine experimental peptic ulceration. 250 18

To study the protective effect of Sucralfate on Naproxen-induced mucosal lesions, 16 healthy, male volunteers were given Naproxen 500 mg b.i.d. together with Sucralfate 2 g b.i.d. or placebo in a double-blind, crossover study. Drug periods were 1 week, with a 3-week wash out in between. Mucosal lesions in stomach and duodenum were assessed by upper endoscopy before and after each drug period, using a visual analogue with separate scoring of mid- and distal duodenal lesions. 51Cr-EDTA absorption tests were performed to demonstrate possible changes in distal gut permeability. In addition, subjective symptoms were registered. Both drug periods induced significant lesions in the stomach and duodenum. Statistically speaking, fewer changes were found in the stomach and duodenal bulb after Sucralfate co-administration, whereas no significant reduction of lesions was seen in the distal duodenum. The 51Cr-EDTA absorption was increased in both periods, indicating deleterious effects to distal parts of the gut, but our results did not demonstrate Sucralfate-mediated protection from these changes. Symptoms were modest, and equal in the two periods. We conclude that Sucralfate may offer protection in the gastric and proximal duodenal mucosa, but no such protective effect was seen distally to the duodenal bulb.
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PMID:Sucralfate for prevention of naproxen-induced mucosal lesions in the proximal and distal gastrointestinal tract. 251 93

Two formulations of [99mTc]sucralfate have been used to image gastric and duodenal ulcers and inflammatory bowel disease. One formulation is a complexation of [99mTc]HSA with sucralfate. The second is prepared by directly labeling sucralfate with [99mTc]pertechnetate in the presence of stannous ion. An in vitro study of the factors affecting the production and stability of these labeled sucralfate preparations was conducted. Both formulations were stable at the acidic pH likely encountered in the stomach. However, at pH greater than 6 the albumin-sucralfate complex began to dissociate while directly labeled sucralfate was stable to a pH of 9. Conversely it was shown that directly labeled sucralfate was more susceptible to loss of 99mTc to other chelating species. Sucralfate complexed with [99mTc]HSA was radiochemically stable up to a specific activity of 26 GBq (700 mCi) per gram while directly labeled sucralfate showed decreased 24-hr stability at specific activities greater than 837 mCi (31 GBq) per gram.
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PMID:Chemical aspects of labeling sucralfate with 99mTcO4. 254 93

Conventional stress bleeding prophylaxis with antacids or histamine (H2)-antagonists, as well as the newer mucosa-protective drugs pirenzepine and sucralfate, are satisfying most of the clinicians with regard to efficacy of stress bleeding prevention. Therefore, potential side effects are attaining crucial importance with regard to the drugs to be used. Pharmacologic blockade of cardiac H2-receptors increases the risk of bradycardia and negative inotropic effects as well as coronary vasoconstriction at least in the presence of elevated plasma histamine levels. Intracardiac injection of pirenzepine can lead to temporary tachycardia. Elderly patients have been shown to be at an increased risk of side effects to the central nervous system when treated with H2-antagonists. These drugs can also induce toxic effects in the liver. Cimetidine leads to interactions with a number of drugs used in the intensive care unit. In patients with pre-existing pulmonary diseases, H2-antagonists have been demonstrated to increase pulmonary bronchoconstriction. Alkalinization of the gastric juice is associated with a significant increase in colonization of gram-negative bacteria in the stomach. In intubated patients, aspiration of stomach contents occurs in 30 to 40 percent of the patients. A number of studies have shown a direct correlation between alkalinization of the gastric juice and pulmonary infections. Sucralfate and to a lesser degree pirenzepine can reduce the risk of pulmonary infections. Sucralfate also exerts a bactericidal effect. Recent investigations support the hypothesis that alkalinization of the stomach also increases the risk of systemic infections. This may be the main reason for the observation that at least in ventilated patients sucralfate, unlike H2-antagonists or antacids, leads to a significant reduction of the mortality rate compared with conventional stress bleeding prophylaxis.
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PMID:Side effects of stress bleeding prophylaxis. 256 72

Sucralfate (55 patients), cimetidine (25 patients), ranitidine (30 patients), antacids and cholinolytics (32 patients) were studied and compared in open clinical trials for the efficacy in the treatment of ulcer disease of the stomach and duodenum. During 5 weeks, ulcers completely healed in 100% of the patients given sucralfate (in 94.5% for 4 weeks), in 90% of the patients treated with ranitidine, in 84% on cimetidine, and in 78% of the patients undergoing treatment with antacids and cholinolytics.
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PMID:[A comparative evaluation of the efficacy of sucralfate and H2-histamine blockaders in treating peptic ulcer]. 257 63

Sucralfate possesses site protective and cytoprotective actions and heals ulcers effectively, but its effect on gastric mucosal blood flow is unknown. Using an ex vivo gastric chamber preparation, we studied the effect of sucralfate on gastric mucosal blood flow in rats by laser doppler flowmetry. Under both fasting and fed states, measurements of gastric mucosal blood flow and damage were made in rats after topical application of absolute ethanol alone or after pretreatment with sucralfate. Gastric mucosal damage was assessed by measuring the total area of haemorrhagic mucosal lesions. Ethanol induced gastric mucosal lesions were significantly less with sucralfate pretreatment than without (p less than 0.008). Mucosal blood flow significantly fell after ethanol application (p less than 0.001). The fall was significantly less in fed than in fasted rats (p less than 0.05), and after pretreatment with sucralfate 100 mg or 200 mg than without in both fasted (p less than 0.0008 and 0.00001, respectively) and fed (p less than 0.002 and 0.001, respectively) rats. Graded doses of sucralfate (25-400 mg) resulted in an increase in gastric mucosal blood flow in a dose dependent manner (r = 0.731, p less than 0.001). In conclusion that sucralfate increases gastric mucosal blood flow in rats and lessens the fall in blood flow in rats treated with ethanol, and this action may contribute to its protection against the vascular damage of mucosa by ethanol.
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PMID:Effect of sucralfate on gastric mucosal blood flow in rats. 259 40

Endoscopic distinction between ulcers and erosions is difficult. Consequently, existing literature, which must be taken at face value, may be misleading. Nevertheless, from published studies most gastric and duodenal ulcers associated with nonsteroidal antiinflammatory drugs appear to heal on antacids or H2-antagonists. Sucralfate appears useful for duodenal but not gastric ulcers. Continuing nonsteroidal antiinflammatory drugs does not prevent or delay healing of duodenal or small gastric ulcers; their effects on large gastric ulcers remain uncertain. Thus far, only full doses of H2-antagonists, or their combinations with antacids, have been shown to heal ulcers and prevent recurrences. Ulcer recurrences and complications have occurred in small numbers of patients on maintenance doses of H2-antagonists. Available antiulcer drugs (antacids, H2-antagonists, sucralfate) reduce severe acute injury when taken before or with nonsteroidal antiinflammatory drugs. They also reduce ulcerlike symptoms due to nonsteroidal antiinflammatory drugs. Inexplicably, chronic prophylaxis with H2-antagonists for 4 wk or more appears ineffective in preventing gastric ulcers, although duodenal injury is reduced. As the efficacy of available prophylactic therapy (H2-antagonists, sucralfate, and antacids) has not been established, routine use in all cases seems unjustified at present.
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PMID:Nonsteroidal antiinflammatory drug-induced ulcers: management by traditional therapies. 264 51

To assess the gastric mucosal protective action of sucralfate against alcohol, a double-blind, controlled, randomized study was carried out in 12 healthy adult men. All subjects received four treatments in a random sequence: sucralfate + ethanol, sucralfate + ethanol placebo, sucralfate placebo + ethanol, and sucralfate placebo + ethanol placebo. Fundal, antral, and duodenal mucosae were submitted to endoscopic examinations, and the antral mucosa underwent histologic examination before and after injury. Biopsy specimens were taken from the antral mucosa to determine by radioimmunoassay its capacity to synthesize prostaglandin E2, thromboxane B2, and 6-keto prostaglandin F1 alpha. In both the fundus and the antrum, the mean endoscopic injury score after sucralfate plus ethanol administration was significantly lower than that after ethanol alone. All treatments tended to increase prostanoid values but 6-keto prostaglandin F1 alpha increased significantly when sucralfate was given. Sucralfate did not affect serum ethanol levels, nor did ethanol affect prostanoid synthesis. It is concluded that sucralfate provides significant protection to the human gastric mucosa against ethanol injury, and that this may be partly due to increased prostanoid synthesis.
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PMID:Sucralfate protection of human gastric mucosa against acute ethanol injury. 264 75

Sucralfate as well as colloidal bismuth subcitrate (CBS) and probably also bismuth subsalicylate (BBS) are effective in the acute treatment of peptic ulcer disease. Sucralfate also has positive effects upon symptoms and healing of peptic lesions in reflux esophagitis. Healing rates in gastric and duodenal ulcers are equal to those obtained with H2-antagonists. Side effects are rare, transient and generally mild. Therapy with bismuth compounds should be restricted to 4-8 weeks (cave: bismuth encephalopathy). Healing rates of smokers with duodenal ulcers were the same as in non-smokers during sucralfate therapy. Sucralfate seems to be useful in the treatment (prophylaxis?) of NSAID-induced lesions in the upper gastrointestinal tract. The question of different recurrence rates in peptic ulcer disease after various kinds of medical treatment still remains open. The relationship between the etiology of peptic ulcer disease and Campylobacter pylori infection, as well as possible medical and therapeutic consequences, should be further investigated.
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PMID:Sucralfate and other non-antisecretory agents in the treatment of peptic ulcer disease. 265 80


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