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 development of acute stress bleeding in intensive-care patients occurs on a multifactorial basis. The basic mechanism lies in the imbalance between aggressive and protective factors. Most intensive care patients show a reduced acid secretion, a reduction of the gastric mucosal blood flow, and a decreased mucus and bicarbonate secretion. Sucralfate enhances most of the defensive mechanisms. These actions are the pathophysiologic basis of the efficacy of sucralfate in the prevention of stress bleeding. Because sucralfate has only a minor influence on the gastric pH and at the same time has proven bactericidal effects, gastric and gut bacterial overgrowth is significantly reduced. These effects explain the observed differences in mortality between sucralfate and alkalinizing drugs like antacids or H2-antagonists. The indications and limits of sucralfate in stress bleeding prophylaxis are pointed out.
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PMID:Stress bleeding prophylaxis with sucralfate. Pathophysiologic basis and clinical use. 169 44

Viable bacteria in the gut of thermally injured patients may be translocated through the gut mucosa, causing widespread infection. Increased flora from optimization of bacterial growth by pH elevation, coupled with the decreased intestinal motility common among patients whose mucosal integrity has been compromised, may increase the incidence of translocation. Gastric pH in these patients is monitored and maintained around pH 6 by various agents to reduce susceptibility to stress ulceration. Whole milk, given as a nutrient source, also raises pH. An in vitro trial simulating gastric fluid under conditions found in patients with burns was conducted to evaluate the growth of commonly ingested bacteria. Bicarbonate buffer containing pepsin and adjusted to pH 2, 4, or 7 with HCl was dosed with magnesium and aluminum hydroxide antacid (Maalox) (10 ml), sucralfate (Carafate) (0.4 gm), or prostaglandin E2 (PGE2) (10 ng) before inoculation with Escherichia coli (3 x 10(2) organisms), Pseudomonas aeruginosa (3 x 10(2) organisms), or Staphylococcus aureus (2 x 10(1) organisms). Bacterial growth and pH were determined periodically over the 24-hour trial. Milk was added at intervals in half the samples to simulate patient feeding. Maalox increased pH in all samples containing milk (initially pH 2, 4, or 7) to over 7.0 in 2 hours, and increased pH more slowly without milk. Carafate had a moderating effect, increasing pH 2 and pH 4 and decreasing pH 7, with a narrower pH range found in the milk groups. PGE2 treatments combined with milk also increased pH 2 and pH 4, but slightly elevated pH 7 within 24 hours. Without milk, PGE2 did not alter pH from initial values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antacid, sucralfate, and prostaglandin E2 effects on the growth and potential for translocation of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus in an in vitro gastric simulation. 190 78

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

A bezoar is a mass of undigested material which may form within the lumen of the gut. Some drugs have the potential to form bezoars. In the majority of patients, there is a clear predisposing factor. We present here the data of the French System of Pharmacovigilance on sucralfate and a literature review. Two distinct populations were involved: 16 adults and 5 newborn babies. All were hospitalized in intensive care units. The children were very low birth weight newborn babies, all of whom presented with abdominal distension or acute occlusion. The abdominal radiograph revealed an opaque mass filling the contour of the stomach. Adults presented an oesophageal bezoar around a nasogastric tube. Risk factors for bezoar formation were severe illness, gut hypomotility, dehydration, overdosage, nasogastric tube feeding. Sucralfate is used in the management of peptic ulcer. At pH < 4, extensive polymerization occurs and a sticky viscid gel is formed. In view of this inquiry, the French System of Pharmacovigilance decided to advise caution for adults in intensive care unit being fed by nasogastric tube and contraindication in premature babies and dysmature newborn babies receiving sucralfate.
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PMID:[Sucralfate and bezoars: data from the system of pharmacologic vigilance and review of the literature]. 1021 23

BACKGROUND: Sucralfate, used in stress ulcer prophylaxis, contains aluminum, which can be absorbed from the gut. OBJECTIVE: To determine whether toxic serum aluminum levels can develop after short-term sucralfate therapy in critically ill children. DESIGN: Retrospective clinical study. SETTING: Pediatric intensive care unit of a pediatric university hospital. PATIENTS: Nineteen patients receiving mechanical ventilatory support (median age, 5 yrs [range, 0.25-16 yrs]; median weight, 17 kg [range, 3.5-60 kg]). INTERVENTIONS: All patients received sucralfate suspension nasogastrically. Measurements and RESULTS: Serum aluminum concentrations were measured after a short period on sucralfate therapy (median time, 7 days [range, 3-14 days]). There was no correlation between total sucralfate dose received (p =.35) or dose of sucralfate per unit of body weight (p =.55) and serum aluminum. Nine patients received peritoneal dialysis. Serum aluminum levels were higher in the nine patients who received peritoneal dialysis (median aluminum concentration, 2.86 &mgr;mol/L [range, 0.19-12.3 &mgr;mol/L]) than the ten patients not dialyzed (median aluminum concentration, 0.55 &mgr;mol/L [range, 0.18-0.94 &mgr;mol/L]) (p =.001). The peak serum creatinine levels were higher in the dialyzed patients (median creatinine level, 500 &mgr;mol/L [range, 163-910 &mgr;mol/L]) than those not dialyzed (median creatinine level, 98 &mgr;mol/L [range, 36-415 &mgr;mol/L]) (p =.006). There was a trend toward correlation between peak serum creatinine and serum aluminum (p =.06). CONCLUSION: Aluminum accumulation occurs in children with acute renal failure on sucralfate, especially those receiving dialysis. If sucralfate is used in children in renal failure, serum aluminum concentrations should be monitored regularly.
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PMID:Aluminum accumulation in critically ill children on sucralfate therapy. 1279 50