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)

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 Treatment was withdrawn in one patient treated with sucralfate because of nausea.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.
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PMID:Comparison of sucralfate and ranitidine in the treatment of chronic nonerosive gastritis. A randomized, multicenter trial. 266 May 57

Sucralfate was evaluated in several clinical studies on reflux esophagitis, a total of over 400 patients were studied worldwide. In this study 49 patients with reflux esophagitis of stage I-III acc. to Savary and Miller were included. The evaluation was based on 41 patients, 22 received sucralfate suspension 1 g in 5 ml qid, 19 ranitidine 150 mg bid. The patients were treated for 8 weeks, endoscopic controls were performed before treatment and after 8 weeks. The healing rates were 64% in the sucralfate group and 68% in the ranitidine group and exhibited no significant difference (p greater than 0.05). Antacid consumption and symptomatic improvement were comparable in both groups. Sucralfate seems to be a valid alternative to H2-blockers in the treatment of reflux esophagitis.
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PMID:Sucralfate in the treatment of reflux esophagitis in adults: an update. 266 89

Sucralfate is known for its gastroprotective properties in humans and rats, but the importance of intragastric pH in this protection is a subject of controversy. This study, performed on healthy young volunteers and rats, was designed to compare the gastroprotective effects of sucralfate with those of sucralfate combined with ranitidine or of sucralfate adjusted to pHs varying from 1 to 7. In humans the mucosal damage induced by 40% ethanol spray after 4 days of pretreatment with placebo, sucralfate (1 g four times daily), ranitidine (150 mg three times daily), or the combination of sucralfate plus ranitidine was evaluated by means of endoscopy with mucosal biopsy and histologic examination. Sucralfate alone reduced the endoscopic score significantly (compared with placebo) and prevented deep necrotic lesions. Neither ranitidine alone nor its combination with sucralfate prevented ethanol-induced endoscopic and histologic mucosal changes. In rats acute gastric lesions were induced by 100% ethanol. Sucralfate was relatively more effective in mucosal protection against ethanol when given at lower pH (1 or 2) than at original pH (4.5) and failed to protect at neutral pH (7.0). Pretreatment with ranitidine, which by itself did not change ethanol damage, greatly reduced the protection afforded by sucralfate. We conclude that sucralfate protects the gastric mucosa against ethanol damage both in humans and in rats and that this protection is dependent on the presence of an acidic intragastric pH.
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PMID:Importance of an acid milieu in the sucralfate-induced gastroprotection against ethanol damage. 267 24

Inhibition of gastric acid secretion is a major factor in protecting the gastric mucosa, although other mechanisms such as bile salt binding may contribute to the protective properties of individual agents. Sucralfate, antacid (Maalox), and Meciadanol, a new flavonoid, were compared with cholestyramine resin for binding bile salts. The free, glycine, and taurine conjugates of the human bile salts, cholate, chenodeoxycholate, and deoxycholate, were incubated with each of the above. Cholestyramine resin adsorbed 91-97% of all bile salts tested. Meciadanol adsorbed all of the bile salts fairly well except for the free forms of chenodeoxycholate and deoxycholate. Meciadanol (53 to 84%) adsorbed bile salts better than sucralfate (4.2 to 61%), and significantly (P less than 0.05) better than Maalox (10 to 47%). In our in vitro studies, sucralfate was not as effective in binding bile salts as previously reported. Patients in the surgical intensive care unit were randomized prospectively to receive nasogastric instillation of Maalox, sucralfate, or Meciadanol to prevent gastrointestinal bleeding. The gastric aspirates were analyzed for bile salt concentration. The mean bile salt concentration of those treated with Maalox (0.24 mM), Meciadanol (0.24 mM), or sucralfate (0.35 mM) was significantly lower than those treated with nasogastric aspiration (0.87 mM) alone (P less than 0.01). This suggests that these substances bind bile salts and may provide additional protection to the gastric mucosa along with their ability to neutralize gastric acid.
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PMID:Bile salt binding by maalox, sucralfate, and meciadanol: in vitro and clinical comparisons. 268 4

Sucralfate is well established in the treatment of upper gastrointestinal inflammation and ulceration, and preliminary evidence suggests it may be of benefit in active colitis. We have therefore undertaken a clinical trial to compare enemas of sucralfate (4 g) and prednisolone metasulphobenzoate (20 mg) in the treatment of active distal ulcerative colitis. Forty-four patients were entered into a 4-week study. Two patients were withdrawn because of non-compliance, and five were unable to complete the study: two developed constipation (both allocated to sucralfate) and three were unable to retain the enemas (two prednisolone and one sucralfate). Intention-to-treat analysis showed significant within-treatment improvement in rectal bleeding, sigmoidoscopic grade, and histologic grade in the prednisolone-treated group, and in stool frequency, rectal bleeding, and sigmoidoscopic grade in the sucralfate-treated group. Between-treatment comparisons, however, showed greater resolution of rectal bleeding and more marked improvements in histologic grade in patients treated with prednisolone metasulphobenzoate enemas. Further studies using higher doses of sucralfate would be useful.
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PMID:A comparison of sucralfate and prednisolone enemas in the treatment of active distal ulcerative colitis. 268 65

Aphthous ulcers are common, painful lesions that affect the oral mucosa and for which no successful treatment has been found. Sucralfate, which acts by locally binding with the proteins at the base of an ulcer to provide a protective covering, has been suggested as a treatment for aphthous ulcers. Forty-five subjects with active aphthous ulcers were recruited into this double-blind study designed to compare treatment of aphthous ulcers using sucralfate or placebo in a powdered spray. Measures of ulcer diameter and area were recorded before and after four days of treatment and the subjects completed a daily log measuring subjective response to the treatment. Sucralfate, as used in this study, was not found to be effective in the treatment of aphthous ulcers.
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PMID:Sucralfate vs. placebo for the treatment of aphthous ulcers: a double-blinded prospective clinical trial. 269 2

Ten cases of gastroduodenal inflammation were diagnosed by endoscopy among a series of 196 children with evidence of Crohn's disease involving other regions of the intestinal tract. Endoscopic and histologic confirmation of upper gastrointestinal tract involvement was performed only in those cases with suggestive symptoms. The mean age at presentation in the 10 cases with gastroduodenal inflammation was 14.6 +/- 1.9 (+/- SD) years, with involvement identified at the time of initial diagnosis of Crohn's disease in five of the 10. Eight of 10 cases occurred in boys. The major presenting symptoms were weight loss in five cases, epigastric pain in three, and recurrent vomiting in two. Hematemesis and melena occurred in only one of the 10 cases. Endoscopic and histological evidence of mucosal inflammation was seen in all 10 cases. Three of 10 cases had noncaseating granuloma present in biopsies of the stomach or duodenum. Two cases also had endoscopic and histological evidence of esophageal involvement. All cases were initially treated with oral corticosteroids, and in each instance a good clinical response was noted. Sucralfate (n = 1), 6-mercaptopurine (n = 1), and H2 receptor antagonists (n = 3) were used as adjunct therapy. After follow-up for 2.7 years (range, 0.5-5.5 years), none of the 10 cases required surgical intervention. Therefore, at least in the short-term, the outlook for adolescents with gastroduodenal Crohn's disease appears to be good and their medical management need not differ from those patients with Crohn's disease involving only more distal portions of the small intestine.
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PMID:Clinical features of gastroduodenal Crohn's disease in adolescents. 270 48

Studies using a gastric chamber model demonstrated that sucralfate protected the rat gastric mucosa against hemorrhagic erosions induced by 40 percent ethanol and by acidified 80 mM sodium taurocholate. Protection required continuous contact of sucralfate with the gastric mucosa but it occurred without the production, by sucralfate alone, of significant damage to the luminal epithelium. Ultrastructural examination indicated that sucralfate stimulated mucus secretion by surface epithelial cells. Furthermore, sucralfate was "cytoprotective" in that, in addition to its anti-ulcer effects, it significantly reduced the damaging effects of luminal ethanol on the surface epithelium. Luminal stasis also significantly reduced the extent of hemorrhagic erosions produced by both ethanol and sodium taurocholate, but the most effective reduction in erosions occurred when sucralfate and luminal stasis were combined. Pretreatment with indomethacin abolished the protection provided by luminal stasis, but this protection was restored by sucralfate. Thus, these studies suggest that protection of the gastric mucosa by sucralfate results in part from effects on the unstirred layer. Sucralfate or its products also interact with the epithelial cells and stimulate mucus release and synthesis or release of inflammatory mediators.
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PMID:Protection of rat gastric mucosa by sucralfate. Effects of luminal stasis and of inhibition of prostaglandins synthesis. 273 27

In a pilot study, 26 rheumatoid arthritic patients taking continuous, stable dosage regimens of nonsteroidal anti-inflammatory drugs and with developed gastric and duodenal lesions were administered sucralfate 1 g four times per day (14 patients) or cimetidine 400 mg twice daily (12 patients) in a single-blind regimen for six weeks. Eleven of the patients given sucralfate and eight of the patients taking cimetidine had improved lesion scores. The lesion score of 10 of the 14 patients taking sucralfate and four of the 12 patients taking cimetidine improved by 50 percent or better (not significant). The antrum and body of the gastric mucosa and the mucosa of the duodenum synthesized prostanoids and thromboxane A2, and there was no significant difference in the synthesis of individual prostanoids at entry to the trial in the groups assigned to sucralfate or cimetidine. After six weeks of administration of sucralfate, prostaglandin E2 (PGE2) synthesis by the antrum and body, but not the duodenum, was significantly greater than observed in the biopsy specimens at entry despite continuation of non-steroidal anti-inflammatory drug therapy. After six weeks of cimetidine treatment, no change in PGE2 synthesis was noted in any biopsy specimens when compared with the synthesis at entry. No change in the synthesis of PGF2 alpha, 6-oxo-PGF1 alpha, or thromboxane B2 was noted in gastric or duodenal biopsy specimens in any treatment group. Sucralfate and cimetidine administration resulted in improved gastroduodenal lesion scores in rheumatoid arthritic patients continuing with nonsteroidal anti-inflammatory drug therapy.
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PMID:Effect of sucralfate and cimetidine on rheumatoid patients with active gastroduodenal lesions who are taking nonsteroidal anti-inflammatory drugs. A pilot study. 273 35

Sucralfate protects the stomach against a number of experimental damaging agents and is efficacious in the treatment of peptic ulcer disease. It binds with acidity to the base of an ulcer to form a protective barrier. Sucralfate also enhances prostaglandin synthesis and release in the mucosa. In this study, the rat stomach was examined to determine sucralfate's interaction with gastric mucus. Mucus in the rat stomach forms a distinct and continuous blanket. In snap-frozen samples, pretreatment with phosphate-buffered saline as a control shows a layer of mucus of homogeneous structure thinner than the homogeneous layer after pretreatment with antibodies developed against rat gastric mucus. Pretreatment with the surface protective agent sucralfate shows some increase in the thickness of mucus with a thin dense sublayer adjacent to the epithelium and a less dense-appearing outer zone of variable thickness. Analysis of x-rays generated by the electron beam on windows of mucus and epithelium showed the expected gradients of sodium, potassium, chloride, and sulfur. The percentage of aluminum and sulfur in the mucus was higher in sucralfate-treated samples than in controls. Interaction between sucralfate and gastric mucus needs further investigation.
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PMID:Sucralfate interactions with gastric mucus. 273 36


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