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)

Reflux esophagitis is encountered quite frequently in clinical practice. Symptoms can be mild, moderate, or severe and complications can occur, particularly if the disorder is untreated or undertreated. Treatment is aimed at relieving symptoms, healing lesions, and preventing complications. Various pharmacologic options are available for treatment, including antacids, alginate/antacid compounds, acid-reducing agents, prokinetic drugs, and agents that protect the mucosa. This article reviews a number of clinical studies evaluating sucralfate in the treatment of reflux esophagitis. Almost all of the investigations were conducted in Europe and encompassed open-label studies, placebo-controlled trials, and comparative studies. From the studies discussed, it can be concluded that sucralfate not only has a place in the treatment of peptic ulcer disease, but is also effective in treating reflux esophagitis. Sucralfate is comparable to H2-receptor antagonists in symptom improvement and healing rates. In addition, the studies reviewed have shown sucralfate to be safe and well tolerated.
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PMID:Clinical studies of sucralfate in reflux esophagitis. The European experience. 188 99

Dyspepsia can be defined as the presence of upper abdominal pain or discomfort; other symptoms referable to the proximal gastrointestinal tract, such as nausea, early satiety, and bloating, may also be present. Symptoms may or may not be meal related. To be termed chronic, dyspepsia should have been present for three months or longer. Over half the patients who present with chronic dyspepsia have no evidence of peptic ulceration, other focal lesions, or systemic disease and are diagnosed as having non-ulcer (or functional) dyspepsia. Non-ulcer dyspepsia is a heterogeneous syndrome. It has been proposed that this entity can be subdivided into a number of symptomatic clusters or groupings that suggest possible underlying pathogenetic mechanisms. These groupings include ulcer-like dyspepsia (typical symptoms of peptic ulcer are present), dysmotility (stasis)-like dyspepsia (symptoms include nausea, early satiety, bloating, and belching that suggest gastric stasis or small intestinal dysmotility), and reflux-like dyspepsia (heartburn or acid regurgitation accompanies upper abdominal pain or discomfort). The aetiology of non-ulcer dyspepsia is not established, although it is likely a multifactorial disorder. Motility abnormalities may be important in a subset of dyspepsia patients but probably do not explain the symptoms in the majority. Epidemiological studies have not convincingly demonstrated an association between Helicobacter pylori and non-ulcer dyspepsia. Other potential aetiological mechanisms, such as increased gastric acid secretion, psychological factors, life-event stress, and dietary factors, have not been established as causes of non-ulcer dyspepsia. Management of non-ulcer dyspepsia is difficult because its pathogenesis is poorly understood and is confounded because of a high placebo response rate. Until more data are available, it seems reasonable that treatment regimens target the clinical groupings described above. Antacids are no more effective than placebo in non-ulcer dyspepsia, although a subgroup of non-ulcer dyspepsia patients with reflux-like or ulcer-like symptoms may respond to H2-receptor antagonists. However, there is no significant benefit of these agents over placebo in many cases. Bismuth has been shown to be superior to placebo in patients with H. pylori in a number of studies, but these trials had several shortcomings and others have reported conflicting findings. Sucralfate was demonstrated in one study to be superior to placebo, but this finding was not confirmed by another group of investigators. Prokinetic drugs appear to be efficacious, and may be most useful in patients with dysmotility-like and reflux-like dyspepsia.
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PMID:Non-ulcer dyspepsia: myths and realities. 188 33

Sucralfate was labelled with 99mTc by the stannous reduction method. Tablets were compressed using 1 g of radioactive sucralfate and suitable additives. On the first test day, five fully informed healthy volunteers were given one radioactive tablet of sucralfate each, following 10 h fasting. On the second test day, the sucralfate tablet was given after a standard meal. The gastrointestinal transit of the 99mTc-labelled sucralfate was evaluated using gamma camera technique. The labelling of sucralfate with 99mTc by the stannous reduction method enables the deposition and the transition of sucralfate in the gastrointestinal tract to be monitored. The tablets disintegrated almost immediately after administration and the released sucralfate distributed homogenously over the entire stomach area, in both fasted and fed subjects. Transit from the stomach into the intestine was noted already 10 min after administration in fasted subjects, whereas the gastric emptying of sucralfate was markedly delayed in fed subjects. To achieve a wider and more homogenous distribution in the GI-tract, sucralfate tablets should be taken before eating.
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PMID:Deposition and gastrointestinal transit of conventional sucralfate tablets. 191 May 51

Sucralfate and ranitidine were compared in the treatment of duodenal ulcer in this multicenter, randomized, double-blind study. A total of 165 patients with endoscopically proven duodenal ulceration were included in the trial and randomized to treatment with sucralfate, 2 g b.i.d. (morning and evening with an empty stomach), or ranitidine, 150 mg twice daily. All patients were endoscopically examined after 4 and, if unhealed, 8 weeks. Of the patients considered suitable for analysis at 4 weeks, 73.5% (61 of 83) of the sucralfate group demonstrated healing of the ulcer in comparison with 63.3% (50 of 79) of the ranitidine group. At 8 weeks cumulative healing rates were 89% (74 of 83) and 84.8% (67 of 79), respectively. When smokers were considered separately, healing rates at 4 weeks were 69.2% (36 of 52) for sucralfate and 53.3% (24 of 45) for ranitidine. At 8 weeks cumulative healing rates were 92.3% (48 of 52) and 77.7% (35 of 45), respectively (p less than 0.05). Overall, there was no difference in the two groups regarding symptom relief and side effects. These results suggest that these drugs are equally effective in the short-term treatment of duodenal ulcer, although in smokers sucralfate appears to be more effective than ranitidine.
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PMID:Comparison of sucralfate and ranitidine twice daily in duodenal ulcer treatment: a multicenter randomized double-blind study. 191 42

In previous studies it has been reported that, after being labeled with technetium, sucralfate, an useful drug in peptic diseases, can be used to detect peptic lesions of the digestive tract. In this work we report our experience with this technique in the diagnosis of esophagitis. 25 studies (11 controls and 14 patients) were undertaken. Sucralfate scintigraphy was normal in the 11 control studies, and abnormal in 10 out of 14 patients. Scintigraphy was abnormal in peptic as well as caustic lesions.
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PMID:[Gammagraphy with sucralfate labelled with technetium in esophagitis]. 193 Dec 38

Sixty patients with endoscopically verified oesophagitis entered a double-blind clinical study comparing 1 g sucralfate granulate given four times daily and 400 mg cimetidine twice daily. The efficacy, as judged by endoscopy and the symptomatic response, were studied after 4, 8, and 12 weeks of treatment. Macroscopic healing of oesophagitis was defined as complete epithelialization of all oesophageal erosive lesions classified in accordance with Savary-Miller. Groups were comparable with regard to demographic data. The healing rate at 12 weeks' end point was 62% in the sucralfate group and 59% in the cimetidine group (NS). Half of the patients in both groups (NS) were relieved of symptoms. No adverse effects were recorded. Sucralfate and cimetidine appear to be equally efficient in the treatment of reflux oesophagitis.
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PMID:Sucralfate versus cimetidine in reflux oesophagitis. A double-blind clinical study. 201 1

The present study was carried out to examine the comparative efficacy of sucralfate and ranitidine in the treatment of duodenal ulcer. Sixty-six patients with endoscopically diagnosed duodenal ulcer were studied in a 4-6 weeks randomised, single blind trial comparing sucralfate 1 gm T.D.S. one hour before meal and 1 gm nocte (34 pts) with ranitidine 300 mg nocte (32 pts). Six patients (four on sucralfate and 2 on ranitidine) failed to complete the study. Endoscopy after four weeks of treatment showed an ulcer healing rate of 57% in the sucralfate group compared with 73% in ranitidine group (p greater than 0.1). At six weeks these figures had risen to 87% and 90% respectively (p less than 0.5). After one year followup study 69% of sucralfate treated ulcers relapsed whereas the relapse rate was 82% in ranitidine treated ulcer group (p less than 0.1). It was observed that the relapse was earlier in the ranitidine group as compared to sucralfate group (p less than 0.01 at 3 months and p less than 0.05 at 6 months). Asymptomatic recurrence was seen in 15% (6/40) patients. Sucralfate was not only as effective as ranitidine in short term healing of duod. ulcer but also delayed the relapse of ulcer in long term followup after initial healing with the drug.
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PMID:A comparative therapeutic trial of sucralfate and ranitidine in initial healing and relapse rate of duodenal ulcer. 209 28

The mucosal protective effect of sucralfate (Ulcogant) was evaluated in a prospective randomised clinical study during radiation therapy. Twenty-four patients received 1 g of a sucralfate suspension 4 times a day orally for 5 min each. This group was compared with a control group of 21 patients receiving standard oral hygiene consisting of frequent tooth cleaning and disinfection of the oral and pharyngeal mucosa. The radiation technique was telecobalt therapy in two opposing fields using the shrinking field technique, with an electron boost to the posterior lymph nodes; the dosage was 60-70 Gy in daily fractions of 2 Gy. Mucosal reactions, pain and difficulty in swallowing were recorded twice a week. We also checked the patient's weight during treatment. The patients showed significant differences in all parameters, and lower weight loss compared with the control group. Minimal or absent mucosal inflammation pain or dysphagia were found in 88%, 79% and 83% respectively, while 43% and 29% and 52% of the controls had such mild radiation side-effects. Local effectivity appeared to be less in the hypopharynx due to shorter time of application compared with mouth and oropharynx. There were no side-effects from the sucralfate. Sucralfate prophylaxis is effective and easy to apply in the protection of mucosa during irradiation therapy.
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PMID:[Radiotherapy of head-neck neoplasms: prevention of inflammation of the mucosa by sucralfate treatment]. 217 76

Sucralfate is a nonsystemic agent that is effective in protecting the gastroduodenal mucosa against injury. In addition, sucralfate is effective in the healing of acute duodenal and gastric ulceration, the therapy of esophagitis, and the prevention of ulcer recurrence. The mechanisms responsible for sucralfate's successful protective and therapeutic actions include the adsorption of pepsin and bile acids, the stimulation of bicarbonate and mucus secretion, and stimulation of endogenous synthesis of prostaglandins. When sucralfate is given to experimental animals or humans, it stimulates endogenous synthesis and release of prostaglandin E2 and inhibits thromboxane release. Pretreatment of animals with the cyclooxygenase inhibitor indomethacin results in a marked decrease in the protective effect of sucralfate against alcohol injury. Sucralfate also increases epidermal growth factor binding to ulcerated areas and stimulates macrophage activity. In addition, sucralfate stimulates endogenous sulfhydryl compounds. At the microscopic level sucralfate protects the vascular integrity of the mucosa and the mucosal proliferative zone. It also stimulates epithelial cell restitution and stimulates cell proliferation. The administration of sucralfate before acute injury results in decreased depth and extent of injury and in acceleration of healing. Because of sucralfate's ability to stimulate the protective and reparative mechanisms of the gastric and duodenal mucosa, it is an important nonsystemic agent for the therapy and prevention of peptic ulceration.
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PMID:The protective and therapeutic mechanisms of sucralfate. 219 Mar 4

Sucralfate plays an important role in peptic ulcer disease, reflux esophagitis, stress erosions and bleeding, and as adjunctive therapy in variceal sclerosis. In accordance with its pharmacologic characteristics, however, one may readily envisage disease states worth investigating, such as irradiation-induced mucosal damage of the esophagus. Especially the combination of external and intraluminal radiotherapy via the after-load technique may cause substantial and occasionally long-standing ulceration of the esophageal lining and discomfort. Several conditions of the stomach deserve further study. Increasingly common is gastric mucosal damage induced by aspirin or non-steroidal anti-inflammatory drugs. On the basis of its various pharmacologic principles sucralfate should theoretically offer protection against such lesions, and, in fact, there are human pharmacologic and clinical studies available supporting this idea. Another disease entity in which sucralfate should be studied in more depth is that of biliary alkaline reflux gastropathy as often seen after gastric surgery. Sucralfate should also be evaluated in those difficult clinical conditions known to be resistant to any therapeutic attempt with currently available drugs, such as erosive varioliform gastritis and hypertrophic gastropathy with heavy inflammation of the mucosa and giant coarsening of the gastric rugae. The results obtained with sucralfate in variceal sclerosis are indeed intriguing, even though the mechanism is not understood. It has been shown that sucralfate has some efficacy in patients with hemorrhagic gastritis. In many patients receiving chemotherapy, mucosal damage may occur both in the mouth and throughout the gastrointestinal tract, including the small bowel.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Future potential applicability of sucralfate in gastroenterology. 219 Mar 5


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