Sucralfate Treatment Research Articles

Comparative study of sucralfate versus cimetidine in the treatment of acute gastroduodenal ulcer: Randomized trial with 667 patients

Six-hundred sixty-seven patients with endoscopically proven peptic ulcer were included in a randomized, multicenter trial to assess the comparative efficacy of sucralfate and cimetidine. One hundred eighty-seven patients with gastric ulcer and 480 patients with duodenal ulcer completed the study. Ulcer healing was evaluated endoscopically at six weeks for duodenal ulcer and at eight weeks for gastric ulcer. Patients with unhealed ulcer at this time were assigned to the other therapy for a second period of six or eight weeks of treatment (crossover). In patients with duodenal gastric ulcer, pain relief and healing were not significantly different in the two groups. Eighty-eight percent of duodenal ulcers and 73 percent of gastric ulcers healed with six weeks of sucralfate treatment. Reported side effects and symptoms, pooled together for duodenal and gastric ulcer, were more significant in the sucralfate group (7.5 percent) than in the cimetidine group (3.7 percent). Constipation was the most frequent symptom recorded. In conclusion, sucralfate and cimetidine are both excellent healing agents for short-term treatment of duodenal and gastric ulcer. Both give rapid relief of symptoms without severe side effects.

Effect of sucralfate on experimental colitis in the rat.

The therapeutic effect of sucralfate on ulcerated gastric and duodenal mucosa is well known. There is, however, almost no information about its activity in colitis. Experimental colitis was produced in rats by rectal instillation of 1 ml of 10 percent acetic acid, and 1.5 ml of a 20 percent suspension of sucralfate was then administered every 12 hours for various lengths of time. Study animals and appropriate controls were killed after 3, 7, 10, or 14 days. The distal colons were studied macroscopically and histologically. Colonic prostaglandin E2 levels were measured in animals killed after 3, 7, 10, or 14 days. The macroscopic score was significantly improved 10 and 14 days after induction of colitis, although the histologic appearance was unchanged. Acetic acid administration increased and sucralfate treatment reduced prostaglandin E2 levels in colitic animals on days 3 and 7, but not later. The present study supports a role for sucralfate in the treatment of colitis, but further studies on the mechanism of its effect and on its clinical activity are indicated.

Na+/H+Ion-Exchange Property of Postmortem Human Gastric Mucus

The effect of Campylobacter pylori infection and sucralfate treatment on the ion-exchange property of human gastric mucus from 17 human postmortem stomachs was investigated in an in vitro chamber. Of the 10 stomachs not infected with C. pylori mucus from 4 stomachs had a 'normal' Na+/H+ exchange capacity, whereas 6 were without a Na+/H+ exchange capacity. The Na+/H+ exchange capacity of the seven stomachs infected with C. pylori was half that of the four 'normal' uninfected stomachs. Sucralfate significantly improved the Na+/H+ exchange capacity of mucus from C. pylori-infected stomachs and from the uninfected stomachs without Na+/H+ exchange. This study shows that impairment of the Na+/H+ exchange capacity of gastric mucus is associated with C. pylori infection and that sucralfate improves the Na+/H+ exchange capacity of gastric mucus.

Circadian rhythms of food intake in gastroduodenally-ulcerated rats: effects of three anti-ulcer drugs.

The effects of three anti-ulcers drugs on the temporal distribution of food intake and of the two parameters, meal size and meal frequency, were studied in ulcerated and non-ulcerated rats exposed to light-dark (LD 12:12) cycles. Experimental ulceration with indomethacin reduces the amplitude of meal frequency and brings the acrophase forward, compared with non-ulcerated animals. These effects were reversed by the oral administration of either ranitidine, sucralfate or pirenzepine along with the food. However, the administration of either pirenzepine or sucralfate alone to non-ulcerated rats is accompanied by significant (P less than 0.05) changes in the circadian patterns of meal size and meal frequency without the total daily food intake being affected in any way (pirenzepine treatment caused large intake of food during the light period while sucralfate treatment resulted in marked food intake during the dark period). The results indicate that circadian modification of meal patterns in the ulcerated rats are attributable to indomethacin-induced gastrointestinal mucosal injury and anti-ulcer medications.

Sucralfate in Duodenal Ulcer Disease: A Double-Blind Trial

ABSTRACT Seventy-five patients with endoscopically confirmed duodenal ulcer disease received either sucralfate (34 patients) or placebo (41 patients) for 6 weeks in a double-blind clinical trial. N...

Clinical efficacy of sucralfate in reflux esophagitis: Comparison with cimetidine

Sucralfate has been evaluated in reflux esophagitis, based on its protective adherence to denuded surfaces, its bile salt-binding properties, and its cytoprotective properties. Histamine H 2-receptor blockers are currently considered the standard therapy. The goal of this study was to compare the potential efficacy of sucralfate with that of cimetidine. A single-blind, randomized, multicenter study was performed in 42 patients with endoscopically documented reflux esophagitis. Patients were randomly given 1 g of sucralfate suspension four times daily or 400 mg of cimetidine four times daily for eight weeks. Forty patients were evaluated after eight weeks. Symptomatic improvement was good and comparable in both groups. In two patients given sucralfate and one given cimetidine, side effects were noted but did not necessitate withdrawal from the study. Endoscopy showed improvement in 53 percent of patients and healing of esophagitis in 31 percent after sucralfate treatment. With cimetidine, improvement was seen in 67 percent and healing occurred in 14 percent. In one patient receiving cimetidine, distal esophageal stenosis developed, requiring dilatation therapy. It is concluded that treatment with sucralfate improves the symptomatology and severity of reflux esophagitis. The results obtained with sucralfate appear comparable to those with cimetidine. Sucralfate may therefore be considered as a valid alternative to H 2-receptor antagonist therapy in treating reflux esophagitis.

Effects of sucralfate or mild irritants on experimental gastritis and prostaglandin production

Rats pretreated with dilute ethanol, dilute hydrochloric acid, or dilute sodium hydroxide had significantly less gastric mucosal damage when they were exposed 15 or 30 minutes later to strong irritants. The dilute agents, known as mild irritants, also caused an increase in the production of gastric mucosal prostaglandin E 2 at the 15- and 30-minutes dosing intervals. This suggests that the mild irritants are only effective in providing gastric mucosal protection when they increase gastric production of prostaglandin E 2. Sucralfate treatment also caused an increase in gastric mucosal production of prostaglandin E 2 at only the 15- and 30-minute dosing intervals. In contrast, pretreatment with sucralfate protected against the damaging effects of the strong irritants for at least 480 minutes. Therefore, prostaglandin E 2 may play a role in sucralfate's protective effect at short dosing intervals, but at longer intervals, when prostaglandin E 2 changes were not observed, sucralfate was still found to be very effective in reducing the severity of gastritis. This suggests that sucralfate acts, at least in part, through some other mechanism(s) besides increasing gastric mucosal prostaglandin E 2 production.

Sucralfate versus placebo in treatment of non-ulcer dyspepsia

One hundred fifty-one patients with non-ulcer dyspepsia, defined as chronic epigastric pain without concomitant symptoms of the irritable bowel syndrome and with no evidence of any organic disease other than macroscopic or microscopic gastritis/duodenitis seen at endoscopy on entry into the trial, were randomly assigned to treatment for four weeks with sucralfate or a placebo, 1 g three times a day one-half hour before meals, according to a double-blind model. Seventy-nine patients received sucralfate and 72 patients received a placebo. According to patients' subjective assessment of their symptoms at four weeks, 61 patients (77 percent) in the sucralfate group and 40 patients (56 percent) in the placebo group had become symptom-free or showed improvement, whereas the condition of 18 (23 percent) in the former group compared with 32 (44 percent) in the latter group remained unchanged or deteriorated. The difference between the groups was significant (p <0.01). The best response to sucralfate treatment (84 percent or more symptom-free or improved) was achieved in patients with mild or moderate symptoms and without macroscopic or microscopic inflammation of their gastric mucosa—a typical patient with non-ulcer dyspepsia. Our results indicate that sucralfate is significantly more effective than placebo in the treatment of non-ulcer dyspepsia.

Multicenter trial of sucralfate suspension for the treatment of reflux esophagitis

The efficacy of sucralfate suspension in the treatment of reflux esophagitis was assessed in a multicenter, randomized, double-blind, placebo-controlled trial. Sixty-eight patients with symptomatic and endoscopic esophagitis received either sucralfate suspension (n= 31) or liquid placebo (n= 37) for eight weeks. The two groups were comparable at entry with the exception that despite randomization, a disproportionately high number of patients with esophageal ulcers were assigned to receive sucralfate. After four and eight weeks of treatment, both groups had reduced heartburn frequency and severity, but there was no difference in improvement between sucralfate and placebo (p >0.05). Endoscopic results after eight weeks of sucralfate treatment revealed complete healing in 36 percent (placebo, 35 percent) and improvement in an additional 45 percent (placebo, 24 percent). Although neither of these differences was significant, the percent of patients in whom healing or improvement occurred with sucralfate (81 percent) was greater than with placebo (59 percent) (p = 0.07). These data fail to establish that eight weeks of treatment with sucralfate suspension improves symptoms or heals lesions in reflux esophagitis at a rate significantly greater than placebo. However, the unequal distribution of patients with ulcers and the trend toward endoscopic improvement indicate that a potential beneficial effect of sucralfate suspension for the treatment of reflux esophagitis cannot be excluded.

Sucralfate treatment of nonsteroidal anti-inflammatory drug-induced gastrointestinal symptoms and mucosal damage

In a randomized, double-blind trial, sucralfate therapy, 1 g four times daily, was compared with placebo in 143 symptomatic patients to assess the treatment of gastrointestinal symptoms and gastric mucosal damage associated with nonsteroidal anti-inflammatory drugs (NSAIDs). All patients followed a fixed regimen of NSAIDs, were assigned to one of two groups based on the presence or absence of gastric erosions at baseline endoscopy, and were then assigned randomly to receive sucralfate or placebo for four weeks. Patients were then followed for up to six months while receiving open-label sucralfate 1 g twice daily to up to 1 g four times daily. After four weeks of double-blind therapy, patients taking either nonsalicylate NSAIDs or long half-life NSAIDs and who were treated with sucralfate experienced a significant reduction in both peptic symptom frequency and intensity (p <0.03) as compared with patients receiving placebo. Sucralfate-treated patients with baseline endoscopic lesions showed a significant reduction in lesion scores (p <0.005) at four weeks as compared with baseline, whereas no improvement was observed in gastric mucosal lesions of patients given placebo. Long-term sucralfate therapy resulted in continued improvement in gastrointestinal symptoms and gastric lesion scores in patients receiving all types of NSAIDs. The results indicate that sucralfate used in conjunction with NSAIDs may allow patients to continue therapy by relieving gastrointestinal symptoms and mucosal damage associated with NSAID therapy.

Medical and Surgical Prophylaxis for Duodenal Ulcer, the Role of Sucralfate

The risk of recurrent duodenal ulcer is high, 70-80% of duodenal ulcer patients having a recurrence during the first year after initial healing. Surgery has so far been the main method for preventing a relapse, but recent studies have shown that it is possible to reduce the risk and the need for surgery with medical maintenance therapy. Five controlled studies are available on the efficacy of sucralfate in prophylaxis for duodenal ulcer. 294 patients participated, 154 having received sucralfate treatment, usually 1 g twice daily. The summarized results indicate that initially healed duodenal ulcers recurred in six months in 60% of cases and in 12 months in 79% of cases in groups receiving placebo therapy or no treatment, the corresponding figures in the groups treated with sucralfate being 21% and 31%. The choice between surgical and medical prophylaxis is discussed, and more liberal use of medical prophylaxis is advocated.

Sucralfate therapy in patients with symptoms of alkaline reflux gastritis: A randomized, double-blind study

The effects of sucralfate (6 g per day) and placebo on symptoms, endoscopic findings, and gastric mucosal histology were compared in 23 patients with symptoms of alkaline reflux gastritis who had undergone Billroth I, Billroth II, or vagotomy and pyloroplasty. Patients were randomly assigned to receive sucralfate (n = 11) or placebo (n = 12) for six weeks. Then all received six weeks of open sucralfate therapy before treatment codes were revealed. Twelve gastric biopsy specimens were obtained before patients began treatment and at six and 12 weeks. The two groups did not differ significantly with respect to symptom scores or endoscopic findings at baseline, after the double-blind phase, or after open sucralfate treatment. There were also no significant differences between the treatment groups with respect to epithelial cell scores and conventional gastritis scores. However, after the six-week, double-blind phase, the inflammatory cell score of the sucralfate-treated group was significantly lower (p < 0.05) than that of the placebo-treated group (1.3 ± 0.3 versus 1.9 ± 0.4). After six weeks of open sucralfate treatment, patients who had initially received placebo had a significant reduction (1.4 ± 0.3 versus 1.9 ± 0.4) in their inflammatory cell score. Sucralfate lowered the inflammatory cell scores of patients with symptoms of alkaline reflux gastritis. This reduction, however, was not associated with an Improvement in symptoms.

Sucralfate and gastric bicarbonate.

The effect of sucralfate treatment (3 g daily for 6 weeks) on gastric HCO3- secretion was investigated in 15 duodenal ulcer patients. After treatment a highly significant (p less than 0.01) increase in gastric bicarbonate output was found. It is suggested that the mode of action of sucralfate includes stimulation of gastric alkaline secretion.