Sucralfate is used in the short-term (up to 8 weeks) treatment of duodenal ulcer. Antacids may be used as adjuncts to sucralfate therapy to relieve pain, but should not be taken within 30 minutes before or after administration of sucralfate.
In controlled studies in patients with duodenal ulcer who were receiving supplemental antacids, reported rates of ulcer healing for sucralfate (3 or 4 g daily as tablets) vs placebo were: 33-39% vs 13-25% at 2 weeks, 69-92% vs 41-64% at 4 weeks, 60% vs 24% at 6 weeks, and 77-86% vs 41% at 12 weeks. Sucralfate also produced greater reductions in severity and occurrence of daytime and nocturnal pain and in antacid consumption than did placebo. In a multicenter, double-blind, controlled study in patients with duodenal ulcer, ulcer healing rates with sucralfate 1 g 4 times daily (as the suspension) versus placebo were: 16 vs 7% at 2 weeks, 46 vs 27% at 4 weeks, and 66 vs 39% at 8 weeks, respectively. The manufactuer states that equivalence of sucralfate suspension and tablets has not been demonstrated.
In a limited number of well-controlled studies comparing 4-12 weeks of oral therapy with 4 g of sucralfate daily to that with 1-1.2 g of cimetidine daily, 87-100% of sucralfate-treated and 83-86% of cimetidine-treated duodenal ulcers were healed as evidenced by endoscopic examination. Based on these limited studies, it appears that the short-term effect of sucralfate on duodenal ulcer healing is comparable to that of cimetidine. In one study, follow-up of sucralfate- and cimetidine-treated patients revealed that the cumulative relapse rate after 1 year was similar in both treatment groups; however, the average duration of remission in patients who developed a recurrence was longer in patients initially treated with sucralfate (7.3 months) than in those initially treated with cimetidine (4.6 months).
In one controlled study comparing 8 weeks of oral therapy with 4 g of sucralfate daily to that with 8 aluminum hydroxide and magnesium trisilicate antacid tablets daily (strength unknown), 93% of sucralfate-treated and 31% of antacid-treated duodenal ulcers were healed. Current epidemiologic and clinical evidence supports a strong association between gastric infection with Helicobacter pylori and the pathogenesis of duodenal and gastric ulcers; long-term H. pylori infection also has been implicated as a risk factor for gastric cancer. For additional information on the association of this infection with these and other GI conditions, .
Conventional antiulcer therapy with H2-receptor antagonists, proton-pump inhibitors, sucralfate, and/or antacids heals ulcers but generally is ineffective in eradicating H. pylori, and such therapy is associated with a high rate of ulcer recurrence (e.g., 60-100% per year). The American College of Gastroenterology (ACG), the National Institutes of Health (NIH), and most clinicians currently recommend that all patients with initial or recurrent duodenal or gastric ulcer and documented H. pylori infection receive anti-infective therapy for treatment of the infection. Although 3-drug regimens consisting of a bismuth salt (e.g., bismuth subsalicylate) and 2 anti-infective agents (e.g., tetracycline or amoxicillin plus metronidazole) administered for 10-14 days have been effective in eradicating the infection, resolving associated gastritis, healing peptic ulcer, and preventing ulcer recurrence in many patients with H. pylori-associated peptic ulcer disease, current evidence principally from studies in Europe suggests that 1 week of such therapy provides comparable H. pylori eradication rates. Other regimens that combine one or more anti-infective agents (e.g., clarithromycin, amoxicillin) with a bismuth salt and/or an antisecretory agent (e.g., omeprazole, lansoprazole, H2-receptor antagonist) also have been used successfully for H. pylori eradication, and the choice of a particular regimen should be based on the rapidly evolving data on optimal therapy, including consideration of the patient's prior exposure to anti-infective agents, the local prevalence of resistance, patient compliance, and costs of therapy.
Current evidence suggests that inclusion of a proton-pump inhibitor (e.g., omeprazole, lansoprazole) in anti-H. pylori regimens containing 2 anti-infectives enhances effectiveness, and limited data suggest that such regimens retain good efficacy despite imidazole (e.g., metronidazole) resistance. Therefore, the ACG and many clinicians currently recommend 1 week of therapy with a proton-pump inhibitor and 2 anti-infective agents (usually clarithromycin and amoxicillin or metronidazole), or a 3-drug, bismuth-based regimen (e.g., bismuth-metronidazole-tetracycline) concomitantly with a proton-pump inhibitor, for treatment of H. pylori infection. For a more complete discussion of H. pylori infection, including details about the efficacy of various regimens and rationale for drug selection, .
Sucralfate is used in reduced dosage as maintenance therapy following healing of active duodenal ulcer to reduce ulcer recurrence. In placebo-controlled studies, duodenal ulcer recurrence (as evidenced by endoscopic examination) rates at 4 months, 6 months, 8 months, and 1 year were 8-42, 19-33, and 27-42%, respectively, for 1 g of sucralfate twice daily versus 38-63, 50-69, and 65-81%, respectively, for placebo. In other studies, recurrence rates for up to 1 year of sucralfate maintenance therapy (2 g daily) were similar to those observed after up to 1 year of cimetidine maintenance therapy (400 mg at bedtime daily).
Sucralfate has been used in the treatment of patients with gastric ulcer, but its efficacy in this condition has not been established. In a limited number of patients in controlled studies, sucralfate was more effective than placebo in healing gastric ulcer. Sucralfate also relieved ulcer-related pain more rapidly than did placebo in patients with gastric ulcer. Based on preliminary data, it had appeared that maintenance administration of sucralfate did not affect the rate of recurrence of gastric ulcer; however, in a limited number of placebo-controlled studies of up to 1 year's duration in patients with healed gastric ulcer, daily maintenance administration of 2-3 of sucralfate reduced the rate of gastric ulcer recurrence.
Sucralfate appears to be as effective as cimetidine in the short-term treatment of gastric ulcer. In a limited number of controlled studies, there was no difference in ulcer healing, symptomatic relief, or antacid consumption between sucralfate- and cimetidine-treated patients.
In one poorly designed study comparing sucralfate and an aluminum hydroxide liquid antacid in patients with gastric ulcer, healing in patients treated with sucralfate was reported to be faster than that in patients treated with aluminum hydroxide; however, patients in this study used only 20 mL of an aluminum hydroxide antacid (concentration unknown) 3 times daily.
Current epidemiologic and clinical evidence supports a strong association between gastric infection with H. pylori and the pathogenesis of duodenal and gastric ulcers, and the ACG, NIH, and most clinicians currently recommend that allpatients with initial or recurrent duodenal or gastric ulcer and documented H. pylori infection receive anti-infective therapy for treatment of the infection. The choice of a particular regimen should be based on the rapidly evolving data on optimal therapy, including consideration of the patient's prior exposure to anti-infective agents, the local prevalence of resistance, patient compliance, and costs of therapy.
(See Duodenal Ulcer: Acute Therapy, in Uses.)For a more complete discussion of H. pylori infection, including details about the efficacy of various regimens and rationale for drug selection, see Helicobacter pylori Infection, under Uses, in Clarithromycin 8:12.12.92.
Sucralfate has been shown to protect the gastric mucosa from aspirin-induced erosions. In one study in healthy adults receiving 3.6 g of aspirin daily, sucralfate (4 g daily) provided complete protection against aspirin-induced mucosal injury (as evidenced by endoscopic examination) in approximately 70% of individuals. Further study is needed to confirm these preliminary findings and to determine the safety and efficacy of sucralfate in the prevention of aspirin-induced gastric erosions.
Sucralfate has been used as an oral suspension for the prevention and treatment of chemotherapy-induced mucositis, but results have been conflicting and additional study is necessary. Although it has been suggested that sucralfate oral suspensions may have a potential beneficial effect in reducing pathogenic gastric microbial colonization in these and other (e.g., intubated) patients, some clinicians have questioned current findings supporting this suggestion.