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ACTAVIS/GREENST
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00591389201

sucralfate 1 gm tablet

Generic
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Uses

Duodenal Ulcer

Acute Therapy

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, .

Maintenance Therapy

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).

Gastric Ulcer

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.

Other Uses

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.

Dosage and Administration

Administration

Sucralfate is administered orally. The drug should be taken on an empty stomach, 1 hour before each meal and at bedtime. Antacids may be used as needed for relief of pain but should not be taken within 30 minutes before or after sucralfate.

Dosage

Duodenal Ulcer

For the treatment of active duodenal ulcer, the usual adult dosage of sucralfate is 1 g 4 times daily. Although healing of the ulcer may occur during the first or second week of therapy, treatment should be continued for 4-8 weeks unless healing has been shown by radiographic or endoscopic examination.

For maintenance therapy following healing of acute duodenal ulcer to reduce ulcer recurrence, the usual adult dosage of sucralfate is 1 g twice daily.

Gastric Ulcer

For the treatment of gastric ulcer, a sucralfate dosage of 1 g 4 times daily has been used in adults.

Cautions

Adverse Effects

Sucralfate is generally well tolerated. The most frequent adverse effect of sucralfate is constipation, which reportedly occurs in about 2% of patients receiving the drug. Other adverse effects of sucralfate reportedly occur in less than 1% of patients and include diarrhea, nausea, vomiting, gastric discomfort, flatulence, indigestion, dry mouth, rash, pruritus, back pain, headache, dizziness, insomnia, sleepiness, and vertigo. Adverse reactions requiring discontinuance of the drug occur rarely. In postmarketing experience, hypersensitivity reactions such as urticaria (hives), angioedema, respiratory difficulty, and rhinitis have been reported with sucralfate tablets. Similar reactions have been reported with sucralfate suspension. In addition, laryngospasm and facial swelling have been reported with sucralfate suspension, but a causal relationship has not been established.

Bezoars have been reported with sucralfate therapy. Most patients who developed bezoars had underlying medical conditions that may have predisposed to bezoar formation (e.g., delayed gastric emplying) or were receiving concomitant enteral tube feedings.

Precautions and Contraindications

Since duodenal ulcer is a chronic recurrent disease, successful therapy with sucralfate should not be expected to alter the post-healing frequency of recurrence or the severity of duodenal ulceration.

Small amounts of aluminum are absorbed from the GI tract when sucralfate is administered orally. Concomitant use of sucralfate with other products that contain aluminum (e.g., aluminum-containing antacids) also can increase the total body burden of aluminum. In patients with normal renal function, this increased body burden of aluminum is excreted in the urine; however, patients with chronic renal failure or those receiving dialysis treatment may not adequately excrete the absorbed aluminum. In addition, because the absorbed aluminum is bound to plasma proteins (e.g., albumin, transferrin) and is not dialyzable, accumulation and intoxication (e.g., aluminum osteodystrophy, osteomalacia, encephalopathy) can occur in patients with impaired renal function. Therefore, sucralfate should be used with caution in patients with chronic renal failure.

Inadvertent injection of sucralfate suspension, which is insoluble and has insoluble excipients, has led to fatal complications, including pulmonary and cerebral emboli. Sucralfate suspension is not intended for IV administration.

Pediatric Precautions

Safety and efficacy of sucralfate in children have not been established.

Mutagenicity and Carcinogenicity

Mutagenicity studies have not been conducted with sucralfate to date. No evidence of carcinogenesis was seen in animals receiving oral sucralfate dosages up to 1 g/kg daily (12 times the usual human dosage) for 24 months.

Pregnancy, Fertility, and Lactation

Pregnancy

Reproduction studies in mice, rats, and rabbits using sucralfate dosages up to 50 times the usual human dosage have not revealed evidence of harm to the fetus. There are no adequate and controlled studies to date using sucralfate in pregnant women, and the drug should be used during pregnancy only when clearly needed.

Fertility

The effect of sucralfate on fertility in humans is not known. A reproduction study in rats using sucralfate dosages up to 38 times the usual human dosage did not reveal evidence of impaired fertility.

Lactation

Since it is not known if sucralfate is distributed into milk, the drug should be used with caution in nursing women.

Drug Interactions

Studies in animals and healthy individuals have shown that concomitant administration of sucralfate with cimetidine, digoxin, ketoconazole, phenytoin, ranitidine, tetracycline, or theophylline results in a reduction in bioavailability of these drugs. These interactions appear to be nonsystemic in origin, apparently resulting from binding of these agents to sucralfate in the GI tract. Although subtherapeutic prothrombin times with concomitant sucralfate and warfarin administration also have been reported, initiation of sucralfate in patients maintained on warfarin therapy reportedly did not alter serum warfarin concentrations or prothrombin times in at least 2 clinical studies. Although the clinical importance of these findings has not been determined in humans, it has been suggested that sucralfate be given 2 hours before or after any of these drugs. Because of the potential of sucralfate to alter the absorption of some drugs from the GI tract, separate administration of sucralfate and other drugs should be considered during concomitant therapy when alterations in bioavailability of the other drug(s) are believed to be critical.

Concomitant sucralfate, presumably because of its aluminum content, decreases GI absorption of ciprofloxacin and norfloxacin and may result in substantial (e.g., 50% or greater) decreases in serum concentrations of the anti-infectives. Patients should be instructed not to ingest sucralfate concomitantly with, or within 2 hours of, a ciprofloxacin or norfloxacin dose.

Pharmacokinetics

Preliminary studies in animals showed sucralfate to be only minimally absorbed following oral administration; thus, extensive pharmacokinetic evaluation of the drug in humans has not been conducted.

Absorption

Sucralfate is only minimally absorbed from the GI tract following oral administration; the drug is absorbed as sucrose sulfate. (See Pharmacokinetics: Elimination.) Poor absorption may result from the high polarity and low solubility of the drug in the GI tract. Studies in animals indicate that only 3-5% of an oral dose of sucralfate reaches systemic circulation as sucrose sulfate. Following oral administration of multiple doses of the drug (200 mg/kg daily) in animals, sucrose sulfate did not accumulate in plasma.

Since sucralfate exerts its therapeutic effects directly at the site of the ulcer, the duration of action depends on the time that the drug is in contact with this site. The drug's viscous adhesiveness, slow reaction with acid, and high affinity for damaged mucosa contribute to its prolonged action. Binding to the ulcer site has been shown for up to 6 hours following oral administration, and 30% of the dose is retained within the GI tract for at least 3 hours.

Distribution

Distribution of sucralfate into human body tissues and fluids following systemic absorption has not been determined. The apparent volume of distribution of sucrose sulfate has been determined in animals and is reported to be approximately 20% of body weight. Following oral administration of sucralfate in animals, the drug is only minimally distributed into tissues. Approximately 95% of the dose remains in the GI tract, with only small amounts being distributed into liver, kidneys, skeletal muscle, adipose tissue, and skin.

It is not known if sucralfate crosses the placenta or is distributed into milk.

Elimination

Following IV administration of sucrose sulfate, plasma concentrations decline rapidly and show first-order elimination. In animals, the elimination half-life of sucrose sulfate ranges from 6-20 hours.

Sucrose sulfate is formed in the GI tract following reaction of sucralfate with hydrochloric acid. (See Pharmacology: Binding to the Ulcer Site.) Sucrose sulfate is not metabolized. In animals, more than 90% of an orally administered dose of sucrose sulfate is excreted unchanged in feces within 48 hours. The small amount (3-5%) of sucralfate that is absorbed as sucrose sulfate is excreted unchanged in urine within 48 hours.

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