Sulcrate

The action of sucralfate is nonsystemic as the drug is only minimally absorbed from the gastrointestinal tract. The minute amounts of the sulfated disaccharide which are absorbed are primarily excreted in the urine.

Each g of sucralfate contains approximately 200 mg of aluminum. The aluminum moiety can dissociate at low pH and aluminum release in the stomach can be expected; however, aluminum is poorly absorbed from the intact gastrointestinal tract. Following administration of 1 g of sucralfate (tablets or suspension) 4 times a day to individuals with normal renal function, approximately 0.001% to 0.017% of sucralfate's aluminum content is absorbed and excreted in the urine. This results in an aluminum load of between 0.008 mg and 0.136 mg following a 4 g daily dose. Individuals with normal renal function excrete absorbed aluminum and can respond to an increased aluminum load by increasing urinary excretion.

These values were determined in individuals with intact gastrointestinal mucosa. Available evidence does not indicate that absorption of aluminum would be different in individuals with ulcerated gastrointestinal mucosa.

Experiments have shown that sucralfate is not an antacid.

Antacids should not be taken within half an hour before or after sucralfate intake because of the possibility of decreased binding of sucralfate with the gastroduodenal mucosa as a consequence of a change of intragastric pH.

Animal studies have shown that simultaneous administration of sucralfate with tetracycline, phenytoin or cimetidine results in a statistically significant reduction in the bioavailability of these agents. Cimetidine absorption was not reduced in humans.

In clinical trials, the concomitant administration of sucralfate reduced the bioavailability of digoxin. In case of simultaneous administration, the extent of absorption of phenytoin, warfarin and fluoroquinolone antibiotics (e.g. ciprofloxacin and norfloxacin) is also reduced. These interactions appear to be nonsystemic and to result from the binding of sucralfate to the concomitantly administered drug in the gastrointestinal tract. In all cases, complete bioavailability was restored by separating the administration of sucralfate from that of the other agent by 2 hours.

Sucralfate, administered respectively 30 and 60 minutes before ASA or ibuprofen did not alter the bioavailability of these agents. In a study comparing the prior administration of a single dose of sucralfate tablets on the bioavailability of naproxen, indomethacin or ketoprofen versus administration in the absence of sucralfate, it was shown that the total amount of these drugs absorbed was not altered; however, the peak concentration of each was reduced, and the time to reach peak concentration was delayed. A single dose of SULCRATE Suspension Plus administered one-half hour before naproxen had a similar effect on the bioavailability of naproxen.

The physician should consider the possible clinical implications of these interactions. It is recommended to separate the administration of any drug from that of sucralfate when the potential for altered bioavailability is felt to be critical to the effectiveness of that drug.

Unless specified, the above data are based on studies carried out with SULCRATE tablets.

Chronic Renal Failure: Dialyzed Patients: Sucralfate should be used with caution in patients with chronic renal failure. When sucralfate is administered orally, small amounts of aluminum are absorbed from the gastrointestinal tract (see Pharmacology). Existing evidence indicates that patients with normal renal function receiving the recommended doses of sucralfate adequately excrete aluminum in the urine; however, patients with chronic renal failure or those receiving dialysis have impaired excretion of absorbed aluminum, and in these individuals, aluminum is known to accumulate in serum and in tissues. In particular, dialysis patients are at greater risk as aluminum does not cross dialysis membranes of the dialysis machine since it is bound to plasma proteins, most notably albumin and transferrin.

In patients with chronic renal failure undergoing dialysis, aluminum-related toxicity (encephalopathy and aluminum-related bone disease), associated with the administration of sucralfate and/or other sources of aluminum has been reported. Consideration should therefore be given to the total daily load of aluminum before administering sucralfate in combination with other aluminum-containing medications, such as aluminum-containing antacids.

Nondialyzed Patients: In a study of 6 nondialyzed chronic renal failure patients with glomerular filtration rates ranging from approximately 10 to 40% of normal, sucralfate administered at a dose of 1 g QID for 3 weeks resulted in elevated serum aluminum concentrations which plateaued at approximately 23 µg/L after 1 week of treatment from a pretreatment level of 3 µg/L. Renal aluminum clearance increased in relation to the increase in serum levels and returned to baseline within 2 weeks following discontinuation of sucralfate as did serum aluminum concentrations. No adverse events were reported in these patients.

These data indicate that the use of sucralfate in nondialyzed chronic renal failure patients requires physician discretion since the excretion of absorbed aluminum may be impaired in these individuals.

The following should be taken into account before treating patients with SULCRATE:

Recurrence may be observed in patients after a successful course of treatment for gastric or duodenal ulcers. While treatment with sucralfate can result in complete healing of the ulcer, a successful course of treatment with sucralfate should not be expected to alter the underlying cause of ulcer disease.

Proper diagnosis is important since symptomatic response to sucralfate therapy does not rule out the presence of a gastric malignancy.

Isolated reports of sucralfate tablet aspiration with accompanying respiratory complications have been received. Therefore, sucralfate tablets should be used with caution by patients who have known conditions that may impair swallowing, such as recent or prolonged intubation, tracheostomy, prior history of aspiration, dysphagia, or any other conditions that may alter gag and cough reflexes, or diminish oropharyngeal coordination or motility.

Each white, capsule-shaped, biconvex tablet, embossed on one side with SULCRATE and debossed on the other side with HMR, contains: sucralfate 1 g. Nonmedicinal ingredients: calcium carboxymethylcellulose, hydrogenated vegetable oil, magnesium stearate and microcrystalline cellulose. Bottles of 100. Store and dispense in a well-closed container.

Each 5 mL of off-white, creamy suspension with a caramel odor contains: sucralfate 1 g. Nonmedicinal ingredients: artificial caramel flavor, glycerin, sodium methylparaben, sodium phosphate monobasic, sodium propylparaben and xanthan gum. Bottles of 500 mL. Shake well before using. Store at room temperature. Avoid freezing.

Clinical experience in children is limited. Therefore, sucralfate therapy cannot be recommended for children under 18 unless, in the judgment of the physician, anticipated benefits outweigh the potential risk.

There has been no experience to date with the use of SULCRATE in pregnant women. Therefore, sucralfate should not be used in pregnant women or women of childbearing potential unless, in the judgment of the physician, the anticipated benefits outweigh the potential risk.

Overdosage has never been observed with SULCRATE (sucralfate) and appears to be unlikely since, using maximal doses of up to 12 g/kg/body weight in a variety of animal species, a lethal dose could not be established.

Overdosage is likely to be associated with symptoms similar to those described in Adverse Effects, such as constipation. These should be treated symptomatically.

See Symptoms.