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 gastro-duodenal mucosa as a consequence of a change of intra-gastric pH.
Animals studies have shown that simultaneous administration of sucralfate with tetracycline, phenytoin or cimetidine results in 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.
These interactions appear to be non-systemic 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.
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.
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 aluminium are absorbed from the gastrointestinal tract (see PHARMACOLOGY under ACTIONS). Existing evidence indicates that patients with normal renal function receiving the recommended doses of sucralfate adequately excrete aluminium in the urine; however, patients with chronic renal failure or those receiving dialysis have impaired excretion of absorbed aluminium, and in these individuals, aluminium is known to accumulate in serum and in tissues. In particular, dialysis patients are at greater risk as aluminium does not cross dialysis membranes of the dialysis machine since it is bound to plasma proteins, most notably albumin and trasferrin.
In patients with chronic renal failure undergoing dialysis, aluminium-related toxicity (encephalopathy and aluminium-related bone disease), associated with the administration of sucralfate and/or other sources of aluminium before administering sucralfate in combination with other aluminium-containing medications, such as aluminium-containing antacids.
Nondialyzed Patients: In a study of six 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 three weeks resulted in elevated serum aluminium concentrations which plateaued at approximately 23 ug/L after one week of treatment from a pretreatment level of 3 ug/L. Renal aluminium clearance increased in relation to the increase in serum levels and returned to baseline within two weeks following discontinuation of sucralfate as did serum aluminium 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 aluminium may be impaired in these individuals.