Effect of sucralfate and an aluminum hydroxide gel on gastric emptying of solids and liquids

ArticleinClinical Pharmacology &#38 Therapeutics 37(6):629-32 · July 1985with37 Reads
DOI: 10.1038/clpt.1985.101 · Source: PubMed
Our purpose was to investigate whether an aluminum-containing compound (sucralfate) and an aluminum-containing antacid (Amphojel; Wyeth Laboratories), both of which are commonly used in peptic ulcer disease, affect gastric emptying. Gastric emptying was studied in ten healthy subjects with the double isotope technique to assess simultaneous emptying rates of the solid and liquid components of a meal. 99mTechnetium sulfur colloid-labeled chicken liver served as the solid component and 111indium diethylenetriamine penta-acetic acid-labeled water was the liquid component. In a randomized, double-blind fashion, 1 gm sucralfate and 30 ml aluminum hydroxide gel were compared with placebo on separate days. Subjects ate the isotope-labeled test meal after dosing, and gastric emptying was monitored for 3 hours by a gamma-camera interfaced with a computer. There was no significant change in gastric emptying of either solids or liquids after sucralfate. The aluminum hydroxide gel slowed the gastric emptying rate for solids more than did the placebo, but this difference was significant only at the intervals of 165 and 180 minutes after the meal. We conclude that aluminum in the form of therapeutic doses of sucralfate does not delay gastric emptying of solids or liquids in normal subjects, while the larger amount of aluminum in therapeutic doses of the antacid gel has some slowing effect on gastric emptying of the solid components of a meal.
    • "Firstly, the more delayed and reduced absorption rate occurred with NSAIDs such as ketoprofen (50 mg dose) and indomethacin (50 mg dose), relative to naproxen (500 mg dose) or diclofenac (50 mg dose), suggesting that there may be an inverse correlation between the oral dose administered of NSAIDs vs. the reduced absorption rate [25, 26] . Second, due to the presence of aluminum hydroxide component, sucralfate may tend to act like an antacid increasing the gastric pH and thus facilitating a faster gastric emptying of NSAIDs and thereby decreasing rate of absorption [31] Third, on the aspects of sucralfate's ability to increase gastric emptying, another clinical study showed that sucralfate had minimal role to play in the gastric emptying of the ingested solids or liquids [32]. Fourth, it has been suggested that sucralfate tended to form a viscous and adhesive moiety immediately upon contact in an acidic environment (i.e., gastric environment for instance). "
    [Show abstract] [Hide abstract] ABSTRACT: Sucralfate, a complex of aluminium hydroxide with sulfated sucrose, forms a strong gastrointestinal tract (GIT) mucosal barrier with excellent anti-ulcer property. Because sucralfate does not undergo any significant oral absorption, sucralfate resides in the GIT for a considerable length of time. The unabsorbed sucralfate may alter the pharmacokinetics of the oral drugs by impeding its absorption and reducing the oral bioavailability. Because of the increased use of sucralfate, it was important to provide a reappraisal of the published clinical drug-drug interaction studies of sucralfate with scores of drugs. This review covers several category of drugs such as non-steroidal anti-inflammatory drugs, fluoroquinolones, histamine H2-receptor blockers, macrolides, anti-fungals, anti-diabetics, salicylic acid derivatives, steroidal anti-inflammatory drugs and provides pharmacokinetic data summary along with study design, objectives and key remarks. While the loss of oral bioavailability was significant for the fluoroquinolone class, it generally varied for other classes of drugs, suggesting that impact of the co-administration of sucralfate is manageable in clinical situations. Given the technology advancement in formulation development, it may be in order feasible to develop appropriate formulation strategies to either avoid or minimize the absorption-related issues when co-administered with sucralfate. It is recommended that consideration of both in vitro and preclinical studies may be in order to gauge the level of interaction of a drug with sucralfate. Such data may aid in the development of appropriate strategies to navigate the co-administration of sucralfate with other drugs in this age of polypharmacy.
    Article · Apr 2016
    • "Drugs that could potentially cause delayed GE leading to gastroparesis include α-2 adrenergic agonists and tricyclic antidepressants which stimulate adrenergic receptors and thus decrease gastrointestinal motility. Also protonpump inhibitors, antacids, H 2 receptor agonists, sucralfate, octreotide, β-adrenergic agonists, calcium channel blockers and diphenhydramine may delay GE leading to gastroparesis1617181920. Viruses (rota virus, Epstein–Barr virus, cytomegalovirus) [15,21] have been implicated as causes of post-infectious gastroparesis. "
    [Show abstract] [Hide abstract] ABSTRACT: Historically, gastroparesis is characterized by delayed gastric emptying of fluids and/or solids without evidence of a mechanical gastric outlet obstruction. To provide a thorough, evidence-based overview of the diagnosis, treatment, outcome and future advances for gastroparesis in children, a web search (PubMed, Cochrane Database of Systematic Reviews, EMBASE, Clinical Evidence) was performed. Original articles and reviews were identified, examined and included as appropriate. The prevalence of gastroparesis is vague in adults and unknown in children. It is suspected on the presence of symptoms indicating gastric dysmotility (nausea, vomiting, early satiety, postprandial fullness, failure to thrive, weight loss) and is confirmed on the demonstration of delayed gastric emptying. It can be assessed with various methods from which gastric emptying scintigraphy of a radiolabeled solid meal is considered as the golden standard. Therapeutic approaches include: dietary modifications, medical treatment (prokinetics, antiemetics, intrapyloric injection of botulinum toxin, enteral feeds via jejunostomy, total parenteral nutrition) and surgical interventions (laparoscopic placement of gastric pacemaker) aiming at alleviating symptoms and maintaining optimal nutritional status. Gastroparesis in children can be challenging to diagnose and treat. Specific protocols for the evaluation of gastric emptying and for a stepwise management are required to optimise future outcomes.
    Full-text · Article · Mar 2013
    • "It is interesting that Piscitelli and colleagues (25) demonstrated an increase in gastric pH of approximately 1 pH unit following administration of ketoconazole alone, as predicted by our in vitro data (14). In contrast, they did not observe a sucralfate-induced increase in gastric pH as predicted by our in vitro data and reported by previous investigators (3, 19, 21, 23), despite the multiple-dose sucralfate regimen employed in their study. Nagashima (21) reported that administration of 1.0 g of sucralfate to 10 healthy volunteers (also monitored with the Heidelberg capsule technique) increased gastric pH approximately 1.5 pH units (from -1.8 to -3.3). "
    [Show abstract] [Hide abstract] ABSTRACT: Absorption of ketoconazole is impaired in subjects with an increased gastric pH due to administration of antacids, H2-receptor antagonists, proton pump inhibitors, or the presence of hypochlorhydria. Sucralfate could provide an attractive alternative in patients receiving ketoconazole who require therapy for acid-peptic disorders. Twelve healthy human volunteers were administered a single 400-mg oral dose of ketoconazole in each of three randomized treatment phases. In phase A, ketoconazole was administered orally with 240 ml of water. In phase B, ketoconazole and sucralfate (1.0 g) were administered simultaneously with 240 ml of water. In phase C, ketoconazole was administered with 240 ml of water 2 h after administration of sucralfate (1.0 g) orally with 240 ml of water. A 680-mg oral dose of glutamic acid hydrochloride was administered 10 min prior to and with each dose of ketoconazole, sucralfate, or ketoconazole plus sucralfate. Simultaneous administration of ketoconazole and sucralfate led to a significant reduction in the area under the concentration-time curve and maximal concentration of ketoconazole in serum (78.12 +/- 12.20 versus 59.32 +/- 13.61 micrograms.h/ml and 12.34 +/- 3.07 versus 8.92 +/- 2.57 micrograms/ml, respectively; P < 0.05). When ketoconazole was administered 2 h after sucralfate, the observed ketoconazole area under the concentration-time curve was not significantly decreased compared with that of ketoconazole alone. The time to maximal concentrations in serum and the ketoconazole elimination rate constant were not significantly different in any of the three treatment phases. In patients receiving concurrent administration of ketoconazole and sucralfate, doses should be separated by at least 2 h.
    Full-text · Article · Mar 1994
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