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At least 19 recordsLinked to original sources
PubMed1989

Combination therapy of sucralfate and cimetidine, compared with sucralfate monotherapy, in patients with peptic reflux esophagitis.

A double-blind multicenter, randomized study was performed in 70 patients with endoscopically documented reflex esophagitis. Patients were randomly given 1 g sucralfate four times a day or the combination of sucralfate 1 g three times a day and 400 mg cimetidine at night. After healing of the esophagitis, patients were randomly given either sucralfate maintenance 2 g daily or placebo for a period of six months. Endoscopy was performed at the beginning of the study, after eight weeks, and, in cases with no healing, after 16 weeks of therapy. Sixty-three of the 70 patients who initially entered the study could be evaluated after eight weeks. Both groups showed good symptomatic improvement, and no side effects necessitated withdrawal of subjects. Endoscopy showed complete healing in 19.4 percent of the sucralfate group and in 21.9 percent of the combination sucralfate and cimetidine group. Endoscopic improvement was found in 50 percent of the sucralfate group and in 50 percent of the combination group. After 16 weeks, 56 patients could be evaluated. In the sucralfate group, improvement was seen in 78.6 percent, and healing in 31 percent. For the combination group these values were 59.3 percent and 37 percent (not significant). Twenty-six patients entered the maintenance phase of the study; 15 received sucralfate and 11 received placebo. Evaluation of 20 patients after six months showed endoscopic and/or symptomatic relapse of esophagitis in three of 12 patients receiving sucralfate and in two of the eight patients receiving placebo. It is concluded that sucralfate monotherapy in patients with reflux-esophagitis is effective and comparable with a combination of sucralfate during the day and cimetidine at night. No difference was found between sucralfate and placebo in terms of the relapse rate of esophagitis during long-term treatment.

Adolescent↗
PubMed1991

Comparative study of sucralfate 2 grams twice daily versus sucralfate 1 gram four times daily in the treatment of benign gastric ulcers in outpatients.

In a double-blind, randomized study, we compared the healing of gastric ulcer during a twice-daily regimen of 2 g sucralfate or sucralfate 1 g q.i.d. Patients receiving the former therapy received the tablets one-half hour before breakfast and at bedtime. Patients receiving sucralfate 1 g q.i.d. received their therapy 30 minutes before breakfast, lunch, and supper, and at bedtime. The study included 52 patients with endoscopically proven gastric ulcer; 41 patients completed the study. Healing was endoscopically assessed at 8 weeks and 12 weeks. After 8 and 12 weeks the healing rate for sucralfate 2 g b.i.d. was 67% and 92%, respectively; the healing rate of sucralfate 1 g q.i.d. was 59% and 71%, respectively. No statistically significant difference was found between the two regimens. The results suggest that 2 g sucralfate twice daily is as effective in the healing of gastric ulcer as 1 g sucralfate q.i.d.

Adult↗
PubMed1992

Combination therapy of sucralfate and ranitidine, compared with sucralfate monotherapy, in patients with peptic reflux esophagitis.

A double-blind, multicenter, randomized study was performed in 75 patients with endoscopically documented reflux esophagitis. Patients were randomly given 1 g sucralfate four times a day or the combination of sucralfate three times a day and 300 mg ranitidine after dinnertime. Endoscopy was performed at the beginning of the study, after 8 weeks, and, if, the reflux esophagitis was not healed, after 16 weeks. Four patients had to be excluded from evaluation; 71 patients could therefore be evaluated. Both groups showed symptomatic improvement to similar extents. Endoscopy showed symptomatic improvement in 67% of the patients treated with sucralfate and in 74% of the combination therapy group. Complete healing or Savary-Miller stage 1 was seen in 26.5% and in 31.4%, respectively. We conclude that sucralfate monotherapy in patients with milder forms of reflux esophagitis is comparable with a combination of sucralfate during the day and ranitidine after dinnertime. This study does not support the commonly used combination of sucralfate and H2-receptor antagonists in reflux esophagitis.

Adolescent↗
PubMed1980

Selective binding of sucralfate to ulcer lesion. III. Experiments in rats with duodenal ulcer receiving 14C-sucralfate.

To determine whether the previously reported mechanisms of action of sucralfate for gastric ulcer are also operative in duodenal ulcer, a single dose of 14C-labelled sucralfate was administered orally to rats with acetic acid-induced duodenal ulcer. Adhesive coating with sucralfate was visible over the duodenal lesion for 6 h in the majority of animals and found localized increasingly selective to the ulcerous area following administration. Visual observations were supported quantitatively by greater than unity mean within-animal ulcer/non-ulcer ratios of binding by 14C-sucrose fulfate moiety and aluminum, with statistical significance at 3 and 6 h post-administration (P less than 0.01 or 0.05). While the aluminum component was found persistent relative to the sucrose sulfate moiety in the adhesive coating, an additional in vitro study revealed that this was due to the pH of duodenal contents and did not lead to a loss of adhesiveness. In addition to these results, the buffering potential of sucralfate coating to control the local pH condition sufficient for binding to ulcer surface proteins to occur support the conclusion that the same mechanisms of action of sucralfate commonly apply to gastric and duodenal ulcers.

Acetates↗
PubMed1994

Sucralfate gel for symptomatic chronic gastritis: multicentre comparative trial versus sucralfate suspension.

The object of this study was to compare the efficacy of a new sucralfate gel formulation and the standard sucralfate suspension in the treatment of chronic gastritis. This multicentre randomized trial included 368 dyspeptic patients with endoscopic features of histologically confirmed chronic gastritis. Patients were randomized to a six week treatment with either 1 g bid sucralfate gel or 1 g qid sucralfate suspension. Endoscopic and histological assessment plus urease test for Helicobacter pylori were performed at 0 and 6 weeks. Clinical evaluation of symptoms were obtained at 0, 3 and 6 weeks. Results showed that both treatments were equally effective in promoting symptom relief, in inducing endoscopic and histological healing or in the improvement of the lesions. Therefore sucralfate gel is as effective as the standard preparation in the treatment of chronic gastritis, with the advantage that its b.i.d. administration improves patients' compliance.

Administration, Oral↗
PubMed1995

Sucralfate maintenance therapy in reflux esophagitis. Sucralfate Investigational Working Team.

OBJECTIVE: to prove in a double-blind placebo-controlled multinational trial the effects of sucralfate suspension 2 g BID and placebo in the prevention of recurrent reflux esophagitis. METHODS: One hundred and eighty-four patients from 16 centers with reflux esophagitis Savary grade 1 and 2 were initially healed with antisecretory therapy before entering the study. They were randomly allocated to sucralfate suspension 2 g BID or placebo for 6 months. Symptoms were monitored monthly. Endoscopy was performed at the end of the trial or earlier in case of clinical suspension of relapse. RESULTS: The two treatment groups were well matched. We were able to analyze 88 sucralfate- and 93 placebo-treated patients. There was a significant reduction in the endoscopic relapse rate (31% in the sucralfate group vs. 65% in the placebo group, p < 0.001). This reduction was especially obvious for symptomatic relapses (10% vs. 34%, respectively, p < 0.001). CONCLUSION: This is the first study to show that sucralfate suspension is capable of preventing recurrent reflux esophagitis in patients with solitary or confluent erosions previously healed with antisecretory therapy.

Double-Blind Method↗
PubMed1980

Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate.

14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.

Acetates↗
PubMed2000

The effect of staggered dosing of sucralfate on oral bioavailability of sparfloxacin.

AIMS: To investigate the effect of sucralfate on sparfloxacin absorption when administered concurrently or at strategically spaced dosing times designed to avoid the potential interaction. METHODS: The study was a four-way crossover design where eight healthy Japanese volunteers were randomized to one of four treatment sequences at entry. A 300 mg dose of sparfloxacin was administered alone for treatment A (control). Treatments B, C and D included sucralfate 1.5 g every 12 h for five doses. For treatment B, the fifth dose of sucralfate was administered concurrently with sparfloxacin 300 mg. For treatment C, 300 mg sparfloxacin was given 2 h prior to the fifth dose of sucralfate. Treatment D consisted of sparfloxacin 300 mg given 4 h prior to the fifth dose of sucralfate. Blood and urine samples were collected at predetermined time intervals for 72 h. Sparfloxacin concentrations in plasma and urine and the concentrations of sparfloxacin metabolite in urine were determined by high performance liquid chromatography assays. RESULTS: Sucralfate administrated concurrently with sparfloxacin decreased the mean AUC(0,infinity) of sparfloxacin 2-fold (P<0.001) and the mean Cmax 2.1-fold (P<0.001) compared with sparfloxacin alone. When sucralfate was administrated 2 h after sparfloxacin, the mean AUC(0,infinity) was decreased 1.5-fold (P<0.01) and the mean Cmax 1.4-fold (P<0.01). Sucralfate did not alter the extent of absorption of sparfloxacin when it was given 4 h after the administration of sparfloxacin. The relative bioavailabilities for treatments B, C and D were 0.50 (95% CI: 0.35-0.65), 0.64 (95% CI: 0. 51-0.77), and 0.92 (95% CI: 0.81-1.03), respectively, relative to sparfloxacin alone. The mean percentage of the sparfloxacin dose recovered in urine was significantly lower after sparfloxacin was administered with sucralfate than after sparfloxacin was administered alone or 2 h before the sucralfate dose (P<0.001). Treatments B, C and D were demonstrated to be equivalent to treatment A in the rate of absorption. The tmax, CLr and t1/2 were not significantly affected by sucralfate. The metabolism of sparfloxacin was not altered in the presence of sucralfate. CONCLUSIONS: Oral administration of sucralfate with sparfloxacin or 2 h after sparfloxacin, decreased the extent of sparfloxacin absorption. When both drugs are to be administered together, sucralfate should be administered 4 h after sparfloxacin, allowing thus sufficient time for sparfloxacin absorption prior to the sucralfate dose and thereby minimizing the chance of a significant interaction.

Administration, Oral↗
PubMed1993

Gastric retention of sucralfate gel and suspension in upper gastrointestinal diseases.

This study was designed to compare by scintigraphy the gastric retention of a new dosage form of sucralfate as gel (Gastrogel) with that of sucralfate suspension in 25 patients with upper gastrointestinal symptoms referred for routine endoscopy. After endoscopy 4 subgroups were defined: macroscopically normal mucosa (n = 7), antral gastritis and/or erosions (n = 6), gastric ulcer (n = 6) and duodenal ulcer (n = 6). Each patient received either sucralfate gel or sucralfate suspension in equivalent doses (5 ml containing 1 g sucralfate). Both formulations were labelled with 111 MBq 99mTc-DTPA before administration. The mean value of t1/2 in the total group was significantly longer when patients were taking sucralfate gel (61.6 min) compared to sucralfate suspension (33.8 min) (P < 0.001). The mean values of t1/2 were significantly longer for sucralfate gel compared to sucralfate suspension also among the subgroups (macroscopically normal P < 0.02, antral gastritis P < 0.05, gastric ulcer P < 0.02 and duodenal ulcer P < 0.05). After 2 and 3 hours, the percentage residual activity in the gastric area was significantly higher following administration of sucralfate gel compared to sucralfate suspension. This study has shown that, compared to sucralfate suspension, sucralfate gel persists longer in the stomach of patients with gastritis and peptic ulcer.

Adolescent↗
PubMed1984

In vitro adsorption of bile salts and aspirin to sucralfate.

Sucralfate, an aluminum salt of sulfated sucrose, is a new drug designed for the treatment of peptic ulcer. Sucralfate has been reported to be useful in a variety of situations including prevention of aspirin-induced gastric mucosal damage. We investigated the in vitro adsorption of bile salts or aspirin to sucralfate in environments simulating the stomach (pH 1.5), small intestine (pH 7), and colon (pH 7.8). Bile salts were incubated with sucralfate, and the quantity of bile salt adsorbed was calculated by subtraction from the amount remaining in solution after centrifugation at 12,500g for 30 min. Adsorption experiments were performed in bile salt solutions at pH 1.5 and 7.0 with 0-10 g/dl sucralfate using glycocholate, glycochenodeoxycholate, taurocholate, taurodeoxycholate, or taurochenodeoxycholate. The dihydroxy-unconjugated bile salts, deoxycholic, and chenodeoxycholic salts were tested at pH 7.8. Binding capacity (micromoles per gram sucralfate) was calculated from the linear regression of micromoles bound vs grams sucralfate incubated. Sucralfate adsorbed all bile salts tested (except taurocholic acid at pH 1.5) but was less effective than cholestyramine. Sucralfate does not adsorb sufficient bile salts at neutral pH to cause bile salt depletion. Aspirin was minimally adsorbed by sucralfate [7.5 mumol (1.4 mg)/g sucralfate, pH 1.5], and thus adsorption of aspirin does not explain the protective effect of sucralfate against aspirin injury.

Adsorption↗
PubMed1993

Sucralfate does not reduce the risk of acid aspiration pneumonitis.

OBJECTIVE: To study the pulmonary effects of aspirating a mixture of sucralfate in water and sucralfate in hydrochloric acid in an animal model of aspiration pneumonia. DESIGN: Prospective, randomized, controlled study with repeated measures. SETTING: University research laboratory. SUBJECTS: Thirty-two in situ, isolated, blood perfused porcine lung preparations. INTERVENTIONS: Five control preparations received no aspiration. Twenty-seven preparations received a standard aspiration of 1.5 mL/kg body of a) distilled water (n = 5), b) sucralfate in distilled water (n = 8), c) 1/10 normal hydrochloric acid (n = 6), and d) mixture of sucralfate in distilled water and hydrochloric acid (n = 8). MEASUREMENTS: The pH measurements were made of all aspirates. Lung weight, airway pressures, and pulmonary artery pressures were continuously monitored before and for 4 hrs after aspiration. Lung wet/dry weight ratio was measured at the completion of the study. RESULTS: The pH of sucralfate mixed with distilled water was 4.9, pH of 1/10 normal hydrochloric acid was 1.0, and pH of equal volumes of a sucralfate-water suspension mixed with hydrochloric acid was 1.5. Airway pressures and pulmonary arterial pressures increased in all aspirate groups over time compared with those values of control lungs. Control lungs gained 18 +/- 3 (SEM) g over 4 hrs and the wet/dry ratio was 4.951 +/- 0.310. Lungs aspirating distilled water gained 147 +/- 49 g and the wet/dry ratio was 5.198 +/- 0.120. Lungs aspirating sucralfate and distilled water increased their weight by 109 +/- 30 g and the wet/dry ratio was 5.380 +/- 0.076. Lungs aspirating a suspension of sucralfate and water and hydrochloric acid were similar to lungs aspirating hydrochloric acid alone with weight increases of 265 +/- 30 g and 346 +/- 81 g, and the wet/dry ratio of 7.011 +/- 0.273 and 7.230 +/- 0.390, respectively. CONCLUSIONS: Sucralfate has minimal acid buffering effect. Aspiration of sucralfate mixed with distilled water causes lung edema similar to aspiration of water alone. Aspiration of a sucralfate-water suspension mixed with hydrochloric acid causes severe lung edema. These results suggest that patients given sucralfate prophylaxis for stress ulceration are at risk for acid aspiration.

Airway Resistance↗
PubMed1989

Sucralfate reduces the gastrointestinal absorption of norfloxacin.

The effect of sucralfate on the bioavailability of norfloxacin after single 400-mg doses of norfloxacin was evaluated in eight healthy males. Subjects received each of the following treatments in random sequence: (i), norfloxacin, 400 mg alone; (ii) sucralfate, 1 g, concurrently with norfloxacin, 400 mg; and (iii) sucralfate, 1 g, followed by norfloxacin, 400 mg, 2 h later. One day before administration of treatments 2 and 3, 1 g of sucralfate was given at 7 a.m., 11 a.m., 5 p.m., and 10 p.m. Blood samples were collected immediately before the norfloxacin dose and at 0.25, 0.5, 0.75, 1.0, 1.5, 2, 3, 4, 6, 8, 12, and 24 h postdose. Urine was collected in divided intervals: from 0 to 12, from 12 to 24, and from 24 to 48 h. Norfloxacin concentrations in plasma and urine were determined by high-performance liquid chromatography. Mean area under the plasma concentration-versus-time curve extrapolated to infinity decreased significantly (P less than 0.001) after norfloxacin was given with and 2 h after sucralfate. The relative bioavailabilities were 1.8% when norfloxacin was taken with sucralfate and 56.6% when it was taken 2 h after sucralfate. After norfloxacin was given alone, the mean norfloxacin concentrations in urine collected during intervals of 0 to 12, 12 to 24, and 24 to 28 h were 118.9 +/- 72.3, 18.8 +/- 12.5, and 2.4 +/- 2.2 micrograms/ml, respectively. After norfloxacin was given with sucralfate, however, the mean norfloxacin concentrations in urine collected during the same time intervals were 6.8 +/- 4.7, 1.8 +/- 1.4, and 0 +/- 0 microgram/ml, respectively. Because of low pH and relatively high magnesium concentration in urine, susceptibilities of bacteria in urine are 8- to 32-fold lower than in broth. This fact, in combination with the reduced bioavailability of norfloxacin in the presence of sucralfate or antacids, is likely to result in treatment failure. The effect of sucralfate given after norfloxacin was not examined, nor was the effect of sucralfate given more than 2 h before norfloxacin. Administration or norfloxacin with sucralfate should therefore by avoided.

Administration, Oral↗
PubMed1987

Protective effect of sucralfate against aspirin-induced damage to the human gastric mucosa.

Sucralfate, an agent that heals peptic ulcers in humans, has been shown to reduce aspirin-induced gastric mucosal damage in experimental animals. It has been suggested that the protective effect of sucralfate is due to stimulation of local prostaglandin production. The purpose of this study was to establish whether sucralfate was capable of reducing aspirin-induced gastric damage in humans. The effect of 1 g of sucralfate or identical placebo was studied in random order in eight healthy subjects. To determine if the effect of sucralfate was related to local prostaglandin synthesis, a second series of studies was performed in which prostaglandin production was inhibited with indomethacin 50 mg given orally eight hours before sucralfate. In each subject, all studies were performed at least one week apart. Following an overnight fast, upper gastrointestinal endoscopy was performed, with sucralfate or placebo given orally 30 minutes before ingestion of 1,200 mg of soluble aspirin in 50 ml of water. Both endoscopist and subject were unaware of the test agent. Ninety minutes after aspirin ingestion, endoscopy was again performed and gastric mucosal lesions were counted and graded to derive an erosion score. Results are expressed as mean +/- SEM. Aspirin produced endoscopic changes (score of 2.75 +/- 0.49) that were significantly (p less than 0.05) inhibited by sucralfate (score of 1.13 +/- 0.44). The protective effect of sucralfate was abolished by pretreatment with indomethacin (scores of 2.88 +/- 0.55 and 1.88 +/- 0.40, respectively). These results demonstrate that sucralfate significantly protects the human gastric mucosa against the acute damaging effects of aspirin. This effect is abolished by indomethacin, suggesting that the protective action of sucralfate on the gastric mucosa of humans may be related to stimulation of endogenous prostaglandins.

Aspirin↗
PubMed1991

Mechanisms of gastroduodenal protection by sucralfate.

Over the past 5-10 years, a number of studies have shown that topical sucralfate enhances a number of gastric and duodenal mechanisms, e.g., the "mucus-bicarbonate barrier," mucosal hydrophobicity, mucosal blood flow, cell viability, and local production of prostaglandins, as well as endogenous mediators of tissue injury and repair. It seems likely that the complex actions of sucralfate are in part related to direct interaction between the drug or its components (aluminum, sucrose, and sulfate) and gastric mucosal tissues, and in part related to effects of the drug on the various mucosal mediators of tissue injury and repair. Local actions may play a role in accelerating healing of ulcer-damaged mucosa, but this does not explain the protective actions of sucralfate on normal mucosa. Thus sucralfate appears to enhance the protective function of the "mucus-bicarbonate" barrier by actions on both components. This may depend in part on an interaction with the unstirred layer overlying gastric epithelium. Sucralfate has also been shown to increase the hydrophobicity of mucus gel. There is little doubt that sucralfate increases local production and release of protective prostaglandins (PGs), but the precise role played by these agents in mediating mucosal protection and in chronic ulcer healing remains uncertain. Currently, the mechanism of action of sucralfate on vascular integrity remains unknown and the role of PGs in this protective function is unclear. There is little evidence that epidermal growth factor plays any role in mediating mucosal protection by sucralfate, but it may be important in its ulcer-healing action. Sucralfate has been shown to be truly "cytoprotective" in that it protects isolated epithelial cells from damage by noxious agents. In animals treated with sucralfate, the surface epithelial cells were disrupted, but necrotic lesions in the deep proliferative zone were virtually absent. It seems likely that investigations of the actions of sucralfate and its components will move ever closer to defining the target cells, the intracellular events, and the mediators that bring about its protective and ulcer-healing activity.

Animals↗
PubMed1989

Importance of an acid milieu in the sucralfate-induced gastroprotection against ethanol damage.

Sucralfate is known for its gastroprotective properties in humans and rats, but the importance of intragastric pH in this protection is a subject of controversy. This study, performed on healthy young volunteers and rats, was designed to compare the gastroprotective effects of sucralfate with those of sucralfate combined with ranitidine or of sucralfate adjusted to pHs varying from 1 to 7. In humans the mucosal damage induced by 40% ethanol spray after 4 days of pretreatment with placebo, sucralfate (1 g four times daily), ranitidine (150 mg three times daily), or the combination of sucralfate plus ranitidine was evaluated by means of endoscopy with mucosal biopsy and histologic examination. Sucralfate alone reduced the endoscopic score significantly (compared with placebo) and prevented deep necrotic lesions. Neither ranitidine alone nor its combination with sucralfate prevented ethanol-induced endoscopic and histologic mucosal changes. In rats acute gastric lesions were induced by 100% ethanol. Sucralfate was relatively more effective in mucosal protection against ethanol when given at lower pH (1 or 2) than at original pH (4.5) and failed to protect at neutral pH (7.0). Pretreatment with ranitidine, which by itself did not change ethanol damage, greatly reduced the protection afforded by sucralfate. We conclude that sucralfate protects the gastric mucosa against ethanol damage both in humans and in rats and that this protection is dependent on the presence of an acidic intragastric pH.

Adult↗
PubMedDate not supplied

Effects of sucralfate and ranitidine on aluminum concentrations in elderly volunteers.

Elevated aluminum concentrations have been implicated in several disease states in the elderly. We examined the effects of sucralfate, a basic aluminum salt of sucrose sulfate, and ranitidine, administered individually and in combination, on plasma and urine aluminum concentrations in the elderly in a prospective, randomized, three-arm crossover study. Subjects were 20 healthy volunteers over age 65 years, with no clinically significant comorbidities or recent use of aluminum-containing drugs or histamine (H)2-antagonists. The three regimens were ranitidine 300 mg at bedtime, sucralfate 1 g 4 times/day, and ranitidine 300 mg at bedtime plus sucralfate 1 g 4 times/day, administered for 4 weeks, with a washout period of at least 1 week between regimens. Plasma and urine aluminum concentrations were measured on days 0, 1, 7, 14, and 28 of each regimen. After 28 days, mean plasma aluminum concentrations were significantly higher in subjects receiving sucralfate alone (8.5 +/- 1.8 micrograms/L) and sucralfate plus ranitidine (5.1 +/- 1.3 micrograms/L) compared with those receiving ranitidine alone (2.4 +/- 0.7 micrograms/L). Urine aluminum concentrations were significantly higher in subjects receiving sucralfate alone (133.2 +/- 32.8 micrograms/g creatinine) and sucralfate plus ranitidine (148.1 +/- 51.9 micrograms/g creatinine) compared with those receiving ranitidine alone (11.0 +/- 3.7 micrograms/g creatinine). There was no significant difference in plasma or urine aluminum concentrations between subjects who received sucralfate alone versus those who received sucralfate plus ranitidine. Sucralfate 4 g/day in elderly subjects produces a significant increase in both plasma and urine aluminum concentrations, compared with ranitidine 300 mg/day. This increase most likely is secondary to gastrointestinal absorption of aluminum in the sucralfate formulation. The clinical relevance of this increase requires further evaluation.

Aged↗