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PubMed2001

Topical use of Sucralfate Cream in second and third degree burns.

This clinical study was undertaken to test the efficacy of topical Sucralfate Cream in second and third degree burns. Topical Sucralfate Cream has been used on a wide variety of lesions from radiation proctitis and dermatitis to keratoconjunctivitis with remarkable results. The study was carried out in two phases. The first phase comprised 60 patients, 30 of whom were treated with Sucralfate Cream while the other 30 were treated with other topical antimicrobial agents. Twenty-one of the patients in the study group had second-degree burns and nine patients' third degree burns. In the second phase, a double blind study was carried out on 25 patients where one area of burns was treated with Sucralfate Cream while another control area of the same patient was treated with a placebo ointment, containing the excipients used during preparation of the Sucralfate Cream, without Sucralfate. In the first phase, it was seen that the period of epithelialisation of second degree burns in the study group treated with Sucralfate Cream was 18.8 days compared with 24.6 days with other topical agents. This difference is statistically significant with a P value of <0.00001. In the double blind study, also healing in the areas treated with Sucralfate was more rapid than those treated with bland placebo ointment. The difference in the two rates of healing was statistically significant with a P value of 0.00067. Histopathological studies were also carried out in 10 patients of phase I of the trial. Sucralfate Cream promotes rapid epithelialisation of second degree burns with minimal said effects and offers another topical agent in the burn care specialist's armamentarium.

Administration, Topical↗
PubMed1993

Fibroblast growth factor in gastroprotection and ulcer healing: interaction with sucralfate.

The study was designed to determine the gastroprotective and ulcer healing efficacy of basic transforming growth factor (bFGF) and to assess whether this peptide contributes to the action of sucralfate on the rat stomach. Application of human recombinant bFGF (1-100 micrograms/kg/hour subcutaneously) failed to affect the formation of acute gastric lesions induced by 100% ethanol and acidified aspirin but reduced the stress induced by gastric lesions. Sucralfate (100-200 mg/kg given orally) protected gastric mucosa against the ethanol, aspirin, and stress induced acute gastric lesions but the addition of bFGF (100 micrograms/kg subcutaneously or intragastrically) failed to affect sucralfate induced protection against ethanol or aspirin but increased that against stress. Administration of bFGF (3-300 micrograms/kg/day) by an intragastric or an intraperitoneal route or sucralfate (400 mg/kg/day) orally to rats with acetic acid induced gastric ulcers, enhanced the healing rate of these ulcers during seven day treatment in a dose dependent manner. This was accompanied by a pronounced increase in the number of capillaries and myofibroblasts and in DNA synthesis and DNA and RNA concentrations in the granulation tissue in the ulcer area. [125I]bFGF (1 microCi) applied subcutaneously or intragastrically accumulated in two to threefold higher amounts in the ulcer area than in the intact mucosa, particularly in rats treated with sucralfate. Concurrent treatment with indomethacin (2 mg/kg intraperitoneally) delayed ulcer healing and reduced the binding of labelled bFGF to the ulcer area, angiogenesis, and DNA synthesis by sucralfate. Addition of [125I]bFGF to sucralfate at various pHs resulted in the coprecipitation of bFGF by sucralfate in a pH dependent manner from about 10% at pH 7.0 to 90% at pH 1.5. Thus bFGF shows little protective activity and is not essential for gastroprotection afforded by sucralfate but plays an important part in healing of gastric ulcers possibly due to its growth promoting and angiogenic actions.

Acetates↗
PubMed1997

Effect of sucralfate on aspirin induced mucosal injury and impaired haemostasis in humans.

BACKGROUND: Sucralfate does not have potent anti-ulcerogenic actions in users of non-steroidal anti-inflammatory drugs (NSAIDs). However, sucralfate may influence intragastric haemostasis favourably. AIM: To investigate separately the effects of sucralfate on acute gastric and duodenal injury and on changes in intragastric bleeding induced by aspirin. METHOD: On three occasions, 24 healthy volunteers received three days' treatment with aspirin 900 mg twice daily together with placebo, sucralfate 2 g twice daily or sucralfate 1 g four times daily. Injury was assessed endoscopically and bleeding by spontaneous and biopsy induced bleeding intragastric washings. Ex vivo prostaglandin E2 (PGE2) synthesis and serum thromboxane were measured by using radioimmunoassay. RESULTS: Aspirin significantly inhibited ex vivo gastric mucosal PGE2 synthesis, reduced serum thromboxane, caused gastric erosions, and increased spontaneous and biopsy induced bleeding. Sucralfate had no significant effects on endoscopic injury but sucralfate 1 g four times daily significantly reduced spontaneous and biopsy induced bleeding. Similar trends were seen with sucralfate 2 g twice daily but the results were less consistent. CONCLUSION: Sucralfate does not affect aspirin induced acute gastric mucosal injury but reduces aspirin associated intragastric bleeding.

Acute Disease↗
PubMed2000

Sucralfate in the prevention of treatment-induced diarrhea in patients receiving pelvic radiation therapy: A North Central Cancer Treatment Group phase III double-blind placebo-controlled trial.

PURPOSE: Randomized studies have suggested that sucralfate is effective in mitigating diarrhea during pelvic radiation therapy (RT). This North Central Cancer Treatment Group study was undertaken to confirm the antidiarrheal effect of sucralfate. Several other measures of bowel function were also assessed. PATIENTS AND METHODS: Patients receiving pelvic RT to a minimum of 45 Gy at 1.7 to 2.1 Gy/d were eligible for the study. Patients were assigned randomly, in double-blind fashion, to receive sucralfate (1.5 g orally every 6 hours) or an identical looking placebo during pelvic RT. RESULTS: One hundred twenty-three patients were randomly assigned and found assessable. Overall, there was no significant difference in patient characteristics between those receiving sucralfate and those receiving placebo. Moderate or worse diarrhea was observed in 53% of patients receiving sucralfate versus 41% of those receiving placebo. Compared with patients receiving placebo, more sucralfate-treated patients reported fecal incontinence (16% v 34%, respectively; P =. 04) and need for protective clothing (8% v 23%, respectively; P =. 04). The incidence and severity of nausea were worse among those taking sucralfate (P =.03). Analysis of patient-reported symptoms 10 to 12 months after RT showed a nonsignificant trend toward more problems in patients taking sucralfate than in those taking placebo (average, 2.3 v 1.9 problems, respectively; P =.34). CONCLUSION: Sucralfate did not decrease pelvic RT-related bowel toxicity by any of the end points measured and seems to have aggravated some gastrointestinal symptoms.

Adult↗
PubMed1995

Stimulation of mucosal glutathione and angiogenesis: new mechanisms of gastroprotection and ulcer healing by sucralfate.

BACKGROUND: Among the endogenous mediators (e.g., PG, SH) of gastroprotection, so far only PG was implicated in the mechanism of acute gastroprotection by sucralfate. Angiogenesis, which is stimulated by bFGF, is a recently recognized element in ulcer healing, and sucralfate binds bFGF in vitro and in vivo. METHODS: In fasted rats the gastric mucosal concentration of GSH and protein SH was measured at 30, 60, 120, and 240 min after a single gastroprotective dose of sucralfate. In normally fed rats, angiogenesis was measured in the subcutaneous sponge assay 7 days after the implantation of sponges containing sucralfate and/or bFGF. RESULTS: A gastroprotective dose of sucralfate time-dependently increased GSH concentration in the gastric mucosa. Sucralfate alone accelerated angiogenesis, which was significantly enhanced by combination with an ineffective dose of bFGF in the subcutaneous sponge assay. The same dose of sucralfate combined with an angiogenic dose of bFGF also resulted in synergistic stimulation (e.g., more than fivefold) of angiogenesis. CONCLUSIONS: It appears that elevated mucosal GSH concentration may represent a new factor in the mechanism of acute gastroprotection by sucralfate, and stimulation of angiogenesis is one of the mechanisms of ulcer healing by sucralfate.

Animals↗
PubMed1989

Chemical aspects of labeling sucralfate with 99mTcO4.

Two formulations of [99mTc]sucralfate have been used to image gastric and duodenal ulcers and inflammatory bowel disease. One formulation is a complexation of [99mTc]HSA with sucralfate. The second is prepared by directly labeling sucralfate with [99mTc]pertechnetate in the presence of stannous ion. An in vitro study of the factors affecting the production and stability of these labeled sucralfate preparations was conducted. Both formulations were stable at the acidic pH likely encountered in the stomach. However, at pH greater than 6 the albumin-sucralfate complex began to dissociate while directly labeled sucralfate was stable to a pH of 9. Conversely it was shown that directly labeled sucralfate was more susceptible to loss of 99mTc to other chelating species. Sucralfate complexed with [99mTc]HSA was radiochemically stable up to a specific activity of 26 GBq (700 mCi) per gram while directly labeled sucralfate showed decreased 24-hr stability at specific activities greater than 837 mCi (31 GBq) per gram.

Chemical Phenomena↗
PubMed1987

The efficacy, safety and dosage of sucralfate in ulcer therapy.

This paper reviews the results of placebo and cimetidine/ranitidine controlled studies in the short-term healing and maintenance therapy of duodenal (DU) and gastric (GU) ulcer, the status of newer dosage regimens, and safety aspects of the drug. The efficacy of sucralfate 1g qid in DU and GU healing has been amply confirmed in placebo and cimetidine or ranitidine-controlled studies. Healing rates have been reported in 60 to 83% DU patients after 4 weeks treatment with sucralfate but as with other drugs the rates tend to be lower in GU patients. The DU relapse rate after sucralfate healing is perhaps lower than after cimetidine healing, and sucralfate healing rates in DU are not compromised by concomitant cimetidine therapy, or by smoking. The value of maintenance therapy with sucralfate 1 g bd in reducing the relapse rate in patients with recently healed DU is well documented. The relapse rate is reduced from the order of 60 to 20% after 6 months, and from 81% to about 30% after one year. Available data also suggests that sucralfate is at least as effective as cimetidine in maintenance therapy. Sucralfate is effective in the prevention of GU relapse in the dose of 1g in the morning and 2g nocte. Sucralfate is particularly well tolerated. Constipation occurs in 2% of patients and nausea is occasionally encountered. The more convenient dose of sucralfate 2g bd is as effective as the conventional one of 1g qid in DU healing and recent evidence suggests that a single nocturnal dose of 2g nocte offers effective maintenance therapy in DU and GU disease.

Clinical Trials as Topic↗
PubMed1979

Sucralfate: antipeptic, antiulcer activities and antagonism of gastric emptying.

The antiulcerogenic and antipeptic activities of sucralfate (Ulcerlmin), a basic aluminum sucrose sulfate complex, were investigated. In rats, sucralfate inhibited the formation of ulcers induced by pyloric ligation, indometacin and cysteamine. In doses antagonizing forestomach ulcer formation, sucralfate increased the pH of the gastric juice in a dose-related manner. In vitro, at pH 1.9, sucralfate inhibited rat, dog and hog pepsin in a concentration-related manner and also the peptic activity in human gastric juice. Sucralfate may act as an inhibitor of pepsin by precipitating the enzyme or by binding with it reversibly. The antipeptic activity appears to be directly related to the amount of sucralfate in suspension rather than that in solution. In the gastrointestinal tract, the basic nature of sucralfate may enhance the antipeptic activity of the sucralfate molecule. In rats, sucralfate decreases the rate of gastric emptying.

Aluminum↗
PubMed1995

Sucralfate in Helicobacter pylori eradication strategies.

BACKGROUND: Sucralfate monotherapy has been shown to suppress but not eradicate Helicobacter pylori. The combination of sucralfate with antibiotic(s) has been evaluated recently in the treatment of H. pylori-positive duodenal ulcer. The aim of this article is to review the efficacy of sucralfate-containing duotherapy and triple therapy in duodenal ulcer healing and H. pylori eradication rates. METHODS: Reports on duotherapy and triple therapy including sucralfate as the mediating agent were analysed to assess the duodenal ulcer healing and H. pylori eradication rates. RESULTS: One study on duotherapy with sucralfate and amoxycillin achieved an ulcer healing rate of 86% and H. pylori eradication rate of 40%, which compared favourably with sucralfate monotherapy that resulted in duodenal ulcer healing and H. pylori eradication rates of 65% and 0% respectively. A total of six studies have examined triple therapy using sucralfate with two antibiotics. The duodenal ulcer healing rates were generally over 90% and the H. pylori eradication rates about 80% (range 59% to 100%). In one comparative study, the 4-week duodenal ulcer healing and H. pylori eradication rates of sucralfate-containing triple therapy were not distinguishable from those of omeprazole-containing triple therapy. CONCLUSIONS: It is concluded that sucralfate is an effective mediating agent for the eradication of H. pylori in patients with duodenal ulcer.

Anti-Bacterial Agents↗
PubMed1987

Short-term treatment of prepyloric ulcer. Comparison of sucralfate and cimetidine.

A double-blind, randomized, multicenter study was performed to compare the effect of sucralfate (1 g qid) and cimetidine (400 mg bid) in the treatment of prepyloric ulcer. Altogether 142 patients (68 in the sucralfate and 74 in the cimetidine group) with endoscopically confirmed ulcer within 2 cm of the pylorus completed the study. Endoscopic follow up was performed after four weeks and, if the ulcer was not healed, after eight weeks of treatment. After four weeks, 65% of the ulcers in the sucralfate group were healed, compared to 70% in the cimetidine group. There was no significant difference between sucralfate and cimetidine at either time point. The 95% confidence interval for the difference in ulcer healing with sucralfate or cimetidine ranged from +4 to -19% at eight weeks. Said another way, with an observed difference of 7% (83% vs 90%), the 95% confidence limit ranged from 4% in favor of sucralfate to 19% in favor of cimetidine. Symptomatic relief, antacid intake, and side effects did not differ significantly between the two groups. The healing rate of prepyloric ulcer in this study is similar to that reported for duodenal ulcer after four and eight weeks when treated with sucralfate or cimetidine. Sucralfate is safe and as effective as cimetidine in the short-term treatment of prepyloric ulcer.

Adolescent↗
PubMed1990

Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture.

The present study evaluated the effect of sucralfate and its components, sucrose octasulfate and aluminum hydroxide, on: (1) damage to rat cultured gastric mucosal cells induced by sodium taurocholate in a neutral environment and in conditions independent of systemic factors, (2) prostaglandin E2 and on 6-keto prostaglandin F1 alpha release by cultured cells, and (3) sulfhydryl content of cultured cells. Cell damage was quantitated by chromium-51 release assay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were measured by radioimmunoassay. Total sulfhydryl content of cultured cells was determined calorimetrically. Microscopically, sucralfate was found to adhere tightly to epithelial cell surfaces despite frequent washings. Sucralfate 2 mg/ml and 5 mg/ml significantly decreased taurocholate-induced damage, reducing taurocholate-induced specific 51Cr release by 11.8 points (equal to 29% decrease in cell damage, P less than 0.01) and 22.9 points (equal to 56% decrease in cell damage, P less than 0.001), respectively. Sucrose octasulfate and aluminum hydroxide did not exert significant protection against damage induced by sodium taurocholate. The protective effect of sucralfate was not prevented by indomethacin, nor was it counteracted by the sulfhydryl blocker, iodoacetamide. Sucralfate, but not its components, significantly and dose-dependently stimulated prostaglandin E2 (r = 0.94, P less than 0.05) and 6-keto prostaglandin F1 alpha (r = 0.89, P less than 0.05) production by cultured cells. Neither sucralfate nor its components affected sulfhydryl content of cultured cells. In conclusion, sucralfate, but not its components, (1) protects rat gastric mucosal cells against taurocholate-induced damage in conditions independent of systemic factors and in a neutral environment and (2) significantly stimulates prostaglandin production by cultured cells. (3) The protection by sucralfate in vitro does not seem to depend on its stimulatory effect on endogenous prostaglandin synthesis.

Aluminum Hydroxide↗
PubMed1994

Antibacterial activity of sucralfate versus aluminum chloride in simulated gastric fluid.

Studies have previously demonstrated that sucralfate possesses intrinsic antibacterial activity. This study was designed to indirectly assess whether aluminum is the active antibacterial component of sucralfate and to further evaluate factors that may influence this agent's antibacterial activity. Utilizing an in vitro model, the antibacterial activity of sucralfate, an equivalent quantity of aluminum in the form of aluminum chloride, and a control were compared. In addition, the influences of bacterial species (Enterobacter cloacae and Pseudomonas aeruginosa), time (0-24 h) and environmental pH (3,5,7) on the agents' antibacterial activities were evaluated. Equivalent quantities of aluminum, as either sucralfate or aluminum chloride, were added to two of three flasks containing approximately 10(5) cfu/ml of bacteria in pH-adjusted simulated gastric fluid. The third flask served as a control. Samples were obtained over 24 h, diluted and subcultured onto agar plates. The experiments demonstrated that bacterial growth was influenced by pH, time and treatment (aluminum chloride or sucralfate). Regardless of pH or bacterial species, bacterial death occurred within 20 min following the addition of aluminum chloride. In contrast, bacterial death following the addition of sucralfate was more variable and appeared to be pH dependent. In conclusion, sucralfate and aluminum chloride both possess antibacterial activity, even at pH values that normally support bacterial growth in gastric fluid. Although differences in the antibacterial activity of the two agents may in part be related to drug-induced changes in pH, these differences also support data suggesting that aluminum release from sucralfate is incomplete and is dependent on pH.

Aluminum↗
PubMed1987

Clinical efficacy of sucralfate in reflux esophagitis. Comparison with cimetidine.

Sucralfate has been evaluated in reflux esophagitis, based on its protective adherence to denuded surfaces, its bile salt-binding properties, and its cytoprotective properties. Histamine (H2)-receptor blockers are currently considered the standard therapy. The goal of this study was to compare the potential efficacy of sucralfate with that of cimetidine. A single-blind, randomized, multicenter study was performed in 42 patients with endoscopically documented reflux esophagitis. Patients were randomly given 1 g of sucralfate suspension four times daily or 400 mg of cimetidine four times daily for eight weeks. Forty patients were evaluated after eight weeks. Symptomatic improvement was good and comparable in both groups. In two patients given sucralfate and one given cimetidine, side effects were noted but did not necessitate withdrawal from the study. Endoscopy showed improvement in 53 percent of patients and healing of esophagitis in 31 percent after sucralfate treatment. With cimetidine, improvement was seen in 67 percent and healing occurred in 14 percent. In one patient receiving cimetidine, distal esophageal stenosis developed, requiring dilatation therapy. It is concluded that treatment with sucralfate improves the symptomatology and severity of reflux esophagitis. The results obtained with sucralfate appear comparable to those with cimetidine. Sucralfate may therefore be considered as a valid alternative to H2-receptor antagonist therapy in treating reflux esophagitis.

Adult↗
PubMed1987

Multicenter trial of sucralfate suspension for the treatment of reflux esophagitis.

The efficacy of sucralfate suspension in the treatment of reflux esophagitis was assessed in a multicenter, randomized, double-blind, placebo-controlled trial. Sixty-eight patients with symptomatic and endoscopic esophagitis received either sucralfate suspension (n = 31) or liquid placebo (n = 37) for eight weeks. The two groups were comparable at entry with the exception that despite randomization, a disproportionately high number of patients with esophageal ulcers were assigned to receive sucralfate. After four and eight weeks of treatment, both groups had reduced heartburn frequency and severity, but there was no difference in improvement between sucralfate and placebo (p greater than 0.05). Endoscopic results after eight weeks of sucralfate treatment revealed complete healing in 36 percent (placebo, 35 percent) and improvement in an additional 45 percent (placebo, 24 percent). Although neither of these differences was significant, the percent of patients in whom healing or improvement occurred with sucralfate (81 percent) was greater than with placebo (59 percent) (p = 0.07). These data fail to establish that eight weeks of treatment with sucralfate suspension improves symptoms or heals lesions in reflux esophagitis at a rate significantly greater than placebo. However, the unequal distribution of patients with ulcers and the trend toward endoscopic improvement indicate that a potential beneficial effect of sucralfate suspension for the treatment of reflux esophagitis cannot be excluded.

Clinical Trials as Topic↗
PubMed1987

Effects of concurrent sucralfate administration on pharmacokinetics of naproxen.

Sucralfate has been reported to protect the gastroduodenal mucosa against a variety of agents and is known to adsorb bile salts. Since gastrointestinal side effects can seriously compromise the efficacy of nonsteroidal anti-inflammatory drug therapy, and since it seems reasonable to assume that sucralfate may adsorb nonsteroidal anti-inflammatory drugs, the influence of sucralfate on the pharmacokinetic parameters of naproxen was assessed in 12 healthy volunteers. To do so, the pharmacokinetic profile of naproxen, administered alone or with sucralfate, singly or repeatedly (twice daily for five days), was compared. No significant difference was observed with any pharmacokinetic parameter between the single administration of naproxen alone or with sucralfate. However, a significantly lower maximum plasma concentration was attained with the repeated administration of naproxen in combination with sucralfate, compared with the repeated administration of naproxen alone. When single- and multiple-dose administration were compared, significant differences were observed in the maximum plasma concentration and the cumulative area under the curve. These results suggest an accumulation of naproxen after five days' administration. This accumulation, however, is not altered by the administration of sucralfate. The results of this study suggest that when naproxen is administered with sucralfate, only a delay in naproxen's absorption may occur, confirmed by a lower maximum plasma concentration, a longer time to reach the maximum plasma concentration, a similar elimination half-life, and equivalence in bioavailability. The clinical importance of such a delay has yet to be proved; however, it is unlikely that the clinical efficacy of naproxen will be altered, since the amount of drug absorbed remains the same.

Absorption↗
PubMed1989

Epidermal growth factor in the gastroprotective and ulcer-healing actions of sucralfate in rats.

Sucralfate exhibits gastroprotective properties in laboratory animals and enhances the healing of chronic gastroduodenal ulcers, but the mechanisms of these actions have not been entirely elucidated. The present study was designed to determine whether or not epidermal growth factor (EGF), which also has gastroprotective and ulcer-healing properties, contributes to the action of sucralfate in rat stomach. It was confirmed that sucralfate, like 16,16-dimethyl prostaglandin E2, protects the gastric mucosa against ethanol damage and increases mucosal generation of prostaglandins. Removal of the endogenous source of EGF (sialoadenectomy) did not abolish the protective and prostaglandin-stimulating effects of sucralfate. Exogenous EGF and 16,16-dimethyl prostaglandin E2 were also protective in rats with intact and removed salivary glands. Sucralfate, like EGF, enhanced the healing of chronic gastric and duodenal ulcerations induced by serosal application of acetic acid. Sucralfate was found to bind EGF in a pH-dependent manner and to accumulate it in ulcer areas. Thus, the peptide is available locally in high concentrations to accelerate tissue repair and the healing process in ulcerated mucosa. The ulcer-healing effects of sucralfate were reduced with sialoadenectomy and partially restored with oral administration of EGF. It was concluded that EGF is not essential for the gastroprotection induced by sucralfate, but seems to play an important role in the ulcer-healing action of this drug.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Effects of food and sucralfate on the pharmacokinetics of naproxen and ketoprofen in humans.

Compliance to nonsteroidal anti-inflammatory drug therapy can be compromised by gastrointestinal side effects. To overcome this problem, food, antacid, or sucralfate are often co-administered with nonsteroidal anti-inflammatory drugs. Three studies were conducted on three groups of 12 volunteers in order to determine the influence of food or sucralfate on the pharmacokinetics of naproxen and ketoprofen. In a crossover experimental design, the first group received a single dose (50 mg) of ketoprofen with and without sucralfate (2 g). The second group received single (100 mg) and multiple (100 mg twice daily for 5 days) doses of enteric-coated ketoprofen with and without food. The third group received single (500 mg) and multiple (500 mg twice daily) doses of naproxen with and without sucralfate. Multiple blood samples were drawn and analyzed by high-pressure liquid chromatography. Short- and long-term pharmacokinetic parameters were determined. Results in group 1 showed that neither ketoprofen bioavailability nor maximal plasma concentration and time to reach maximal concentration were affected by the administration of sucralfate. However, in group 2 absorption of ketoprofen was markedly affected by food. In the presence of food, maximal plasma concentration decreased from 10.7 to 6.3 micrograms/ml after single-dose administration and 12.1 to 8.0 micrograms/ml after multiple-dose administration. The time to reach maximal plasma concentration was also modified by food, increasing from 2.8 to 7.1 hours after single-dose and 2.8 to 7.6 hours after multiple-dose administration. Food caused a significant decrease in the bioavailability of ketoprofen (over 40 percent) following both single-dose (23.8 versus 13.1 micrograms.hour/ml) and multiple-dose (29.3 versus 16.8 micrograms.hour/ml) administration. Results obtained in group 3 showed that sucralfate reduced the absorption rate constant of naproxen, from 1.7 to 1.2 hours-1 and from 1.5 to 0.7 hour-1 following single- and multiple-dose administration, respectively. However, bioavailability of naproxen was not affected by sucralfate administration. Overall, these studies have shown that sucralfate does not alter the pharmacokinetics of naproxen and ketoprofen; the amount of drug absorbed remains constant. However, plasma concentrations of ketoprofen after single- and multiple-dose administration were greatly affected by food, with a decrease of greater than 40 percent in bioavailability.

Adolescent↗
PubMed1991

Prevention of irradiation-induced bowel discomfort by sucralfate: a double-blind, placebo-controlled study when treating localized pelvic cancer.

Sucralfate, an aluminum hydroxide complex of sulfated sucrose used in the treatment of gastric ulcer, was shown to prevent irradiation-induced diarrhea and bowel discomfort significantly in patients treated for pelvic cancer with external radiotherapy with intent to cure. The double-blind placebo-controlled study included 70 patients with carcinoma of the prostate and urinary bladder without distant metastasis (T1-4NO1xMO) and performance status of greater than or equal to 90% Karnofsky scale. Radiotherapy was administered in a conventional manner with MeV photons and a four-field technique. The total dose was 62-66 Gy and total treatment time of 6.5 weeks. Dose granules of sucralfate or placebo were dispensed to each patient 2 weeks after radiation started and continued for 6 weeks. All analyses were performed blindly. Seven of 34 evaluable patients in the placebo group and 18 of 32 evaluable patients in the sucralfate group did not present with diarrhea during the observation period. The frequency of defecation and stool consistency were significantly improved by sucralfate. Fourteen patients in the placebo group and only three in the sucralfate group required symptomatic therapy with loperamide. There was no evidence of adverse effects associated with the use of sucralfate. Sucralfate can be of beneficial value in diminishing the bowel discomfort during radiotherapy of pelvic malignancies, and the earlier proposed mechanisms of action (e.g., protection of denuded mucosa, cytoprotective properties, binding bile acids) can also be valid for the current effects of sucralfate.

Diarrhea↗