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PubMed1985

Sucralfate prevents experimental peptic esophagitis in rabbits.

Sucralfate was tested in a rabbit model for its ability to prevent experimental esophagitis. Esophagitis was assessed by gross appearance and microscopic examination by an uninformed observer. In addition, the permeability of the esophagus to a number of probe molecules was measured to assess barrier function. Animals were exposed for 1 h to either acid alone (HCl at pH 2), acid plus pepsin (0.8 mg/ml), or acid plus taurocholic acid (5 mM), as well as to the same injurious agents with the addition of 1 g of sucralfate. At the completion of this hour, the perfusate was removed and all animals were again perfused for 1 h with HCl at pH 2 while mucosal permeability was assessed by measuring erythritol, glucose, potassium, and sodium fluxes. The animals were then killed. Sucralfate significantly diminished esophagitis and the attendant mucosal permeability changes induced by pepsin. The viscous sucralfate gel was shown to adhere tenaciously to the esophageal mucosa, but this characteristic of sucralfate was found not to be critical for its protective action because a clear sucrose sulfate solution with no gel present was also protective. Hence, it was not necessary for the gel to be present for the drug to be effective. Several in vitro tests suggested that the clear sucrose sulfate solution, like the sucralfate gel, probably acts through a topical protectant effect, rather than through pepsin inactivation. Although the degree of esophagitis induced by the bile acid was significantly less than that observed with pepsin, the mucosal permeability changes were comparable. Sucralfate did not significantly reduce the flux rates of glucose, potassium, and sodium nor did it affect the morphology of the mucosa after exposure to taurocholic acid. In conclusion, the binding of sucralfate to pepsin substrates in tissue results in this agent being very effective in preventing experimental peptic esophagitis.

Aluminum↗

PubMed1990

Gastric mucosal protection by sucralfate involves phosphoinositides participation.

1. The mechanism of gastroprotective action of an antiulcer drug, sucralfate, was investigated. Studies in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received sucralfate followed by ethanol. In the in vitro system, gastric mucosa was cultured in the presence of sucralfate with and without indomethacin. 2. The in vivo experiments revealed that ethanol caused extensive gastric lesions which were significantly reduced following sucralfate pretreatment. Furthermore, sucralfate was also capable of preventing the detrimental effect of indomethacin on gastric mucus gel dimension and its mucin content. 3. The data with gastric mucosal culture showed that the sucralfate elicited increase in mucin was accompanied by the enhanced turnover of mucosal phosphoinositides. 4. Regardless of the inclusion of indomethacin, sucralfate evoked 23% reduction in phosphatidylinositol, 24% increase in inositol-1-phosphate and 3.4-fold increase in inositol-1,4,5-trisphosphate, thus indicating the activation of phosphoinositide-specific phospholipase C. 5. The results demonstrate that the gastric mucosal protective action of sucralfate is not mediated by endogenous prostaglandins, but appears to involve the metabolism of phosphoinositide-derived messenger molecules.

Animals↗

PubMed1997

A phase III double-blind randomised study of rectal sucralfate suspension in the prevention of acute radiation proctitis.

BACKGROUND AND PURPOSE: A limited number of studies have suggested that oral sucralfate reduces the acute and late gastro-intestinal side-effects of pelvic radiotherapy and sucralfate enemas ameliorate symptoms of chronic proctitis. Sucralfate may act via local bFGF at the mucosal level in promoting angiogenesis and reducing epithelial associated microvascular injury. This multi-institutional study was designed to test the hypothesis that sucralfate given as an enema would have a significant protective effect against acute radiation induced rectal injury by direct application to the mucosa. MATERIALS AND METHODS: Eighty-six patients having radiotherapy for localised carcinoma of the prostate were randomised in a double-blind placebo-controlled study to receive either 15 ml of placebo suspension or 3 g of sucralfate in 15 ml suspension, given as a once daily enema during and for 2 weeks following radiotherapy. Assessment was based on the EORTC/RTOG acute toxicity criteria and a patient self-assessment diary. RESULTS: There was no significant difference between placebo and sucralfate for peak incidences of EORTC/RTOG proctitis. For the placebo and sucralfate arms 95 and 88% (difference 7 +/- 11%) suffered some degree of proctitis, with 71 and 61% (difference 10 +/- 19%) reaching grade 2, respectively. The median period to onset of grade 2 proctitis was 33.5 and 36 days, with the median duration being 9.5 and 15 days, respectively, again these difference being non-significant. Thirty-five and 37% of patients rated the effect of radiotherapy on bowel habit as 'a lot' with a moderate or severe effect on normal daily living in 52 and 49%, respectively. CONCLUSION: This study suggests that sucralfate given as a once daily enema does not substantially reduce the incidence of symptoms associated with acute radiation proctitis and its routine clinical use cannot be recommended. This cohort of patients will be followed to determine if any difference develops in relation to late toxicity.

Acute Disease↗

PubMed2001

The effect of oral sucralfate on the acute proctitis associated with prostate radiotherapy: a double-blind, randomized trial.

PURPOSE: Acute rectal complications occur in the majority of patients receiving external-beam radiotherapy for carcinoma of the prostate. Sucralfate has been proposed to reduce radiation-induced mucosal injury by forming a protective barrier on ulcer bases, binding local growth factors, and stimulating angiogenesis. However, there is conflicting clinical evidence as to whether sucralfate, taken prophylactically during radiotherapy, can ameliorate the symptoms of acute radiation proctitis. METHODS AND MATERIALS: A double-blind randomized trial was conducted at four Radiation Oncology Departments in Sydney, Australia, between February 1995 and June 1997. A total of 338 patients with clinically localized prostate cancer receiving small volume radiotherapy, of whom 335 were evaluable, were randomized to receive either 3 g of oral sucralfate suspension or placebo twice a day during radiotherapy. Patients kept a daily record of their bowel symptoms and were graded according to the RTOG/EORTC acute toxicity criteria. RESULTS: One hundred sixty-four patients received sucralfate and 171 received placebo. Both groups were well balanced with regard to patient, tumor, treatment factors, and baseline symptoms, except that the placebo group had a significantly more liquid baseline stool consistency score (p = 0.004). Patients kept a daily diary of symptoms during radiotherapy. After adjusting for baseline values, there was no significant difference between the two groups with regard to stool frequency (p = 0.41), consistency (p = 0.20), flatus (p = 0.25), mucus (p = 0.54), and pain (p = 0.73). However, there was more bleeding in the sucralfate group, with 64% of patients noticing rectal bleeding, compared with 47% in the placebo group (p = 0.001). There was no significant difference between the two groups with respect to RTOG/EORTC acute toxicity (p = 0.88; sucralfate 13%, 44%, 43% and placebo 15%, 44%, 40% for grade 0, 1, and 2, respectively). CONCLUSION: This study suggests that oral sucralfate taken prophylactically during radiotherapy does not ameliorate the symptoms of acute radiation proctitis and may increase acute bleeding. The cause of the increased bleeding in the sucralfate group is unclear. As the pathogenesis of acute and late reactions are different, late follow-up, which includes sigmoidoscopic evaluation, is currently being performed on this cohort of patients.

Administration, Oral↗

PubMed2002

Comparison of granulocyte-macrophage colony-stimulating factor and sucralfate mouthwashes in the prevention of radiation-induced mucositis: a double-blind prospective randomized phase III study.

PURPOSE: To compare granulocyte-macrophage colony-stimulating factor (GM-CSF) mouthwashes with sucralfate mouthwashes in the prevention of radiation-induced mucositis. METHODS AND MATERIALS: Forty patients with radically operated head-and-neck cancer were randomly allocated to use either GM-CSF (n = 21) or sucralfate (n = 19) mouthwashes during postoperative radiotherapy (RT). All patients received conventionally fractionated RT to a total dose of 50-60 Gy in 2-Gy daily fractions during 5-6 weeks to the primary site and regional lymphatics. A minimum of 50% of the oral cavity and oropharyngeal mucosa was included in the clinical target volume. GM-CSF mouthwashes consisted of 37.5 microg GM-CSF and sucralfate mouthwashes of 1.0 g of sucralfate distilled in water. Both washes were used 4 times daily, beginning after the first week of RT and continued to the end of the RT course. Symptoms related to radiation mucositis and body weight, serum prealbumin level, and blood cell counts were monitored weekly. RESULTS: Oral mucositis tended to be less severe in the GM-CSF group (p = 0.072). Complete (n = 1) or partial (n = 4) healing of mucositis occurred during the RT course in 5 patients (24%) in the GM-CSF group and in none of the patients in the sucralfate group (p = 0.049). Patients who received GM-CSF had less mucosal pain (p = 0.058) and were less often prescribed opioids for pain (p = 0.042). Three patients in the sucralfate group needed hospitalization for mucositis during RT compared with none in the GM-CSF group. Four patients (21%) in the sucralfate group and none in the GM-CSF group required an interruption in the RT course (p = 0.042). No significant differences in weight, prealbumin level, or blood cell count were found between the groups, and both mouthwashes were well tolerated. CONCLUSION: GM-CSF mouthwashes may be moderately more effective than sucralfate mouthwashes in preventing radiation-induced mucositis and mucositis-related pain, and their use may lead to less frequent RT course interruptions from mucositis. The present findings need to be confirmed before adopting GM-CSF mouthwashes in routine clinical use.

Adult↗

PubMed2001

Detection of caustic oesophageal injury with technetium 99m-labelled sucralfate.

BACKGROUND/PURPOSE: Radiolabelled sucralfate has been used to show the extent and severity of reflux oesophagitis, peptic ulceration, and inflammatory bowel disease. Endoscopy under general anaesthetic has been the preferred method to assess the injury after caustic ingestion. The aim of this study was to assess whether sucralfate has an affinity for the chemically injured oesophageal mucosa and, if so, to assess the accuracy of radiolabeled sucralfate as an indicator of presence and extent of oesophageal injury. METHODS: A prospective study was conducted of 22 patients with mean age of 30 months (range, 13 to 90) admitted consecutively with a history of caustic ingestion between January 1998 and January 2000. A sucralfate-labelled scan followed by endoscopic assessment of upper gastrointestinal tract with documentation of extent and grade of injury was performed in all patients within 24 hours of admission except the first 6 who underwent scan after the endoscopy. The sucralfate was labelled by the direct stannous reduction method. Oesophageal transit was studied by recording 120 images (64 x 64 matrix size) at 1 image per second while the child swallowed 5 mL of labelled sucralfate containing 2 to 3 MBq Technetium 99m. Retention of radiolabelled oesophageal activity was considered abnormal. RESULTS: The caustic substances ingested were household cleaners in 18, potassium permanganate in 3, and pool chlorine in 1. There were 11 scans that showed residual activity in the oesophagus, which correlated exactly with endoscopic findings. The other 11 patients had normal oesophageal mucosa, but 2 were found to be falsely positive on scanning. In 2 cases repeat sucralfate scan results correlated well with the healing process assessed endoscopically. CONCLUSIONS: The results indicate that technetium 99m sucralfate swallow is an accurate technique for assessing oesophageal injury after ingestion of caustic substances. In addition, it may be used to document healing.

Burns, Chemical↗

PubMed2005

Effect of residual water content on the physico-chemical properties of sucralfate dried gel obtained by microwave drying.

The purpose of this study was to investigate the physico-chemical characteristics of sucralfate humid gel dried by microwaves, in relation to the residual water content. Differential scanning calorimetry (DSC) allowed for the determination of the water state in sucralfate samples. Fourier-transform infrared (FT-IR) spectroscopy was used to monitor the changes in sucralfate gel structure induced by the microwave drying. A boundary value of total water content for sucralfate gel samples was found at 42% (w/w). Below this value only bound water was present, whereas above this value, the increase in total water was due to free water. In the physical form of gel, the strength of the coordination between sulfate anions and the positively charged aluminum hydroxide was dependent on the residual water content. The study of the sedimentation behavior of water suspensions prepared with dried sucralfate allowed for the evaluation of the retention of gel properties. We found that the microwave drying process affected the sedimentation of sucralfate dried gel suspensions independent of the residual water content: when suspensions were prepared from sucralfate dried gel powders containing more than 42% (w/w) of residual water, the sedimentation ratio was higher than 0.9. The non-gel powder suspension showed a sedimentation ratio of 0.68 +/- 0.02, whereas the sucralfate humid gel suspension did not sediment.

Anti-Ulcer Agents↗

PubMed1991

A comparison of the frequency of stress ulceration and secondary pneumonia in sucralfate- or ranitidine-treated intensive care unit patients.

OBJECTIVE: To compare the frequency of acute stress ulceration and secondary pneumonia caused by aerobic Gram-negative bacilli in ICU patients treated with either sucralfate or ranitidine. DESIGN: Prospective, randomized study. SETTING: ICU, university hospital. PATIENTS: Sixty adult patients who were mechanically ventilated and at risk of developing stress ulceration. INTERVENTION: The patients were randomized to receive either sucralfate (1 g every 6 hrs) via the nasogastric tube or iv ranitidine (50 mg every 6 hrs). If the gastric pH was less than 3.5 in the latter group, 30 mL of 0.3M sodium citrate was given via the nasogastric tube. MEASUREMENTS AND MAIN RESULTS: On admission, the frequency rate of erosion/ulceration (assessed with the endoscope) was 13.5%. After 4 days, this rate had increased to 18% in sucralfate-treated patients and 36% in ranitidine-treated patients (NS). Mean gastric pH was more alkaline in the ranitidine-treated patients (5.50) compared with the sucralfate-treated patients (4.26) (p less than .01). This pH permitted a higher occurrence rate of gastric colonization by aerobic Gram-negative bacilli in ranitidine-treated patients (64.3%) compared with sucralfate-treated patients (23.8%) (p less than .01). Retrograde bacterial colonization from the stomach to oropharynx and trachea occurred more frequently in ranitidine-treated patients compared with sucralfate-treated patients. Ultimately, the occurrence rate of pneumonia was greater in the ranitidine-treated (35.7%) than in the sucralfate-treated patients (10.3%) (p less than .05). CONCLUSION: Based on our findings, we recommend the adoption of sucralfate for routine prophylaxis against stress ulceration.

Administration, Oral↗

PubMed1994

Effect of sucralfate on absorption of norfloxacin and ofloxacin.

The effect of sucralfate on the pharmacokinetics of norfloxacin and ofloxacin was assessed in two separate crossover studies with healthy volunteers. In both studies, eight subjects were randomized to one of the following three regimens: a 400-mg dose of norfloxacin or ofloxacin alone, norfloxacin or ofloxacin given simultaneously with sucralfate (1 g), or norfloxacin or ofloxacin given 2 h before sucralfate. Coadministration of sucralfate reduced the bioavailability of norfloxacin and ofloxacin by 91% (P < 0.001) and 61% (P < 0.001), respectively. However, when norfloxacin and ofloxacin were given 2 h before sucralfate, there were no significant alterations in the pharmacokinetics of either fluoroquinolone. Similar results were obtained when the cumulative amount of each fluoroquinolone recovered in the urine was used to calculate bioavailability. To avoid these interactions and potential therapeutic failures, norfloxacin and ofloxacin should not be used concurrently with sucralfate. The interaction can be minimized by maximizing the time between the fluoroquinolone dose and the previous sucralfate dose and giving the fluoroquinolone at least 2 h before another sucralfate dose.

Absorption↗

PubMed1994

In vivo interaction of ketoconazole and sucralfate in healthy volunteers.

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.

Absorption↗

PubMed2004

Effect of sucralfate on antibiotic therapy for Helicobacter pylori infection in mice.

It has been documented that sucralfate, a basic aluminum salt, enhances the efficacies of antibiotics against Helicobacter pylori, resulting in eradication rates comparable to those associated with the use of proton pump inhibitors. However, its mechanism of action remains unclear. The aim of the present study was to investigate sucralfate's ability to complement antibiotic treatment of H. pylori infection in vivo. Four weeks following induced H. pylori infection, clarithromycin (CAM) and amoxicillin (AMPC) were administered orally to C57BL/6 mice for 5 days, both with and without sucralfate or lansoprazole. When sucralfate was concurrently given with CAM and AMPC at the maximum noninhibitory doses for the treatment of H. pylori infection, the bacterial clearance rates were comparable to those achieved by treatment with lansoprazole plus those antibiotics. The results of pharmacokinetic studies showed that lansoprazole delayed gastric clearance and accelerated the absorption of CAM, whereas sucralfate suppressed both gastric clearance and absorption. AMPC was undetectable in all samples. Scanning electron microscopy with a microscope to which a energy dispersive spectrometer was attached revealed that aluminum-containing aggregated substances coated the mucosa surrounding H. pylori in mice receiving sucralfate plus antibiotics, whereas the gastric surface and pits where H. pylori had attached were clearly visible in mice receiving lansoprazole plus antibiotics. The addition of sucralfate to the antibiotic suspension resulted in a more viscous mixture that bound to the H. pylori-infected mucosa and that inhibited the loss of CAM bioavailability in the acidic environment. Sucralfate delays gastric clearance of CAM and physically captures H. pylori through the creation of an adherent mucus, which leads to bacterial clearance.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1990

Sucralfate in the treatment and prevention of gastric ulcer: multicentre double blind placebo controlled study.

A randomised controlled multicentre trial was performed in 160 patients with gastric ulcer, proved by endoscopy and biopsy, to compare ulcer healing with sucralfate and ranitidine (double blind double dummy design) and to assess the effect of maintenance treatment with sucralfate on ulcer recurrence (double blind placebo controlled design). The healing rates were similar with 4 g sucralfate suspension per day and 300 mg ranitidine per day (82% and 88% after 12 weeks, respectively). Of the 109 patients with healed ulcers, 92 were entered into the maintenance trial and treated with sucralfate tablets (2 g per day) or placebo tablets. Maintenance treatment with sucralfate delayed symptoms of gastric ulcer recurrence. Lifetable analysis showed significant differences between sucralfate and placebo, both after six months (p = 0.018) and after 12 months (p = 0.044). The rates of symptom recurrences were 13% and 34% after six months and 34% and 55% after 12 months for sucralfate and placebo, respectively. The rate of asymptomatic recurrences after 12 months was similar in the two groups (9% and 10%, respectively). The recurrence rate was higher in patients who had never taken non-steroidal anti-inflammatory drugs than in those who had but had stopped on admission to the study. It was also higher in patients with recurrent ulcer and in those with scarring deformation and narrowing of the pylorus. Maintenance treatment with sucralfate slowed the appearance of symptom recurrences of gastric ulcer.

Adult↗

PubMed1991

Combined use of ciprofloxacin and sucralfate.

The effect of sucralfate on the bioavailability of ciprofloxacin hydrochloride was assessed in 12 healthy male volunteers. The study was a four-period crossover design where subjects were randomized to one of four treatment sequences at entry. Treatments A, B, and C included sucralfate 2 g q12h for five doses. For treatment A, the fifth dose sucralfate was administered concurrently with ciprofloxacin 750 mg. For treatment B, 750 mg of ciprofloxacin was administered two hours before the fifth dose of sucralfate. Treatment C consisted of ciprofloxacin 750 mg six hours before the fifth dose of sucralfate. A 750-mg dose of ciprofloxacin was administered alone for treatment D. Blood and urine samples were collected at predetermined time intervals for 24 hours. Ciprofloxacin concentrations were determined by HPLC. The area under the concentration versus time curve from zero to infinity and the urinary recovery of ciprofloxacin were used for determining relative bioavailability. Concurrent administration of ciprofloxacin and sucralfate (treatment A) resulted in a significant decrease (p less than 0.05) in ciprofloxacin absorption. The relative bioavailabilities for treatments A, B, and C were 0.0429 +/- 0.0202, 0.829 + 0.21, and 0.965 + 0.32, respectively, relative to ciprofloxacin alone. In normal volunteers, ciprofloxacin may be administered between two and six hours before sucralfate, allowing sufficient time for ciprofloxacin absorption prior to the sucralfate dose and thereby minimizing the chance of a significant interaction. In patients with decreased gastric emptying the interaction may be more difficult to avoid.

Adolescent↗

PubMed2006

The effect of residual water on antacid properties of sucralfate gel dried by microwaves.

The aim of this work was to study the acid neutralization characteristics of microwave-dried sucralfate gel in relation to the water content and physical structure of the substance. Several dried sucralfate gels were compared with humid sucralfate gel and sucralfate nongel powder in terms of neutralization rate and buffering capacity. Humid sucralfate gel and microwave-dried gel exhibited antacid effectiveness. In particular, the neutralization rate of dried gel powders was inversely related to the water content: as the water content of dried powders decreased, the acid reaction rate linearly increased. The relationship was due to the different morphology of dried sucralfate gels. In fact, the porosity of the dried samples increased with the water reduction. However, the acid neutralization equivalent revealed that the dried sucralfate gel became more resistant to acid attack in the case of water content below 42%. Then, the microwave drying procedure had the opposite effect on the reactivity of the aluminum hydroxide component of dried sucralfate gel powders, since the rate of the reaction increased whereas the buffering capacity decreased as the amount of water was reduced.

Antacids↗

PubMed2001

Use of sucralfate in renal failure.

OBJECTIVE: To assess the potential for the development of aluminum toxicity in patients with renal insufficiency or chronic renal failure who are taking sucralfate. DATA SOURCES: Clinical literature accessed through MEDLINE (1966-December 1999) and International Pharmaceutical Abstracts (1970-December 1999). Key search terms included sucralfate, renal failure, renal insufficiency, and end-stage renal disease. DATA SYNTHESIS: Urinary excretion is an important route of elimination for systemically absorbed aluminum. Accumulation of aluminum in patients with impaired renal function may lead to significant toxicity. A potential source of aluminum is the antiulcer medication sucralfate. Studies and case reports evaluating the use and toxicity of sucralfate in patients with normal renal function, as well as those with renal failure or renal insufficiency, were reviewed. CONCLUSIONS: Aluminum accumulation and toxicity have been reported with the use of sucralfate in patients with compromised renal function. The risk of toxicity most likely represents a long-term complication of sucralfate use in this patient population. Toxicity may be enhanced by concurrent use of other aluminum-containing medications, such as phosphate binders or antidiarrheal preparations. These medications, in addition to sucralfate, should be avoided if possible in patients with end-stage renal disease. Patients with renal failure or renal insufficiency who are undergoing prolonged sucralfate therapy should be monitored for potential signs of aluminum toxicity.

Aluminum↗

PubMed1991

Longer relapse-free period after sucralfate than after H2-blocker treatment of duodenal and gastric ulcers.

In a prospective investigation of 2,045 patients with recurrent peptic ulcer disease, the relapse-free period after acute treatment with sucralfate was evaluated over 1 year. This remission period was compared retrospectively with that achieved by previous treatment with a histamine-H2-blocker in the same patients. Only patients who had a symptomatic relapse within 1 year after H2-blocker therapy were included. Patients with no relapses within 1 year after sucralfate were assumed to have a relapse on day 366, in order to compare the two periods. In 73% of the evaluable 2,045 patients, remission after sucralfate was longer than after H2-blocker, and 23% of these patients had no symptomatic relapse at all within 1 year after sucralfate. The average relapse-free period after sucralfate was 212 days, as compared with 132 days after H2-blockers (difference = 80 days; p less than 0.0001). Elderly and nonsmoking patients and those experiencing their first recurrence, or who had a duodenal ulcer, benefited especially from acute treatment with sucralfate. It can be concluded that peptic ulcer patients with a relapse after treatment with an H2-blocker are suitable candidates for sucralfate therapy. There is a high probability that the relapse-free period after sucralfate is longer than after H2-blocker treatment in both gastric and duodenal ulcer patients.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1990

Sucralfate protection of gastric mucosa against alcohol-induced injury: a phosphoinositide mediated process.

The mechanism of protection by sucralfate against gastric mucosal injury induced by ethanol was investigated. The experiments in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received sucralfate followed by ethanol. In the in vitro experiments, gastric mucosa was cultured in the presence of sucralfate, ethanol, or both. The in vivo experiments revealed that ethanol caused extensive gastric hemorrhagic lesions which were significantly reduced following sucralfate pretreatment and that this effect of sucralfate was not prevented by indomethacin. The data with gastric mucosal culture demonstrated that ethanol caused a 24% decrease in mucin synthesis, while mucin synthesis in the presence of sucralfate increased by 32%. This increase was accompanied by the enhanced metabolism of mucosal phosphoinositides, as reflected by a 22% decrease in PI, 1,2-fold increase in IP1 and 3.4-fold increase in IP3. In contrast, ethanol, caused 1.5-fold increase in IP1 and PIP2, and 35% decrease in PIP, 47% decrease in IP2 and 38% decrease in IP3. However, when the mucosal culture was carried out in the presence of both sucralfate and ethanol, the detrimental changes evoked by ethanol in mucin synthesis were prevented. The results suggest that the mucosal protective action of sucralfate involves the metabolism of phosphoinositide-derived messenger molecules.

Animals↗

PubMed1986

Sucralfate protection against gastrointestinal damage: possible role of prostanoids.

The protective effect of sucralfate against gastric and intestinal mucosal damage was studied in rats. Sucralfate (125 mg) significantly reduced gastric mucosal lesion formation induced by s.c. administration of indomethacin (30 mg/kg) or intragastric administration of aspirin (100 mg/kg), HCl (0.6 N), NaOH (0.2 N) or sodium taurocholate (30 mM). Furthermore, when given in three doses of 125 mg each, sucralfate significantly decreased the development of small intestinal lesions induced by indomethacin in the re-fed rat. Gastric mucosal cyclooxygenase activity in sucralfate-treated rats expressed as prostaglandin E2 formation--388 +/- 140 (ng/g wet weight; mean +/- SE)--was significantly higher (P less than 0.01) than its activity in the control--264 +/- 62 (ng/g wet weight). Sucralfate also slightly, but significantly, decreased indomethacin-induced gastric mucosal cyclooxygenase inhibition. Intestinal mucosal cyclooxygenase activity was not affected by sucralfate. The results suggest that gastric and intestinal mucosal damage induced by various ulcerogens is significantly reduced by sucralfate. Sucralfate-induced stimulation of endogenous gastric mucosal prostanoid formation may in part explain its effective protective properties.

6-Ketoprostaglandin F1 alpha↗