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At least 19 recordsLinked to original sources

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↗

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↗

PubMed1991

The effects of sucralfate and luminal stasis on recovery of the chambered rat gastric mucosa from taurocholate-induced damage.

We have previously shown, using a gastric chamber model, that both sucralfate and luminal stasis protected the rat gastric mucosa against the development of hemorrhagic erosions produced by subsequent exposure for 10 minutes to acidified (50 mM HCl) 80 mM sodium taurocholate (NaT). The protection afforded by sucralfate was abolished by inhibition of cyclooxygenase activity but restored by sucralfate. In this study we demonstrate that indomethacin pretreatment decreases both the depth (in microns) and magnitude (in pH units) of the juxtamucosal pH gradient, but that sucralfate restores these parameters to levels characteristic of normal mucosae. The cytoprotective effect of sucralfate is thus prostaglandin-independent and, at least in part, a consequence of sucralfate-induced increases in the thickness of the juxtamucosal pH gradient/unstirred layer. We have also examined the ability of sucralfate to prevent the otherwise inevitable development of hemorrhagic erosions when it was applied after the gastric mucosa was exposed to NaT. When 100 mg sucralfate in 50 mM HCl was applied for 10 minutes, without stirring, subsequent to a 10-minute exposure of the mucosa to NaT, the average lesion area was reduced from about 15% to less than 3%. Unlike its cytoprotective property, the ability of sucralfate to accelerate the recovery process after damage was abolished by indomethacin pretreatment. Studies using antimony microelectrodes revealed that indomethacin pretreatment resulted in reductions in both the depth and magnitude of the pH gradient that resulted from plasma efflux from the mucosa after exposure to the acidified bile salt. These studies demonstrate that sucralfate is capable not only of prevention or attenuation of acute damage when administered prior to damaging agents, but is also capable of arresting the sequence of events that produces hemorrhage in the previously inflamed or damaged stomach.

Animals↗

PubMed1991

Enhancement of the protective qualities of gastric mucus by sucralfate: role of phosphoinositides.

The effects of intragastric administration of sucralfate on the physicochemical properties of gastric mucus, and the mechanism of its protective action against alcohol-induced mucosal injury were investigated using in vivo and in vitro models. The experiments in vivo were conducted with groups of rats receiving a dose of 100 mg sucralfate twice daily for 5 consecutive days. The animals were sacrificed 16 hours after the last dose, their stomachs dissected, and the mucosa subjected to physicochemical measurements. In the in vitro studies, gastric mucosa was cultured in the presence of sucralfate, ethanol, or both. The in vivo results revealed that sucralfate elicited an 8% increase in mucus gel dimension, while its sulfo- and sialomucin content increased by 63% and 81%, respectively. The changes in mucus gel mucin content with sucralfate were accompanied by a 9.5% increase in mucus hydrogen ion (H+) retardation capacity, 1.9-fold increase in viscosity, and a 60% increase in the gel hydrophobicity. The mucus elaborated in the presence of sucralfate exhibited 14% lower protein content and 62% higher content of carbohydrate than that of control, and contained more neutral lipids. Furthermore, the gastric mucus of the sucralfate group showed a marked increase in mucus glycoprotein polymeric form. The data obtained with gastric mucosal culture demonstrated that sucralfate elicited a significant increase in mucin synthesis, which was reflected in the enhanced metabolism of mucosal phosphoinositides. In contrast, ethanol, which exhibited detrimental effects on mucin synthesis, also caused alterations in the phosphoinositide signal pathway. The changes in mucin and phosphoinositide distribution patterns evoked by ethanol were prevented by sucralfate. Our results suggest that the mucosal strengthening action of sucralfate occurs through the stimulation of the metabolism of phosphoinositide-derived messenger molecules.

Animals↗

PubMed1992

Effects of sucralfate on acute and late bowel discomfort following radiotherapy of pelvic cancer.

PURPOSE: Radiotherapy, a cornerstone in the management of pelvic cancer, is accompanied by intestinal reactions. Therefore, we investigated the possible effects of sucralfate, an aluminium hydroxide complex of sulfated sucrose used in the treatment of gastric ulcer, in preventing radiation-induced diarrhea and bowel discomfort in patients treated with curative intention for pelvic cancer with external radiotherapy. PATIENTS AND METHODS: The study was double-blind and placebo-controlled and included 70 patients with carcinoma in the prostate or urinary bladder without distant metastases (T1-4No1xMo) and a performance status of greater than or equal to 90% on the Karnofsky scale. Radiotherapy was conventionally delivered with high-energy photons (four-field technique, the total dose 64 Gy, 2 Gy daily, total treatment time 5 to 6 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. RESULTS: The frequency of defecation and stool consistency were significantly improved by sucralfate. Fourteen patients in the placebo group and three in the sucralfate group required symptomatic therapy with loperamide. One year later, the patients in the sucralfate group displayed significantly less problems with frequency of defecation, mucus, and blood in the stools compared with the placebo group. There was also a lower intake of loperamide and the weight decrease was less pronounced in the sucralfate group. There was no evidence of adverse effects associated with the use of sucralfate. CONCLUSION: It is suggested that sucralfate can be of beneficial value in diminishing bowel discomfort during treatment and, most importantly, sucralfate also reduces the late bowel disturbances that follow radiotherapeutic treatment of pelvic malignancies. The earlier proposed mechanisms of action (eg, protection of denuded mucosa, cytoprotective properties, binding bile acids) seem adequate to explain the present effects of sucralfate.

Diarrhea↗

PubMed1991

Deposition and gastrointestinal transit of conventional sucralfate tablets.

Sucralfate was labelled with 99mTc by the stannous reduction method. Tablets were compressed using 1 g of radioactive sucralfate and suitable additives. On the first test day, five fully informed healthy volunteers were given one radioactive tablet of sucralfate each, following 10 h fasting. On the second test day, the sucralfate tablet was given after a standard meal. The gastrointestinal transit of the 99mTc-labelled sucralfate was evaluated using gamma camera technique. The labelling of sucralfate with 99mTc by the stannous reduction method enables the deposition and the transition of sucralfate in the gastrointestinal tract to be monitored. The tablets disintegrated almost immediately after administration and the released sucralfate distributed homogenously over the entire stomach area, in both fasted and fed subjects. Transit from the stomach into the intestine was noted already 10 min after administration in fasted subjects, whereas the gastric emptying of sucralfate was markedly delayed in fed subjects. To achieve a wider and more homogenous distribution in the GI-tract, sucralfate tablets should be taken before eating.

Adult↗

PubMed1992

Effect of sucralfate on components of mucosal barrier produced by cultured canine epithelial cells in vitro.

The mucous gel maintains a neutral microclimate at the epithelial cell surface, which may play a role in both the prevention of gastroduodenal injury and the provision of an environment essential for epithelial restitution and regeneration after injury. Enhancement of the components of the mucous barrier by sucralfate may explain its therapeutic efficacy for upper gastrointestinal tract protection, repair, and healing. We studied the effect of sucralfate and its major soluble component, sucrose octasulfate (SOS), on the synthesis and release of gastric mucin and surface active phospholipid, utilizing an isolated canine gastric mucous cells in culture. We correlated these results with the effect of the agents on mucin synthesis and secretion utilizing explants of canine fundus in vitro. Sucralfate and SOS significantly stimulated phospholipid secretion by isolated canine mucous cells in culture (123% and 112% of control, respectively). Indomethacin pretreatment significantly inhibited the effect of sucralfate, but not SOS, on the stimulation of phospholipid release. Administration of either sucralfate or SOS to the isolated canine mucous cells had no effect upon mucin synthesis or secretion using a sensitive immunoassay. Sucralfate and SOS did not stimulate mucin release in the canine explants; sucralfate significantly stimulated the synthesis of mucin, but only to 108% of that observed in untreated explants. No increase in PGE2 release was observed after sucralfate or SOS exposure to the isolated canine mucous cells. Our results suggest sucralfate affects the mucous barrier largely in a qualitative manner. No increase in mucin secretion or major effect on synthesis was noted, although a significant increase in surface active phospholipid release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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↗

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↗

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↗

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↗

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↗

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↗

PubMed1991

Effects of sucralfate, lansoprazole, and cimetidine on the delayed healing by hydrocortisone sodium phosphate of chronic gastric ulcers in the rat.

We have previously shown that chronic sucralfate ingestion stimulates gastric epithelial proliferation in rats, which may explain one of the beneficial effects of sucralfate in healing of peptic ulcers. In a separate study, we have found that chronic steroid administration delays the healing of experimental gastric ulcers in rats. This study was designed to test the beneficial effects of sucralfate, cimetidine, and lansoprazole (AG-1749, a new proton pump inhibitor), on the delayed healing by steroids in rat chronic gastric ulcers. Chronic gastric ulcers were produced in male Wistar rats, weighing 180 g, by the application of 100% acetic acid. The rats were randomly divided into five groups; (1) control, (2) vehicle alone, (3) 10 mg/kg lansoprazole, (4) 500 mg/kg sucralfate, and (5) 100 mg/kg cimetidine. Except for controls, all rats received daily intraperitoneal injections of 2.5 mg/kg hydrocortisone sodium phosphate. Tested drugs were administered intragastrically (lansoprazole and sucralfate) or intraperitoneally (cimetidine) twice a day for 2 weeks. Rats were sacrificed 14 days later and ulcer size was measured. Chronic administration of hydrocortisone sodium phosphate resulted in a significant delay of ulcer healing induced by acetic acid. Treatment with either lansoprazole or sucralfate abolished the deleterious effect of steroids, whereas cimetidine had no effect. These results indicate that lansoprazole and sucralfate overcome the delayed healing by steroids of chronic gastric ulcers in the rat.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1991

Role of acid milieu in the gastroprotective and ulcer-healing activity of sucralfate.

Sucralfate prevents the formation of acute gastric lesions induced by various ulcerogens and enhances the healing of chronic gastroduodenal ulcerations, but the mechanism of these effects has not been fully explained. This study was designed to determine the importance of intragastric pH in the sucralfate-induced gastroprotection against 100% ethanol, acidified aspirin, taurocholate, or stress, and in the healing of chronic gastroduodenal ulcerations induced by acetic acid. Sucralfate acidified to pH 2.0 showed significantly stronger protective activity against all four irritants, its protective potency against 100% ethanol being about eight times greater and the duration of the protection about four times longer than those obtained with sucralfate at its pH of 5.0. Pretreatment with indomethacin to suppress mucosal generation of prostaglandin or the removal of salivary glands to eliminate the endogenous source of epidermal growth factor failed to affect sucralfate-induced gastroprotection. In contrast, the rate of healing of chronic gastric ulcerations was significantly delayed by indomethacin or sialoadenectomy; but sucralfate enhanced the healing, and a marked inhibition of gastric acid secretion by ranitidine did not eliminate this enhancement. We conclude that the protective activity of sucralfate depends on the presence of acid milieu in the stomach, but that the ulcer-healing effects of this drug occur even after a marked inhibition of gastric acid secretion.

Animals↗

PubMed1991

Maintenance therapy with sucralfate in duodenal ulcer: genuine prevention or accelerated healing of ulcer recurrence?

We sought to compare the efficacy of sucralfate to placebo for the prevention of duodenal ulcer recurrence and to determine that the efficacy of sucralfate was due to a true reduction in ulcer prevalence and not due to secondary effects such as analgesic activity or accelerated healing. This was a double-blind, randomized, placebo-controlled, parallel groups, multicenter clinical study with 254 patients. All patients had a past history of at least two duodenal ulcers with at least one ulcer diagnosed by endoscopic examination 3 months or less before the start of the study. Complete ulcer healing without erosions was required to enter the study. Sucralfate or placebo were dosed as a 1-g tablet twice a day for 4 months, or until ulcer recurrence. Endoscopic examinations once a month and when symptoms developed determined the presence or absence of duodenal ulcers. If a patient developed an ulcer between monthly scheduled visits, the patient was dosed with a 1-g sucralfate tablet twice a day until the next scheduled visit. Statistical analyses of the results determined the efficacy of sucralfate compared with placebo for preventing duodenal ulcer recurrence. Comparisons of therapeutic agents for preventing duodenal ulcers have usually been made by testing for statistical differences in the cumulative rates for all ulcers developed during a follow-up period, regardless of the time of detection. Statistical experts at the United States Food and Drug Administration (FDA) and on the FDA Advisory Panel expressed doubts about clinical study results based on this type of analysis. They suggested three possible mechanisms for reducing the number of observed ulcers: (a) analgesic effects, (b) accelerated healing, and (c) true ulcer prevention. Traditional ulcer analysis could miss recurring ulcers due to an analgesic effect or accelerated healing. Point-prevalence analysis could miss recurring ulcers due to accelerated healing between endoscopic examinations. Maximum ulcer analyses, a novel statistical method, eliminated analgesic effects by regularly scheduled endoscopies and accelerated healing of recurring ulcers by frequent endoscopies and an open-label phase. Maximum ulcer analysis reflects true ulcer recurrence and prevention. Sucralfate was significantly superior to placebo in reducing ulcer prevalence by all analyses. Significance (p less than 0.05) was found at months 3 and 4 for all analyses. All months were significant in the traditional analysis, months 2-4 in point-prevalence analysis, and months 3-4 in the maximal ulcer prevalence analysis. Sucralfate was shown to be effective for the prevention of duodenal ulcer recurrence by a true reduction in new ulcer development.

Double-Blind Method↗

PubMed1991

A comparison of sucralfate with placebo in the treatment of esophageal ulcers following therapeutic endoscopic sclerotherapy of esophageal varices--a prospective controlled randomized trial.

In 1984 Roark published the first report of a sucralfate treatment of esophageal ulcers after sclerotherapy. Because this was an uncontrolled trial we planned a prospective double-blind placebo-controlled study with 60 patients. After therapeutic paravariceal injection-sclerotherapy of esophageal varices, patients were randomly treated with sucralfate suspension or placebo. Time of treatment was limited to a maximum of 3 weeks and the dosage of sucralfate was 1 g q.i.d. (Ulcogant-Suspension). Healing was assessed by endoscopy at weekly intervals. Fifty-three patients (25 sucralfate, 28 placebo) were evaluable according to the protocol. No patient left the study because of side effects. At the start of the trial, the patients in the sucralfate group showed a larger ulcer area than the placebo group. There was a tendency to faster healing in the sucralfate group, especially in patients with deeper ulcerations. However, there was no significant difference in global healing between both treatment groups after 3 weeks. Sucralfate suspension may be of value in accelerating the healing process in esophageal ulcers after sclerotherapy, especially in patients with deep ulcers. These results should be confirmed in further trials, in which patients should be stratified with respect to their ulcer volume and severity of liver disease.

Aged↗