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PubMed1987

Role of mucus and prostaglandins in the gastric mucosal protective actions of sucralfate against ethanol-induced injury in the rat.

This study investigated the relationship between the protective effect of sucralfate against ethanol-induced gastric mucosal injury in the rat and the effects of sucralfate on prostaglandin and mucus synthesis and secretion. Sucralfate at 200, 400, and 800 mg/kg significantly reduced gastric ulceration. Intragastric administration of sucralfate increased luminal mucus and prostaglandin E2 levels but did not affect prostaglandin or mucus synthesis in gastric mucosal biopsy specimens from sucralfate-treated animals. Pretreatment with indomethacin partially reduced the protective effect of sucralfate. However, sucralfate 200 mg/kg, a dose that completely prevented ulceration, did not increase the levels of luminal prostaglandin E2. In vitro incubation with sucralfate did not stimulate mucosal prostaglandin synthesis. Longer-term administration of sucralfate for 48 or 96 hours did not stimulate mucus or prostaglandin synthesis but did increase luminal prostaglandin E2 and mucus. Although sucralfate increased the gastric juice content of prostaglandin E2 and mucus, the two did not appear to be mechanistically related, and only mucus release was consistently associated with mucosal protection.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Differences in mucosal appearances and in relapse rates in duodenal ulceration treated with sucralfate or cimetidine.

A total of 46 patients with duodenal ulcer were randomly assigned, without the knowledge of the investigators, to treatment with cimetidine 200 mg three times daily and 400 mg at night or sucralfate 1 g four times daily followed by one year of maintenance treatment with cimetidine 400 mg at night or sucralfate 1 g twice daily, respectively, in those patients with healed ulcers. The endoscopic healing rates and relapse rates during the maintenance period were similar, four relapses occurring in each group. All four relapses in the sucralfate group occurred at 12 months and only two were symptomatic. All the cimetidine relapses were symptomatic, two occurring at six months, one at nine months, and one at 12 months. Following the one year maintenance period, 13 cimetidine patients and 11 sucralfate patients were followed up for 36 months. During the first two years, nine of 13 (69 percent) cimetidine-treated and two of 11 (18 percent) sucralfate-treated patients had relapses. During the third year, three more sucralfate-treated patients and one more cimetidine-treated patient had relapses, making a total of 10 of 13 (77 percent) and five of 11 (45 percent) in the cimetidine and sucralfate groups, respectively. Duodenal biopsy specimens obtained before and after healing and after one year of maintenance were examined by light and electron microscopy. The sucralfate group showed greater improvement after one year of maintenance therapy than did the cimetidine group, although the appearances in either group were not predictive of subsequent relapse. The results show that relapses are less frequent and occur later after sucralfate therapy and also that the morphologic appearances are more normal after treatment with sucralfate than after treatment with cimetidine.

Adolescent↗
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↗
PubMed1994

Sucralfate causes malabsorption of L-thyroxine.

PURPOSE: To determine if sucralfate causes malabsorption of L-thyroxine. PATIENTS AND METHODS: Five healthy volunteers ingested L-thyroxine, 1,000 micrograms, administered orally (1) without sucralfate, (2) with sucralfate, 1 g, and (3) 8 hours after sucralfate, 2 g. The amount of L-thyroxine absorbed was calculated from the peak increase in serum T4 levels within 6 hours of hormone ingestion multiplied by the volume of distribution for the hormone. RESULTS: Peak absorption of L-thyroxine in the absence of sucralfate was 796 micrograms (95% confidence interval (CI): 515-1,074 micrograms). Coadministration of sucralfate, 1 g, with L-thyroxine reduced thyroid hormone absorption to 225 micrograms (95% CI: 151-299 micrograms) (P = 0.0029 compared with control). Peak hormone absorption was delayed 2 hours by simultaneous sucralfate ingestion. Separation of administered L-thyroxine and sucralfate doses by 8 hours returned hormone absorption to control values. Maximum T3 levels did not differ, regardless of drug regimen, but suppression of thyroid-stimulating hormone (TSH) by L-thyroxine was reduced by coadministration of sucralfate. CONCLUSIONS: Sucralfate causes malabsorption of L-thyroxine, presumably by intraluminal binding of hormone.

Adult↗
PubMed1994

In vitro analysis of the interaction between sucralfate and ketoconazole.

In healthy volunteers, the bioavailability of ketoconazole is significantly decreased during simultaneous administration with sucralfate. In an effort to address this problem, we examined the interaction between sucralfate and ketoconazole in aqueous solutions and in simulated gastric fluid (SGF) at various initial pHs (1, 2, 3, and 6) in the presence or absence of glutamic acid hydrochloride (GA). Samples from each solution were taken 30 min and 2 h after the addition of ketoconazole to evaluate the solubility of ketoconazole over the usual time period of maximal absorption of ketoconazole in humans. The addition of GA to SGF leads to an increase in solution acidity, while the pHs of SGF at a pH of 1, 2, or 3 are markedly increased by the addition of sucralfate. There is a net decrease in acidity from initial pHs for the pH 1, 2, and 3 solutions when GA and sucralfate are combined. The concentration of ketoconazole in SGF at pHs of 1, 2, 3, 4, and 6 was evaluated in order to assess the pH-dependent solubility properties of the drug in the absence of other interacting species. Regardless of the initial pH, combinations of GA plus ketoconazole showed high concentrations of ketoconazole (approximately 100%) in solution. In contrast, significant decreases in the concentration of soluble ketoconazole were observed when sucralfate was mixed with ketoconazole, and, in some cases, soluble ketoconazole was not detectable. The addition of GA to a mixture of sucralfate and ketoconazole leads to a significant increase in the concentration of solubilized ketoconazole. Nonetheless, important sucralfate-ketoconazole interactions are still observed. After 2 h, approximately 35% of the maximal ketoconazole concentration remained in solution. Comparison of the ketoconazole concentrations at different pHs with the predicted concentrations of the three protonation species of ketoconazole [H2(ketoconazole)(2+), H(ketoconazole)(+), or ketoconazole] showed no correlation. Therefore, the decrease in ketoconazole solubility is not simply a reflection of pH perturbation associated with the dissolution of sucralfate. The observed data are most consistent with a model that has H2(ketoconazole)(2+) or H(ketoconazole)(+) forming an electrostatic interaction with the sucralfate polyanion. The findings of this study suggest that the coadministration of sucralfate with other azole antifungal agents should be investigated.

Chemistry, Pharmaceutical↗
PubMed1988

Effects of sucralfate on gastric prostaglandin and leukotriene synthesis: relationship to protective actions.

The mechanism of the protective actions of sucralfate against ethanol-induced gastric mucosal damage in the rat has been investigated. In particular, the role of prostaglandins as mediators of such protection was assessed. Oral administration of sucralfate at a dose causing a significant reduction of ethanol-induced gastric damage (500 mg/kg) did not significantly alter gastric 6-ketoprostaglandin F1 alpha synthesis. Pretreatment with indomethacin at a dose that inhibited gastric cyclooxygenase activity by an average of 88% did not affect the protective actions of sucralfate. To further investigate the mechanism of action of sucralfate, an ex vivo gastric chamber model was used in which sucralfate could be applied to only one side of the mucosa. Sucralfate did not affect gastric prostaglandin synthesis, but did cause a significant increase in leukotriene C4 synthesis, a fall in transmucosal potential difference, and a significant decrease in gastric myeloperoxidase activity on the side exposed to sucralfate. These observations suggest that sucralfate has an irritant action on the mucosa. The release of mediators in response to such irritation may play an important role in the protective action of sucralfate. The present study supports the hypothesis that prostaglandins do not mediate the protection afforded by exposure to sucralfate.

6-Ketoprostaglandin F1 alpha↗
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↗
PubMed1990

The protective and therapeutic mechanisms of sucralfate.

Sucralfate is a nonsystemic agent that is effective in protecting the gastroduodenal mucosa against injury. In addition, sucralfate is effective in the healing of acute duodenal and gastric ulceration, the therapy of esophagitis, and the prevention of ulcer recurrence. The mechanisms responsible for sucralfate's successful protective and therapeutic actions include the adsorption of pepsin and bile acids, the stimulation of bicarbonate and mucus secretion, and stimulation of endogenous synthesis of prostaglandins. When sucralfate is given to experimental animals or humans, it stimulates endogenous synthesis and release of prostaglandin E2 and inhibits thromboxane release. Pretreatment of animals with the cyclooxygenase inhibitor indomethacin results in a marked decrease in the protective effect of sucralfate against alcohol injury. Sucralfate also increases epidermal growth factor binding to ulcerated areas and stimulates macrophage activity. In addition, sucralfate stimulates endogenous sulfhydryl compounds. At the microscopic level sucralfate protects the vascular integrity of the mucosa and the mucosal proliferative zone. It also stimulates epithelial cell restitution and stimulates cell proliferation. The administration of sucralfate before acute injury results in decreased depth and extent of injury and in acceleration of healing. Because of sucralfate's ability to stimulate the protective and reparative mechanisms of the gastric and duodenal mucosa, it is an important nonsystemic agent for the therapy and prevention of peptic ulceration.

Animals↗
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↗
PubMedDate not supplied

Sucralfate--alternative therapy for peptic-ulcer disease.

The pharmacology, pharmacokinetics, clinical studies, adverse reactions, and dosage of sucralfate (Carafate, Marion Laboratories), a unique drug for peptic-ulcer disease, are reviewed. Sucralfate exerts its antiulcer effect by binding with proteinacious material, neutralizing local acidity without affecting gastric pH, and forming a protective barrier at the ulcer site. It also inhibits the diffusion of hydrogen ion, inhibits the action of pepsin, and adsorbs bile salts. Approximately 3-5% of an orally administered dose of sucralfate is absorbed; more than 90% of the dose is excreted unchanged in the feces. Sucralfate remains at the site of gastric ulcers for up to six hours. In the treatment of duodenal ulcers, sucralfate is more effective than placebo and comparable with cimetidine and intensive antacid therapy. Healing rates for gastric ulcers are less impressive but are comparable with those produced by cimetidine and antacids. Additive or synergistic effects of sucralfate with cimetidine or intensive antacid therapy have not been studied. Sucralfate has few side effects because it is not absorbed; most frequently reported are constipation (3-4%), xerostomia (1%), and skin eruptions (0.6%). No drug-drug interactions have been reported. The recommended dose of sucralfate is 1 g four times a day one hour before meals and at bedtime. Sucralfate is a unique antiulcer drug that compares favorably with cimetidine and antacid therapy in terms of safety and efficacy. Sucralfate is FDA-approved for short-term (up to eight weeks) treatment of duodenal ulcers.

Aluminum↗
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↗
PubMed1989

Protection of rat gastric mucosa by sucralfate. Effects of luminal stasis and of inhibition of prostaglandins synthesis.

Studies using a gastric chamber model demonstrated that sucralfate protected the rat gastric mucosa against hemorrhagic erosions induced by 40 percent ethanol and by acidified 80 mM sodium taurocholate. Protection required continuous contact of sucralfate with the gastric mucosa but it occurred without the production, by sucralfate alone, of significant damage to the luminal epithelium. Ultrastructural examination indicated that sucralfate stimulated mucus secretion by surface epithelial cells. Furthermore, sucralfate was "cytoprotective" in that, in addition to its anti-ulcer effects, it significantly reduced the damaging effects of luminal ethanol on the surface epithelium. Luminal stasis also significantly reduced the extent of hemorrhagic erosions produced by both ethanol and sodium taurocholate, but the most effective reduction in erosions occurred when sucralfate and luminal stasis were combined. Pretreatment with indomethacin abolished the protection provided by luminal stasis, but this protection was restored by sucralfate. Thus, these studies suggest that protection of the gastric mucosa by sucralfate results in part from effects on the unstirred layer. Sucralfate or its products also interact with the epithelial cells and stimulate mucus release and synthesis or release of inflammatory mediators.

Animals↗
PubMed1989

Prevention of upper gastrointestinal bleeding in long-term ventilated patients. Sucralfate versus ranitidine.

Thirty-two long-term ventilated patients were randomly selected for a study of the efficacy of sucralfate (1 g six times per day via gastric tube) versus ranitidine (six 50-mg to six 100-mg doses per day intravenously) for the prevention of upper gastrointestinal bleeding. The patients of the two treatment groups (each 16) were comparable with respect to diseases precipitating acute respiratory failure and risk factors of bleeding, e.g., renal failure, thrombopenia, coagulopathy, and anticoagulant treatment. Mean duration of mechanical ventilation was 7.4 in sucralfate- and 7.7 days in ranitidine-treated patients. During mechanical ventilation, macroscopically visible bleeding developed in three of the sucralfate-treated (18.7 percent) and seven of the ranitidine-treated (43.7 percent) patients. Until the end of the study, only three of the sucralfate-treated but nine of the ranitidine-treated (56.2 percent) patients bled; the difference between the two treatment groups was at all times significant (p less than 0.05). Packed red blood cells had to be administered to the three bleeding patients in the sucralfate group and to seven bleeding in the ranitidine group. Therefore it seems that sucralfate prevented mostly minor bleeding. The high bleeding rate during ranitidine treatment was presumably due to the high number of pH-nonresponders, as almost 30 percent of the gastric aspirates of this group had a pH less than 5. During treatment no difference was found in positive blood culture specimens and bronchial secretions between the two groups. However, nosocomial pneumonia developed in two ranitidine-treated patients, whereas that complication developed in none of the sucralfate-treated patients. In long-term ventilated patients, sucralfate prevented minor upper gastrointestinal bleeding significantly better than ranitidine. However, this does not imply that major upper gastrointestinal bleeding can be prevented by either sucralfate or ranitidine in these patients.

Adolescent↗
PubMed1989

Sucralfate tablets 1 g twice a day for the prevention of duodenal ulcer recurrence.

Sucralfate 1 g twice daily was found to be significantly better than placebo for the prevention of duodenal ulcer recurrence. This was a double-blind, randomized, placebo-controlled, parallel groups study. A total of 254 patients with a history of two or more duodenal ulcers, the most recent event diagnosed within three months of study entry, were entered into the trial after healing was documented. Patients received sucralfate 1 g twice daily or placebo for four months, or until recurrence. Endoscopies and symptom assessments were scheduled monthly and at investigator discretion upon symptom development. Treatment groups were comparable with regard to number of patients, age, sex, smoking status, and ulcer history. Traditional ulcer prevalence and point prevalence analyses were performed. Traditional ulcer prevalence included all ulcers found at scheduled visits and interim recurrences. Point prevalence included only ulcers found at scheduled visits. In the traditional analysis, sucralfate was significantly better than placebo in reducing ulcer recurrence for all months of the study. The life table estimate of the cumulative percent with ulcer at four months was 42 percent for the sucralfate group and 63 percent for the placebo group (p = 0.002). At four months, there were 49 recurrences among 122 patients in the sucralfate group and 71 among 117 patients for the placebo group. In the point prevalence analysis, sucralfate was significantly better than placebo in reducing ulcer recurrence at Months 2 through 4. The life table estimate of the cumulative percent with ulcer at four months was 36 percent for the sucralfate group and 55 percent for the placebo group (p = 0.005). At four months, there were 38 recurrences among 114 patients in the sucralfate group and 54 among 104 patients for the placebo group. Both analyses demonstrated that sucralfate 1 g twice daily was significantly better than placebo for the prevention of duodenal ulcer recurrence. Symptom development was associated with recurrence in both treatment groups. Smoking was associated with a greater tendency to recur in placebo-treated patients only.

Clinical Trials as Topic↗
PubMed1989

Sucralfate protection of human gastric mucosa against acute ethanol injury.

To assess the gastric mucosal protective action of sucralfate against alcohol, a double-blind, controlled, randomized study was carried out in 12 healthy adult men. All subjects received four treatments in a random sequence: sucralfate + ethanol, sucralfate + ethanol placebo, sucralfate placebo + ethanol, and sucralfate placebo + ethanol placebo. Fundal, antral, and duodenal mucosae were submitted to endoscopic examinations, and the antral mucosa underwent histologic examination before and after injury. Biopsy specimens were taken from the antral mucosa to determine by radioimmunoassay its capacity to synthesize prostaglandin E2, thromboxane B2, and 6-keto prostaglandin F1 alpha. In both the fundus and the antrum, the mean endoscopic injury score after sucralfate plus ethanol administration was significantly lower than that after ethanol alone. All treatments tended to increase prostanoid values but 6-keto prostaglandin F1 alpha increased significantly when sucralfate was given. Sucralfate did not affect serum ethanol levels, nor did ethanol affect prostanoid synthesis. It is concluded that sucralfate provides significant protection to the human gastric mucosa against ethanol injury, and that this may be partly due to increased prostanoid synthesis.

Adult↗
PubMedDate not supplied

Acute effects of sucralfate aspiration: clinical and laboratory observations.

STUDY OBJECTIVE: To assess the complications associated with the aspiration of sucralfate. DESIGN: Clinical (case report) and bench observations. SETTING: Inpatient intensive care unit and experimental animal laboratory. SUBJECTS: The case of a critically ill patient who aspirated sucralfate is presented. Fifteen Sprague-Dawley rats served as experimental animals to investigate the acute histologic effects of large-volume aspiration of sucralfate. INTERVENTIONS: The patient underwent emergent intubation to relieve acute upper airway obstruction. All the animals were anesthetized and had tracheostomies performed. The experimental groups had acidic intratracheal injections of 2 ml/kg of a nonparticulate liquid (pH, 2.3; n = 6) or a sucralfate aspirate (1 ml/kg of a 5% sucralfate suspension of pH 3.6, followed by 1 ml/kg 0.1 of normal hydrochloric acid of pH 1.0; n = 4). Four hours after simulated aspiration, the rats were sacrificed and their lungs removed for histologic examination by light microscopy. MEASUREMENTS AND MAIN RESULTS: Differences were noted in histopathologic injury in the experimental groups compared to the control group using a numeric scoring scale. Nonparticulate acidic liquid aspiration caused a significant increase (p < 0.05) in inflammation. Sucralfate caused a significant increase (p < 0.05) in lung hemorrhage. A nonsignificant trend was seen with simulated sucralfate aspiration for edema and inflammation. No long-term sequelae were attributed to the clinical aspiration episode. CONCLUSIONS: Acute complications associated with aspiration of sucralfate have been identified. In the laboratory setting, simulated aspiration of sucralfate led to acute lung injury.

Acute Disease↗
PubMed1987

Sucralfate overcomes adverse effect of cigarette smoking on duodenal ulcer healing and prolongs subsequent remission.

A unicenter, single-blind, randomized study was conducted on 283 patients with active duodenal ulcer to compare possible factors that may affect healing and relapse in patients treated with a potent antisecretory agent, cimetidine, or a site-protective and cytoprotective agent, sucralfate. The endoscopic healing rates at 4 wk were 76% and 79%, respectively, and cross-over treatment of the failures for a further 4 wk resulted in 68% healing with cimetidine and 69% healing with sucralfate, both differences being not statistically different. Unlike cimetidine, healing by sucralfate was unaffected by cigarette smoking, reluctance to give up smoking, habitual use of alcohol, high maximal acid output, and large ulcer diameter. In particular, the healing rate of smokers treated with sucralfate (82%) was significantly greater than that of smokers treated with cimetidine (63%). Duodenal bulb deformity significantly affected healing in both groups, and was the only offsetting factor identifiable for sucralfate out of 46 factors examined. Of the patients with healed ulcers, 238 participated in a 24-mo follow-up study consisting of interviews at 2-mo intervals and endoscopy at 4-mo intervals or whenever symptoms recurred. The cumulative relapse rate was significantly (p less than 0.007) greater in patients healed with cimetidine than with sucralfate, 50% relapse occurring at 6 and 12 mo, respectively. In both, the cumulative relapse rate was significantly greater in cigarette smokers than in nonsmokers, but smokers and nonsmokers treated with cimetidine relapsed (50% at 4 and 8 mo, respectively) faster than the corresponding smokers and nonsmokers treated with sucralfate (50% at 8 and 18 mo, respectively). Furthermore, in cimetidine- but not sucralfate-healed patients, early ulcer relapse (within 6 mo) was associated with short duration of illness, short remission period, long symptomatic spell, and reluctance to give up smoking. We conclude that smoking adversely affects duodenal ulcer healing by cimetidine and hastens subsequent relapse, and that sucralfate overcomes the adverse effect of smoking on healing as encountered with cimetidine, and results in a subsequent remission period double that of cimetidine.

Adult↗