Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D00446 (Sucralfate)
 278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sucralfate is used to induce healing of gastrointestinal tract ulcers. We evaluated its potential utility in the healing of skin wounds. Initial experiments examined the effects of the sucralfate on proliferation of cultured dermal fibroblasts and keratinocytes. Sucralfate induced proliferation in quiescent cultures of both cell types. Additionally, sucralfate enhanced prostaglandin E2 synthesis in basal keratinocytes and in interleukin-1-stimulated keratinocytes and dermal fibroblasts. Basal interleukin-1 and 6 release were not affected by sucralfate, but the agent enhanced interleukin-1-stimulated interleukin-6 release from fibroblasts. When applied daily to full-thickness wounds in rats, sucralfate increased the thickness of granulation tissue when assessed at day 12.
Agents Actions 1991 Sep
PMID:Sucralfate induces proliferation of dermal fibroblasts and keratinocytes in culture and granulation tissue formation in full-thickness skin wounds. 179 36

The present study was carried out to examine the comparative efficacy of sucralfate and ranitidine in the treatment of duodenal ulcer. Sixty-six patients with endoscopically diagnosed duodenal ulcer were studied in a 4-6 weeks randomised, single blind trial comparing sucralfate 1 gm T.D.S. one hour before meal and 1 gm nocte (34 pts) with ranitidine 300 mg nocte (32 pts). Six patients (four on sucralfate and 2 on ranitidine) failed to complete the study. Endoscopy after four weeks of treatment showed an ulcer healing rate of 57% in the sucralfate group compared with 73% in ranitidine group (p greater than 0.1). At six weeks these figures had risen to 87% and 90% respectively (p less than 0.5). After one year followup study 69% of sucralfate treated ulcers relapsed whereas the relapse rate was 82% in ranitidine treated ulcer group (p less than 0.1). It was observed that the relapse was earlier in the ranitidine group as compared to sucralfate group (p less than 0.01 at 3 months and p less than 0.05 at 6 months). Asymptomatic recurrence was seen in 15% (6/40) patients. Sucralfate was not only as effective as ranitidine in short term healing of duod. ulcer but also delayed the relapse of ulcer in long term followup after initial healing with the drug.
J Assoc Physicians India 1990 Sep
PMID:A comparative therapeutic trial of sucralfate and ranitidine in initial healing and relapse rate of duodenal ulcer. 209 28

More than a dozen NSAIDs are commercially available in the United States. Diclofenac may not be as effective for dysmenorrhea. Although most are equally efficacious, indomethacin is the preferred agent for hemicrania continua and chronic paroxysmal hemicrania. Although all NSAIDs should theoretically be beneficial in gout, the greatest experience is with indomethacin. Sulindac may be the preferred agent for diabetic neuropathy. Fenoprofen appears to be the most offensive NSAID in terms of nephrotoxicity. NSAIDs may antagonize antihypertensive therapy, although this effect may not persist beyond 1 month. Generally, use of NSAIDs in pediatric patients is limited to naproxen and tolmetin. Concomitant therapy with methotrexate, lithium, and AZT should be approached with caution. NSAIDs have similar propensities to cause gastrointestinal side effects. Sucralfate has consistently proved beneficial as cytoprotective therapy for use with NSAIDs without impairing absorption of the NSAID, NSAIDs generally should be avoided prior to surgery, although sulindac or nonacetylated salicylates have a negligible effect on platelet function and may be used if continued NSAID therapy is required. Hepatotoxicity, although rare with NSAIDs, is most common with phenylbutazone and least common with the fenamates.
Prim Care 1990 Sep
PMID:Current issues in NSAID therapy. 223 38

Sucralfate is known for its gastroprotective properties in humans and rats, but the importance of intragastric pH in this protection is a subject of controversy. This study, performed on healthy young volunteers and rats, was designed to compare the gastroprotective effects of sucralfate with those of sucralfate combined with ranitidine or of sucralfate adjusted to pHs varying from 1 to 7. In humans the mucosal damage induced by 40% ethanol spray after 4 days of pretreatment with placebo, sucralfate (1 g four times daily), ranitidine (150 mg three times daily), or the combination of sucralfate plus ranitidine was evaluated by means of endoscopy with mucosal biopsy and histologic examination. Sucralfate alone reduced the endoscopic score significantly (compared with placebo) and prevented deep necrotic lesions. Neither ranitidine alone nor its combination with sucralfate prevented ethanol-induced endoscopic and histologic mucosal changes. In rats acute gastric lesions were induced by 100% ethanol. Sucralfate was relatively more effective in mucosal protection against ethanol when given at lower pH (1 or 2) than at original pH (4.5) and failed to protect at neutral pH (7.0). Pretreatment with ranitidine, which by itself did not change ethanol damage, greatly reduced the protection afforded by sucralfate. We conclude that sucralfate protects the gastric mucosa against ethanol damage both in humans and in rats and that this protection is dependent on the presence of an acidic intragastric pH.
Scand J Gastroenterol 1989 Sep
PMID:Importance of an acid milieu in the sucralfate-induced gastroprotection against ethanol damage. 267 24

The effect of Campylobacter pylori infection and sucralfate treatment on the ion-exchange property of human gastric mucus from 17 human postmortem stomachs was investigated in an in vitro chamber. Of the 10 stomachs not infected with C. pylori mucus from 4 stomachs had a 'normal' Na+/H+ exchange capacity, whereas 6 were without a Na+/H+ exchange capacity. The Na+/H+ exchange capacity of the seven stomachs infected with C. pylori was half that of the four 'normal' uninfected stomachs. Sucralfate significantly improved the Na+/H+ exchange capacity of mucus from C. pylori-infected stomachs and from the uninfected stomachs without Na+/H+ exchange. This study shows that impairment of the Na+/H+ exchange capacity of gastric mucus is associated with C. pylori infection and that sucralfate improves the Na+/H+ exchange capacity of gastric mucus.
Scand J Gastroenterol 1989 Sep
PMID:Na+/H+ ion-exchange property of postmortem human gastric mucus. The effects of Campylobacter pylori infection and sucralfate. 279 81

Standard oesophageal scintigraphic techniques using 99mTc-colloids rarely identify oesophageal mucosal damage. Sucralfate can be labelled with 99mTc for the detection of oesophageal mucosal ulceration. This method uses two separate supine swallows of 10 MBq 99mTc-colloid in 10 ml, followed by a single supine swallow of 30 MBq 99mTc-sucralfate. The data are processed to give time-activity curves, mean transit times and condensed dynamic images. When oesophageal ulceration is detected, the time-activity curves using sucralfate show residual activity in the oesophagus after the transit time indicated by the colloid swallow. The condensed dynamic image shows a persistence of activity at the level of the ulceration. Erect sucralfate images taken immediately after the dynamic sequence show no oesophageal localisation. The results from a study of 62 patients have shown excellent correlation between the dynamic 99mTc-sucralfate images and endoscopy findings. Sequential sucralfate studies for healing also correlate well. The use of labelled sucralfate to detect oesophageal ulceration could modify the indications for endoscopy in gastrooesophageal reflux disease.
Gut 1989 Sep
PMID:Dynamic radionuclide imaging with 99mTc-sucralfate in the detection of oesophageal ulceration. 280 94

Fifty patients in whom endoscopy revealed peptic esophagitis were included in a double-blind study in which either sucralfate (1 g four times a day) or an alginate/antacid compound (5 g four times a day) were randomly assigned. After six weeks of treatment, efficacy and clinical safety were evaluated in 23 patients in the sucralfate group and 22 patients in the alginate/antacid group. No significant difference between the two treatments was detected with regard to efficacy, evaluated on the basis of clinical and endoscopic criteria. Clinical safety was also good in both groups. Sucralfate was, therefore, found to be as effective and as well tolerated as the alginate/antacid compound in the treatment of peptic esophagitis.
Am J Med 1987 Sep 28
PMID:Sucralfate versus alginate/antacid in the treatment of peptic esophagitis. 282 8

Syrup of ipecac (SOI) is a commonly used emetic for toxic ingestions. A preliminary study was undertaken to quantify the efficacy of SOI-induced emesis. Three groups of adult subjects fasted overnight before ingestion of 1 mCi of Tc-99m human serum albumin-sucralfate. Sucralfate is minimally absorbed from the gastrointestinal tract and has a gastric clearance half-time of 90 minutes, approximately equal to that of solid foods. At 5, 30, and 60 minutes after ingestion of radiolabeled sucralfate (RSC), subjects were given a standard dose of 30 ml SOI and 240 ml of water. Gastrointestinal tract images were obtained both at the time of ingestion of RSC and 60 minutes after ingestion of SOI. Regions-of-interest were drawn and activity measured over the stomach and small bowel with correction for physical decay. Those subjects (N = 10) treated at 5 minutes after ingestion retained a mean value of 17% of the administered RSC by 60 minutes. The group (N = 5) treated at 30 minutes after ingestion retained a mean value of 41%, while those (N = 5) treated at 60 minutes retained a mean value of 56%. The results tend to confirm the efficacy of SOI-induced emesis when SOI is given promptly (i.e., 5 minutes) following ingestion, and generally support efforts to assure widespread immediate availability of SOI for toxic ingestions.
Clin Nucl Med 1988 Sep
PMID:Efficacy of syrup of ipecac-induced emesis for emptying gastric contents. 290 46

In a prospective, controlled, randomized study of the prophylaxis of stress bleeding, 100 ventilated high-risk patients in a surgical intensive care unit received, on a daily basis, 1 g of sucralfate suspension (n = 50) every four hours, or an antacid (n = 50) every two hours. The mean duration of the treatment was about six days in both of the groups. Gastric pH was determined every eight hours. Bleeding was defined as macroscopically visible bleeding. The intragastric pH was less than 4 significantly more often in patients treated with sucralfate. In each group, one case of macroscopically visible bleeding occurred. Both of the patients had a very high risk of bleeding. None of the bleedings influenced the outcome of the patients. When patients with primary thoracic trauma or pneumonia were excluded, nosocomial pneumonia developed in significantly fewer (p less than 0.05) patients in the sucralfate group (three of 29) than in the antacid group (11 of 32). In four of the latter patients, pneumonia influenced the outcome of the patients. Sucralfate provides adequate protection against stress bleeding while also minimizing the danger of pneumonia caused by infection via the gastropulmonary route.
Am J Med 1987 Sep 28
PMID:Risk of acute stress bleeding and nosocomial pneumonia in ventilated intensive care unit patients: sucralfate versus antacids. 331 Jun 26

In a randomized, double-blind trial, sucralfate therapy, 1 g four times daily, was compared with placebo in 143 symptomatic patients to assess the treatment of gastrointestinal symptoms and gastric mucosal damage associated with nonsteroidal anti-inflammatory drugs (NSAIDs). All patients followed a fixed regimen of NSAIDs, were assigned to one of two groups based on the presence or absence of gastric erosions at baseline endoscopy, and were then assigned randomly to receive sucralfate or placebo for four weeks. Patients were then followed for up to six months while receiving open-label sucralfate 1 g twice daily to up to 1 g four times daily. After four weeks of double-blind therapy, patients taking either nonsalicylate NSAIDs or long half-life NSAIDs and who were treated with sucralfate experienced a significant reduction in both peptic symptom frequency and intensity (p less than 0.03) as compared with patients receiving placebo. Sucralfate-treated patients with baseline endoscopic lesions showed a significant reduction in lesion scores (p less than 0.005) at four weeks as compared with baseline, whereas no improvement was observed in gastric mucosal lesions of patients given placebo. Long-term sucralfate therapy resulted in continued improvement in gastrointestinal symptoms and gastric lesion scores in patients receiving all types of NSAIDs. The results indicate that sucralfate used in conjunction with NSAIDs may allow patients to continue therapy by relieving gastrointestinal symptoms and mucosal damage associated with NSAID therapy.
Am J Med 1987 Sep 28
PMID:Sucralfate treatment of nonsteroidal anti-inflammatory drug-induced gastrointestinal symptoms and mucosal damage. 331 Jun 31


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