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)

Twelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s. for 1 month. Ulcers healed in 8 of the 12 patients without an alteration in the H. pylori-associated antral gastritis. Sucralfate produced a significant fall in basal acid output in all the patients, from a median of 4.8 (range 2.1-12.1) to 1.6 (0.4-8) mmol/h, P less than 0.01, whereas peak acid output was unchanged from 41 (21-59) before to 38 (24-55) mmol/h after treatment. Basal plasma gastrin concentrations and the meal-stimulated integrated gastrin response were not altered significantly by sucralfate: 8 (2-17) pmol/L and 732 (188-1045) pmol. min/L pre-treatment and 6 (2-17) pmol/L and 600 (140-1302) pmol. min/L post-treatment, respectively. The fall in basal acid output observed may contribute to prolonged duodenal ulcer remission after treatment with sucralfate.
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PMID:Sucralfate diminishes basal acid output without affecting gastrin, H. pylori or gastritis in duodenal ulcer patients. 160 44

The end point in peptic ulcer disease is a crater in the mucosa. The cause of gastric ulcers seems to be the breakdown of defensive factors, which then allows damage from endogenous and/or exogenous aggressive factors. Aggressive factors are more important in duodenal ulcer formation. Treatment options discussed herein have similar clinical effectiveness, and all have better results than placebo. Selection of a specific agent should be individualized. Helicobacter pylori infection has been implicated in both gastric and duodenal ulcer formation, and use of triple-drug therapy to eradicate or suppress the organism has decreased recurrence rates when maintenance therapy is not used. However, first-line treatment in acute peptic ulcer disease remains the use of antacids, sucralfate (Carafate), or histamine2 receptor antagonists. This approach to therapy is inexpensive, safe, and effective.
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PMID:Uncomplicated peptic ulcer disease. An overview of formation and treatment principles. 809 30

In some patients, peptic lesions fail to heal after 2 to 3 months of standard histamine2 (H2) receptor antagonist or sucralfate (Carafate) therapy. Noncompliance with prescribed treatment, cigarette smoking, gastric acid hypersecretory states (including Zollinger-Ellison syndrome), Helicobacter pylori infection, the use of nonsteroidal anti-inflammatory drugs, abdominal radiation therapy, and malignant tumors are all causes of refractory disease. Treatment options include high-dose H2 receptor antagonist therapy or switching to a more potent drug or one with a different mechanism of action. Occasionally, drug combinations (eg, H2 receptor antagonist plus misoprostol [Cytotec] for gastric ulcers or H2 receptor antagonist plus metoclopramide [Octamide, Reglan] for reflux disease) are effective. Triple-drug therapy for H pylori infection with refractory duodenal ulcers may allow healing and dramatically decrease recurrence rates. When surgery is required, vagotomy and antrectomy is probably the procedure of choice in patients with peptic ulcer disease that is refractory to medical management. Nissen fundoplication is effective in patients with reflux esophagitis who have adequate esophageal motility.
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PMID:Refractory peptic lesions. Therapeutic strategies for ulcers and reflux esophagitis that resist standard regimens. 809 31