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)

Pharmacologic management of peptic ulcer disease continues to evolve with the introduction of diverse types of new therapeutic agents. The ideal aims of treatment of peptic ulcer disease are to relieve pain, heal the ulcer, and delay ulcer recurrence. This article provides a broad perspective on the pharmacology and therapeutic actions of antiulcer drugs. To date, no drug meets all goals of therapy. Drug treatment of peptic ulcers is targeted at either counteracting aggressive factors or stimulating the mucosal defense. Drugs that inhibit or neutralize gastric acid secretion include histamine H2-receptor antagonists, proton pump inhibitors, anticholinergics, prostaglandins, and antacids. H2-receptor antagonists have become first-line drugs for treatment of uncomplicated duodenal ulcers, gastric ulcers, prevention of ulcer relapse, and mild esophagitis. However, H2-receptor antagonists, like other gastric antisecretory/antiulcer drugs, have high rates of ulcer recurrence following discontinuation of therapy. They therefore need to be administered continuously in patients prone to such recurrences. Omeprazole has emerged as a major drug for the treatment of severe erosive esophagitis, refractory ulcers, and Zollinger-Ellison syndrome. The major disadvantage of proton pump inhibitors is the concern for their long-term safety. The roles of M1-antimuscarinic agents and antacids have not been fully defined. Misoprostol, effective for the treatment of gastric and duodenal ulcers, is now the only drug that prevents ulcers induced by nonsteroidal anti-inflammatory drugs. Mucosal protective drugs that do not inhibit gastric acid secretion include sucralfate and organic bismuth salts. Sucralfate is a nonsystemic, well-tolerated, effective drug for treatment of duodenal ulcers and prevention of duodenal ulcer relapse. The organic bismuth salt bismuth subcitrate is efficacious in the treatment of duodenal and gastric ulcers. Furthermore, it has also been established that it alters the course of ulcer recurrence. However, bismuth encephalopathy is a major toxicity concern that needs to be addressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Drugs for treatment of peptic ulcers. 135 99

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

With rare exception, peptic ulcers can now be classified as either Helicobacter pylori-related, induced by nonsteroidal anti-inflammatory drugs (NSAIDs), or related to Zollinger-Ellison syndrome. Helicobacter pylori-related ulcers can be treated by eradication of H pylori or by traditional therapies, including antisecretory drugs or sucralfate. Successful eradication of H pylori requires compliance with a multidrug regimen. Therefore, candidates should demonstrate substantial motivation. In general, the greater the degree of ulcer recurrence or resistance, the stronger the indication for H pylori eradication. Sucralfate is effective in healing H pylori-related duodenal ulcers, and H2 receptor antagonists heal H pylori-related duodenal and gastric ulcers. Omeprazole provides faster healing of H pylori-related ulcers, and is particularly useful in treating large gastric ulcers. Dyspepsia induced by NSAIDs and NSAID-related endoscopic erosions are managed by stopping NSAID use or reducing the dosage; administering NSAIDs with meals; and administering H2 receptor antagonists in full split-doses. NSAID-induced duodenal ulcers and small gastric ulcers can be healed with full split-doses of H2 receptor antagonists, even while the NSAID is continued. Large (> 5 mm) NSAID-induced gastric ulcers are most efficiently treated with omeprazole, particularly if the patient continues to take the NSAID.
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PMID:An etiologic approach to management of duodenal and gastric ulcers. 828 53