Matching articles for "Duodenal ulcers"

Primary Prevention of Ulcers in Patients Taking Aspirin or NSAIDs

   
The Medical Letter on Drugs and Therapeutics • March 8, 2010;  (Issue 1333)
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are common causes of peptic ulcer disease. Patients infected with Helicobacter pylori who take aspirin or another NSAID have an especially high...
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are common causes of peptic ulcer disease. Patients infected with Helicobacter pylori who take aspirin or another NSAID have an especially high risk. Drugs that have been tried for prevention of ulcers in patients taking NSAIDs including H2-receptor antagonists, proton pump inhibitors (PPIs), aluminum- or magnesium-containing antacids, the prostaglandin misoprostol (Cytotec, and others), and antibiotics to eradicate H. pylori.

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Med Lett Drugs Ther. 2010 Mar 8;52(1333):17-9 | Show Full IntroductionHide Full Introduction

Treatment of Peptic Ulcers and GERD

   
The Medical Letter on Drugs and Therapeutics • August 1, 2008;  (Issue 72)
Peptic ulcers caused by treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) are mainly gastric ulcers. Most duodenal and other gastric ulcers are caused by the gram-negative bacillus Helicobacter...
Peptic ulcers caused by treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) are mainly gastric ulcers. Most duodenal and other gastric ulcers are caused by the gram-negative bacillus Helicobacter pylori. Gastroesophageal reflux disease (GERD) is caused by gastric acid reflux into the esophagus. Drugs that suppress gastric acid production are the primary treatment for GERD and peptic ulcers.
Treat Guidel Med Lett. 2008 Aug;6(72):55-60 | Show Full IntroductionHide Full Introduction

Drugs for Peptic Ulcers

   
The Medical Letter on Drugs and Therapeutics • February 1, 2004;  (Issue 18)
Most peptic ulcers not caused by nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with infection of the gastric mucosa by the gram-negative bacilli Helicobacter pylori. The majority of NSAID-related...
Most peptic ulcers not caused by nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with infection of the gastric mucosa by the gram-negative bacilli Helicobacter pylori. The majority of NSAID-related ulcers are gastric. H. pylori infection causes both duodenal and gastric ulcers. Eradication of H. pylori promotes healing and markedly decreases recurrence of both duodenal and gastric ulcers (A Shiotamni and DY Graham, Med Clin North Am 2002; 86:1447; FKL Chan and WK Leung, Lancet 2002; 360:933). The first step in the management of peptic ulcers is the diagnosis and treatment of H. pylori.
Treat Guidel Med Lett. 2004 Feb;2(18):7-12 | Show Full IntroductionHide Full Introduction

Pantroprazole (Protonix)

   
The Medical Letter on Drugs and Therapeutics • July 24, 2000;  (Issue 1083)
Pantoprazole, the fourth benzimidazole proton pump inhibitor to become available in the United States, has been marketed for short-term oral treatment of erosive gastroesophageal reflux disease...
Pantoprazole, the fourth benzimidazole proton pump inhibitor to become available in the United States, has been marketed for short-term oral treatment of erosive gastroesophageal reflux disease (GERD).
Med Lett Drugs Ther. 2000 Jul 24;42(1083):65-6 | Show Full IntroductionHide Full Introduction

Rabeprazole

   
The Medical Letter on Drugs and Therapeutics • November 19, 1999;  (Issue 1066)
Rabeprazole, a benzimidazole proton pump inhibitor similar to omeprazole and lansoprazole, has been approved by the FDA for treatment of duodenal ulcers, healing and maintenance treatment of erosive or...
Rabeprazole, a benzimidazole proton pump inhibitor similar to omeprazole and lansoprazole, has been approved by the FDA for treatment of duodenal ulcers, healing and maintenance treatment of erosive or ulcerative gastroesophageal reflux disease, and for long-term treatment of chronic hypersecretory conditions, including Zollinger-Ellison syndrome
Med Lett Drugs Ther. 1999 Nov 19;41(1066):110-2 | Show Full IntroductionHide Full Introduction