misoprostol and Peptic-Ulcer-Perforation

Despite the progress in the diagnosis and treatment of Helicobacter pylori-related peptic ulcer disease, it has become apparent that we may be in the midst of an epidemic of nonsteroidal anti-inflammatory drug ulcers and ulcer complications. We also have almost no information about whether there is a link between ulcers in NSAID users and H. pylori infection or whether clinically significant interactions occur.. Current data regarding the diagnosis, prevention, and treatment of NSAID-induced ulcers and the possible relationship between H. pylori ulcers and NSAID use is reviewed.. We need to rethink past conclusions about NSAIDs and gastroduodenal complications and also re-do many of the experiments, taking into account the H. pylori status of the patient (infected, uninfected, cured). It is predicted that the epidemic of NSAID complications will only get worse. Only the future will tell whether selective COX II inhibitors or NO-NSAIDs that incorporate a nitroxybutyl moiety will actually provide the same benefit at lower risk. Until then we must rely on more rational use of NSAIDs, and misoprostol to keep the number of complications at a minimum.

Topics: Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Cyclooxygenase Inhibitors; Helicobacter Infections; Helicobacter pylori; Humans; Misoprostol; Peptic Ulcer; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; United States

The role is reviewed of gastric antisecretory and mucosal protective drugs in the prevention of NSAID-induced gastric and duodenal mucosal lesions. The results of the randomized, double-blind, controlled trials show that misoprostol is the only antiulcer drug proven to be effective in the prevention of NSAID-induced gastric and duodenal ulcers as well as for reducing serious upper gastrointestinal complications (perforation and/or haemorrhage). However, recent data suggest that even omeprazole and high dose of H2-receptor antagonists may have a role in the prevention of NSAID-induced gastric and duodenal ulcerations.

Topics: Adult; Age Factors; Aged; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Duodenal Ulcer; Histamine H2 Antagonists; Humans; Misoprostol; Omeprazole; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Risk Factors; Sialoglycoproteins; Stomach Ulcer

Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with an increased risk of clinical upper gastrointestinal tract (UGI) events, namely, symptomatic ulcer, perforation, bleeding, and obstruction. Our objective in this study was to compare the cost-effectiveness of several strategies aimed at reducing the risk of clinical UGI events in NSAID users.. A decision tree model was used for patients requiring long-term treatment with NSAIDs to compare conventional NSAID therapy alone with 7 other treatment strategies to reduce the risk of NSAID-related clinical UGI events (cotherapy with proton-pump inhibitor, cotherapy with misoprostol, cyclooxygenase [COX]-2-selective NSAID therapy, or Helicobacter pylori treatment followed by each of the previous strategies, including conventional NSAID treatment, respectively). The outcome measure is the incremental cost per clinical UGI event prevented compared with conventional NSAID treatment over 1 year.. The use of a COX-2-selective NSAID and cotherapy with proton-pump inhibitors were the 2 most cost-effective strategies. However, the incremental cost associated with these strategies was high (>$35 000) in persons with a low risk of clinical UGI event with conventional NSAIDs (eg, 2.5% per year). If the baseline risk of clinical UGI events is moderately high (eg, 6.5%), using a COX-2-selective NSAID becomes the most effective and least costly (dominant) treatment strategy, followed closely by cotherapy with a daily proton-pump inhibitor. Because small changes in costs or assumed efficacy of these drugs could change the conclusions, the incremental cost-effectiveness ratios between any 2 strategies were presented in a nomogram that allows the flexible use of a wide range of values for costs and rates of clinical UGI events.. The risk of clinical UGI events in NSAID users depends on their baseline risk, the added risk associated with the individual NSAID, and the protection conferred by cotherapy. A nomogram can be used to incorporate these factors and derive estimates regarding cost-effectiveness of competing strategies aimed at reducing the risk of clinical UGI events.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Cost-Benefit Analysis; Decision Support Techniques; Drug Costs; Health Care Costs; Helicobacter Infections; Humans; Misoprostol; Peptic Ulcer; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Primary Prevention; Proton Pump Inhibitors; Risk Assessment; Risk Factors; United States

Sucralfate is the first drug to be shown to prevent ulceration in bile duct-ligated pigs. Usually such ulceration is uniformly fatal. Seven pigs in each of four groups in this study received only saline, or sucralfate (1 g every six hours), famotidine (40 mg per day), or misoprostol (200 micrograms every six hours). A Foley catheter was placed into a gastrectomy after bile duct ligation. Similar groups of sham-operated pigs were also prepared. After 48 hours, all saline-, famotidine-, or misoprostol-treated pigs showed severe macroscopic ulceration, whereas only two of those treated with sucralfate showed minimal macroscopic ulceration. Until now, only highly selective vagotomy has reduced ulceration caused by bile duct ligation. The present results suggest that acid inhibition is not the only important factor in healing bile duct ligation-induced peptic ulceration.

Topics: Alprostadil; Animals; Anti-Ulcer Agents; Bile Ducts; Famotidine; Ligation; Misoprostol; Peptic Ulcer Perforation; Sucralfate; Swine; Thiazoles