Nonsteroidal anti-inflammatory drugs and peptic ulcer hospitalization rates in New South Wales

NSAID‐induced antral ulcers are associated with distinct changes in mucosal gene expression

“…Major inclusion criteria included: age 50 to 75 years; generally good health; willingness to sign the informed consent. Major exclusion criteria included: (1) use of any NSAID (including aspirin) within past 2 weeks, or history of chronic NSAID use; (2) use of antacids, H-2 blocker within past 2 weeks, or PPI within past 30 days; (3) use of any corticosteroid within past 60 days; (4) history of bleeding tendencies or warfarin use within past 60 days; (5) history of previous bleeding ulcer; (6) consumption of 3 or more alcoholic beverages a day; (7) hypersensitivity or allergy to NSAIDs or other contraindications to their use; (8) baseline abdominal pain, nausea and/or cramping; and (9) the presence of one or more gastroduodenal mucosal breaks (erosions or ulcerations) at a baseline endoscopy. As part of the clinical trial, patients provided consent for biopsies.…”

“…Our secondary objectives were to evaluate: (1) fold changes in subjects treated with placebo; (2) fold changes in duodenal mucosa in patients with antral ulcers compared to fold changes in the duodenum in non-ulcer subjects; and (3) fold changes at the ulcer margin.…”

“…1 Strategies to minimize NSAID-related adverse events include the use of lower drug doses or of less toxic NSAIDs such as COX-2-selective inhibitors, the co-administration and co-packaging of NSAIDs with gastro-protective agents, and the stratification of patients based on risk factors for bleeding. [2][3][4][5][6][7][8] Unfortunately, these strategies have been only partially effective: patient and physician adherence with experts' prescribing recommendations is only fair, 9 while the GI-safety advantage of the COX-2 inhibitors is mitigated by such factors as concurrent aspirin use 10 and cardiovascular safety concerns. 11 It has been observed across different studies and in clinical practice that individuals vary in their vulnerability to gastroduodenal NSAID injury.…”

Outcomes of an educational‐outreach service for community medical practitioners: non‐steroidal anti‐inflammatory drugs

“…It has been estimated that 20% of ulcer haemorrhage or perforation events are attributable to the use of NSAIDs,19 and that NSAIDs are responsible for 30% or more of admissions for these events among elderly people. 12,20 It would be unreasonable to suggest that the DATIS program eliminated the fraction of peptic event admissions attributable to NSAID therapies. Equally, it would be unreasonable to assume that the program has not contributed to the observed effects: there has been a background of reduced community consumption of NSAIDs, and our analysis identified a single change point in hospitalisations at the time of the NSAID focus program.…”

Primary Prevention of Adverse Gastroduodenal Effects from Short-Term Use of Non-Steroidal Anti-Inflammatory Drugs by Omeprazole 20 mg in Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled Study

“…Strategies to minimize NSAID adverse effects include using the smallest effective doses and treating for the fewest effective number of days; avoiding (when possible) the co-prescription of other potentially ulcerogenic agents such as aspirin; prescribing (when appropriate) relatively GI-sparing NSAIDs, such as the cyclo-oxygenase-2 (COX-2) selective inhibitors [3][4][5][6]; and co-prescribing (when indicated) gastro-protective agents (GPAs) [7][8][9]. Many experts recommend stratifying chronic NSAID users according to their risk for GI toxicity [10][11][12][13], but this strategy remains under-utilized in ''realworld'' practice [14][15][16][17][18].…”