NSAID-induced gastrointestinal and cardiovascular injury.
OBJECTIVE
To review recent publications related to NSAID-induced adverse effects on the gastrointestinal and cardiovascular systems.


RESULTS
This paper explores novel mechanisms of NSAID-induced gastrointestinal injury, highlights new composite endpoints evaluating adverse events of NSAIDs in the entire gastrointestinal tract, and combines published data to establish evidence-based guidance on the best use of NSAIDs to achieve optimal clinical outcomes whilst minimizing cardiovascular and gastrointestinal injuries.


CONCLUSIONS
NSAIDs can induce peptic ulcers via epithelial cell membrane disruption and the renin angiotensin system, independent of the cyclooxygenase (COX) pathways, whereas mast cells and bile acid sensors may have a protective effect on NSAID-induced gastrointestinal damage. Patients with arthritis treated with a COX-2 inhibitor are less likely to develop upper and lower gastrointestinal complications than those who are treated with diclofenac plus a proton pump inhibitor (PPI). PPI therapy is recommended in patients receiving dual antiplatelet treatment but observational studies show that clopidogrel users taking PPIs have an increased risk of cardiovascular events. Until further reliable controlled data are available, this potential, but currently unproven, clinical interaction can be minimized by widely separating the dosing of clopidogrel and PPI. Histamine-2 antagonists may be an alternative to PPI for the prevention of peptic ulcers in patients taking low-dose aspirin.
Ng
Siew C
SC
Institute of Digestive Disease, Chinese University of Hong Kong, Department of Medicine and Therapeutics, Prince of Wales Hospital, Shalin, NT, Hong Kong.
Chan
Francis K L
FK
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D001241:Aspirin / Q000009:adverse effects; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000453:epidemiology; D000077144:Clopidogrel; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects; D004347:Drug Interactions; D005767:Gastrointestinal Diseases / Q000139:chemically induced* / Q000453:epidemiology; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects; D054328:Proton Pump Inhibitors / Q000009:adverse effects; D018570:Risk Assessment; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D006635:Histamine H2 Antagonists; D010975:Platelet Aggregation Inhibitors; D054328:Proton Pump Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin