Ulcers, Helicobacter pylori infection, platelets and gastrointestinal complications of non-steroidal anti-inflammatory drugs: what are the connections?
The term "gastropathy", and discussion surrounding the adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) on the gastrointestinal (GI) tract, suggests that most of the complications arise from injury to the gastric mucosa, resulting in gastric ulcers that develop complications. The commonest GI complication is bleeding, which results principally from thrombocytopathy or impaired platelet function in the presence of various underlying GI conditions, including but not confined to antecedent peptic ulcer disease, and in some cases ulcers caused by NSAIDs. In unselected cases, bleeding as a result of aspirin or NSAID may occur early in the course of treatment, much of it predictable from a careful history, taken to identify well-defined risk factors, including previous peptic ulcer disease, GI bleeding, or concomitant treatment with steroids, anticoagulants, or anti-platelet drugs. Only in the presence of such risk factors is NSAID use likely to be associated with a serious GI complication. Although GI complications are common in such cases, attributability of the event solely to NSAIDs is low. Attributability of the complication to the drug is highest when NSAID use is the sole risk factor: the estimated incidence of complications in this setting is only about 10% of all NSAID-associated GI complications. In estimating the likely outcome of therapy, the risk factors identifiable from the history in each case before treatment are more important than the choice of NSAID. Independently analysed, the VIGOR and CLASS trials showed that use of rofecoxib or celecoxib caused fewer clinical ulcers and bleeding, but much of the bleeding observed did not arise from ulcers or from sites proximal to the ligament of Treitz. This suggests that the main value of these drugs is the absence of thrombocytopathy: their safety is substantially reduced by concomitant treatment with low doses of aspirin. This paper analyses the separate roles of COX 2-selective agents, H. pylori eradication, and concomitant aspirin prophylaxis or treatment with acid-suppressant drugs.
McCarthy
Denis M
DM
Veterans Administration Medical Center and University of New Mexico School of Medicine, Albuquerque, New Mexico 87108, USA. denis.mccarthy2@med.va.gov
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D004008:Diclofenac / Q000494:pharmacology / Q000627:therapeutic use; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced* / Q000453:epidemiology; D016481:Helicobacter Infections; D006801:Humans; D007052:Ibuprofen / Q000627:therapeutic use; D007783:Lactones / Q000627:therapeutic use; D009288:Naproxen / Q000494:pharmacology / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000188:drug therapy* / Q000382:microbiology*; D012307:Risk Factors; D013450:Sulfones / Q000627:therapeutic use
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D007783:Lactones; D013450:Sulfones; C116926:rofecoxib; D004008:Diclofenac; D009288:Naproxen; D007052:Ibuprofen