Adverse drug reactions from - non-steroidal anti-inflammatories

Reaction systems

Reactions cluster around four systems: GI, renal, cardiovascular, and hypersensitivity/pseudoallergy
Mechanism-based (COX inhibition) rather than idiosyncratic - predictable, dose- and duration-dependent for most effects

Among the commonest causes of drug-related hospital admission (GI bleeding, AKI)
Risk inc sharply with age >65, polypharmacy, and pre-existing renal/cardiac/GI disease

COX-1 inhibition: dec protective gastric prostaglandins -> mucosal injury -> ulceration/bleeding; dec thromboxane A2 -> antiplatelet effect
COX-2 inhibition: dec renal prostaglandins -> afferent arteriolar vasoconstriction -> dec GFR -> AKI, esp. with volume depletion, ACEi/ARB + diuretic ("triple whammy")
- Also -> Na/water retention -> oedema, worsens heart failure, raises BP
Cardiovascular: COX-2 selective inhibition shifts the thromboxane/prostacyclin balance towards thrombosis -> inc MI/stroke risk (class effect, worse for COX-2 selective and diclofenac)
Pseudoallergic reactions: NSAID-exacerbated respiratory disease (Samter's triad - asthma + nasal polyps + NSAID sensitivity) via leukotriene shunting, not IgE-mediated - cross-reacts across the whole class

Clinical + UEC before/during use in at-risk patients (elderly, renal impairment, ACEi/ARB + diuretic combination)
GI: consider gastroprotection (PPI) rather than waiting for symptoms in high-risk patients
Respiratory hypersensitivity - history of worsening asthma/rhinitis with any NSAID -> avoid the whole class (paracetamol and, cautiously, COX-2 selective agents are usually tolerated but should be introduced with care)

Stop the NSAID - most toxicity (renal, GI risk) reverses over days once withdrawn
Avoid the "triple whammy": NSAID + ACEi/ARB + diuretic together - counsel explicitly, this combination causes a disproportionate share of NSAID-related AKI
GI bleeding - manage per gastrointestinal-gi-bleeding pathway; PPI co-prescription for ongoing NSAID use in at-risk patients
Use the lowest effective dose for the shortest duration; consider topical NSAIDs for localised musculoskeletal pain (comparable efficacy, far less systemic exposure)
NSAID-exacerbated respiratory disease - avoid all NSAIDs; aspirin desensitisation is a specialist option if aspirin needed for cardiac indication

Peptic ulcer disease, upper GI bleeding
AKI, hyperkalaemia, worsening heart failure/hypertension
Increased cardiovascular thrombotic events (all NSAIDs except low-dose aspirin)
Interaction with warfarin/DOACs - inc bleeding risk beyond the GI mucosal effect

Renal and GI effects are generally reversible on stopping, provided recognised before severe complication (bleed, dialysis-requiring AKI)
Cardiovascular risk elevation may persist for a period after cessation and inc with cumulative exposure

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