NSAIDs

Yes, and the better agents clear the bar convincingly. In a network meta-analysis of 76 trials, diclofenac 150 mg/day and etoricoxib 60 mg/day both reached the pre-specified minimum clinically important effect with 100% probability. This is a real drug effect, not a marginal one — which is precisely why the harms matter enough to be worth understanding.

There is not. The risks run in opposite directions. Naproxen has the least vascular risk of the traditional NSAIDs — but the HIGHEST upper-gastrointestinal complication risk of the common agents. Diclofenac, the most-used NSAID globally and available over the counter in many countries, carries vascular risk comparable to the COX-2 inhibitors it is often chosen instead of. Celecoxib has the best gastrointestinal profile and, at moderate doses in a 24,081-patient randomised trial, was non-inferior to ibuprofen and naproxen for cardiovascular safety. The right choice is the one that avoids the organ most likely to be your problem — and that is a conversation with a clinician, not a ranking.

They beat placebo, but barely. Across 32 trials, NSAIDs improved acute back pain by about 7 points on a 100-point scale versus placebo; the Cochrane authors' own verdict is that 'the magnitude of these effects is small and probably not clinically relevant'. For chronic back pain the difference shrinks to about 3 points, and shrank further when only low-risk-of-bias trials were included. Paracetamol, meanwhile, does nothing at all here. The honest summary for back pain is that neither drug class is a good answer, and BioSignal would rather say that than pick the less-bad one and call it a treatment.

This is two different claims and only one of them is supported. ACUTE kidney injury risk is real: pooled odds ratio about 1.7 in the general population, and higher in older people. But ACCELERATED PROGRESSION of chronic kidney disease at regular doses is NOT supported — the pooled odds ratio is 0.96, spanning no effect, and only high-dose use showed an association (OR 1.26). The reviewers' own conclusion is that medium-term avoidance of NSAIDs in moderate-to-severe CKD is 'unnecessary' if not otherwise contraindicated. Guidelines still counsel caution and monitoring, which is reasonable. But the popular claim that ordinary NSAID use destroys kidneys over time is an overstatement, and BioSignal corrects it in the anti-alarmist direction.

For knee osteoarthritis, topical NSAIDs are the guideline's FIRST-LINE drug — NICE offers them before an oral NSAID — and head-to-head Cochrane data show similar efficacy to oral, albeit at low certainty. The effect is modest in absolute terms (about one additional person in ten achieves at least 50% pain relief beyond the carrier gel), and the evidence is derived almost entirely from KNEE osteoarthritis, not hand. Systemic adverse events were not increased where reported, though that evidence is graded very low certainty. Under-used, not weaker.

PPIs clearly reduce ULCERS SEEN ON ENDOSCOPY — a large reduction, at moderate certainty. Whether they reduce the outcomes that actually matter — perforation, bleeding, obstruction — is a weaker claim: the pooled estimate points in the right direction but the confidence interval crosses no effect, and the certainty is low. PPIs also protect only the upper gut: in a trial of high-risk patients, a COX-2 inhibitor alone caused far fewer combined upper AND lower gastrointestinal events than diclofenac plus a PPI. Co-prescription is sensible and guideline-recommended. It is not a licence to ignore the risk.

There is a genuine pharmacodynamic interaction — ibuprofen competes with aspirin at the same site on the COX enzyme — and the FDA advises taking ibuprofen at least 30 minutes after, or at least 8 hours before, immediate-release low-dose aspirin. But the FDA is far more hedged than the popular framing: the clinical impact has never been tested in an endpoint trial, the epidemiological data are equivocal, and a negative effect on aspirin's cardioprotection is 'unlikely from an occasional dose'. Regular daily ibuprofen in someone on aspirin is worth a conversation. One tablet for a headache is not a crisis.