Painkillers for Gout: What to Take
For most people, the over-the-counter painkiller that works for a gout attack is a non-steroidal anti-inflammatory — ibuprofen or naproxen — taken as early in the flare as possible. Paracetamol (acetaminophen) takes the edge off the pain but does nothing to the inflammation causing it. And aspirin, the one many people reach for first, is the wrong choice here for two separate reasons.
The complication is that NSAIDs are not safe for everyone, and many people with gout fall into exactly the groups who should avoid them. This page is about working out which category you are in — then checking it with a pharmacist or doctor, a five-minute conversation that can save you a hospital admission.
Why NSAIDs are the usual answer
A gout flare is an inflammatory event: urate crystals activate the NLRP3 inflammasome, interleukin-1β is released, neutrophils pour into the joint. NSAIDs block prostaglandin production through COX inhibition, damping that response rather than masking the result. That is why they shorten the misery instead of muffling it.
Timing matters more than which one you pick. An NSAID started within the first few hours of a flare works dramatically better than the same drug started on day three, once the cascade is fully amplified. If you get gout regularly, the practical implication is to have a plan agreed with your doctor in advance, so you are not starting from scratch at 2am. What to do first in a gout attack covers the sequence.
Ibuprofen and naproxen are the two commonly sold without prescription in the UK and US. No strong evidence says one full-dose NSAID beats another for gout; naproxen is longer-acting, ibuprofen more flexible. Dosing is a matter for the label and your pharmacist — it depends on your age, kidneys and other medicines, which is why this article gives no numbers.
When NSAIDs are not a good idea
This list is longer than most people expect, and it overlaps heavily with the population that gets gout.
- Reduced kidney function. NSAIDs cut blood flow to the kidneys. In chronic kidney disease — common alongside gout — they can precipitate a sharp deterioration.
- Heart failure. NSAIDs cause fluid retention and can tip decompensation.
- Anticoagulants or antiplatelets. Warfarin, apixaban, rivaroxaban, clopidogrel: combining these with an NSAID raises bleeding risk substantially.
- Peptic ulcer or a previous gastrointestinal bleed. NSAIDs are a leading cause of upper GI bleeding.
- Older adults. Risk rises with age across all of the above; many guidelines advise caution above 65 and real reluctance above 75.
- Uncontrolled high blood pressure or established cardiovascular disease. NSAIDs nudge blood pressure up and carry a small excess cardiovascular risk.
- Asthma worsened by aspirin or NSAIDs — a recognised pattern in some people with asthma and nasal polyps.
- Already taking an NSAID for something else, including a topical one. Doubling up adds risk without adding benefit.
If any of these apply, the answer is not “take it anyway and hope”. Colchicine and corticosteroids exist precisely for these situations, and both need a prescription — see colchicine for gout and gout medications compared. Ask rather than improvise.
Paracetamol: useful, but not for the inflammation
Paracetamol (acetaminophen) works centrally on pain perception. It has no meaningful anti-inflammatory action, so it does not touch the swelling, heat or redness, and on its own it is usually underwhelming against a serious flare — people describe it as taking a flare from unbearable to merely awful.
It earns its place as an add-on: combined with an NSAID it gives better pain control than either alone, and it is often the only option for someone who cannot take NSAIDs and is waiting to be seen. Stay within the label’s daily maximum — paracetamol overdose is silent at first and damages the liver — and watch for it hidden inside combination cold and flu remedies.
Aspirin: the trap
Aspirin looks like it should fit: a non-steroidal anti-inflammatory, on every shelf, cheap. It is still the wrong choice, for two reasons.
First, low-dose aspirin — the 75–100 mg cardiovascular kind — raises serum urate by reducing renal excretion. At that dose it works against you rather than for you. Second, the anti-inflammatory doses of aspirin that might actually help a flare are far higher, and at those doses the side-effect profile is worse than the alternatives; nobody uses aspirin for gout in modern practice.
One thing this article will not tell you to do: if you take low-dose aspirin for your heart or after a stroke, keep taking it. Its cardiovascular benefit outweighs a modest urate effect, and stopping it is a decision only the doctor who started it should make. Mention it at your next gout review instead.
The three options side by side
| Option | Effect on a flare | Main cautions |
|---|---|---|
| Ibuprofen / naproxen (NSAID) | Reduces pain and the inflammation driving it; best started early | Kidney disease, heart failure, anticoagulants, ulcer history, older age |
| Paracetamol / acetaminophen | Reduces pain only; no effect on swelling or heat | Daily maximum; hidden in combination remedies; liver disease |
| Aspirin | Not used for gout; low doses raise urate | Keep taking prescribed low-dose aspirin — just do not use it as your flare painkiller |
What else genuinely helps while you wait
- Rest and elevate the joint. Weight-bearing on an inflamed toe prolongs the pain.
- Cold packs, wrapped and for about twenty minutes at a time. A small randomised trial found ice added to usual treatment improved pain.
- Keep drinking water. It will not end the flare, but dehydration does you no favours.
- Nothing heavy on the joint — a duvet cradle or keeping the foot outside the covers is a reasonable trick.
No food, drink or supplement stops an attack in progress. Cherry juice, apple cider vinegar and bicarbonate of soda all circulate as flare cures; none of them works on the timescale of an acute attack, and the last is a genuinely bad idea for anyone watching their blood pressure. Fast gout pain relief goes through what has evidence behind it.
When over-the-counter is the wrong plan entirely
A hot, swollen joint with a fever, rigors or feeling generally unwell can be septic arthritis — infection in the joint — and that is an emergency. It needs same-day assessment, joint aspiration and antibiotics, not painkillers and a wait-and-see. Having had gout before does not exclude it, and the two can occur in the same joint at the same time.
Also worth same-day advice: a first-ever undiagnosed attack, several joints at once, spreading redness up the foot or leg, or a flare not budging after a few days of treatment.
The larger point
Painkillers manage flares. They do nothing about the cause: serum urate above the level at which crystals form, with targets below 6 mg/dL (360 µmol/L), or below 5 mg/dL (300 µmol/L) with tophi. If you reach for the ibuprofen more than a couple of times a year, the conversation is not about painkillers but about testing your urate and whether urate-lowering treatment is due. Gout is not cured, but controlled to zero attacks is realistic.
Frequently Asked Questions
Can I take ibuprofen with my allopurinol?
Generally yes — there is no direct interaction, and allopurinol is continued through a flare rather than paused. Still worth confirming with your pharmacist, who can check everything else you take at the same time.
Is ibuprofen gel a safer option for a gout toe?
Topical NSAIDs produce far lower blood levels and are gentler on the stomach and kidneys, but penetration into a deep joint is limited and the skin over a flare is often too tender to rub anything into. Ask your pharmacist whether it is worth trying in your situation.
How long should I keep taking an over-the-counter NSAID for a flare?
A gout flare course is short, and the label will give a limit for self-treatment. If you need it beyond that, you should be reviewed rather than continuing on your own.
What to read next
- Fast Gout Pain Relief: What Works
- Colchicine for Gout: Dose and Timing
- Gout Medications Compared
- How Long Does a Gout Attack Last?
