Excruciating, and one of the few forms of arthritis that can be prevented almost entirely.
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Gout is a form of inflammatory arthritis caused by urate crystals forming inside a joint. The immune system attacks the crystals, and the result is one of the most severe pains in medicine — typically arriving overnight, in one joint, from nothing.
It affects around one in forty adults in the UK and is becoming more common. It is also, unusually among forms of arthritis, completely controllable — keep the urate level low enough for long enough and the crystals dissolve and the attacks stop permanently.
Despite that, gout is badly managed nationally. Two misunderstandings account for most of it.
The first is that gout is caused by diet and rich living. It is not, mainly. Around 90% of people with gout have kidneys that excrete urate less efficiently — which is largely genetic. Diet contributes at the margin, and blaming the patient has meant decades of dietary advice instead of the treatment that works.
The second is that allopurinol is for after attacks. Starting urate-lowering treatment can trigger an attack in the first months, people assume the drug caused their gout, and they stop — losing the one treatment that would have cured it. Taken with cover for the first six months, that does not happen.
Untreated, an attack settles over one to two weeks. Treated early, in a day or two.
Urate is a normal waste product. When the blood level stays high, crystals form in cooler peripheral joints — which is why the big toe is the classic site. In around nine out of ten people the problem is reduced excretion by the kidneys rather than excess production, and that is largely inherited.
Diet raises urate modestly, and its role is consistently overstated. The items with the clearest effect:
Dietary change alone rarely lowers urate enough to stop attacks. It is worth doing, and it is not a substitute for treatment.
Gout is an independent marker of cardiovascular risk and is strongly associated with kidney disease, high blood pressure and diabetes. A gout diagnosis is a reason to check blood pressure, cholesterol, glucose and kidney function — not just to treat the toe.
In a typical case — sudden severe pain, redness and swelling of the big toe in a middle-aged man — gout is diagnosed clinically and treatment starts immediately. Photographs help and this assesses well remotely.
Serum urate is frequently normal during an acute attack. The level often falls as crystals precipitate into the joint — so a normal result in the middle of an attack does not exclude gout, and it is one of the commonest reasons the diagnosis is missed or doubted.
The urate level should be measured four to six weeks after the attack settles, when it reflects your true baseline. That figure is what treatment is then aimed at.
Septic arthritis — infection in the joint — looks almost identical to gout. Hot, red, swollen, exquisitely painful, and it destroys the joint within days if untreated.
Fever, feeling systemically unwell, or being unable to move the joint at all mean urgent in-person assessment, not a remote prescription. Joint aspiration distinguishes them definitively, and where there is any real doubt we send you to be seen rather than treating for gout and hoping.
Pseudogout, which favours the knee and wrist in older people; a flare of osteoarthritis; cellulitis; reactive arthritis; and psoriatic arthritis.
Treatment works best within the first 24 hours, which is another reason for a same-day appointment. Options, chosen to fit your kidney function and other conditions:
Rest the joint, keep it elevated, and use an ice pack.
Allopurinol lowers urate, dissolves existing crystals, and stops gout permanently if the level is kept low enough. It is not merely a preventive — given long enough it clears the crystal deposits entirely, and tophi disappear.
Current guidance is to offer it to anyone who has had a single attack and wants to avoid another — not to wait for repeated attacks, which was the old approach and left people suffering unnecessarily.
One serious interaction: allopurinol with azathioprine or mercaptopurine can be dangerous. Always mention them.
Reviewing diuretics, and treating blood pressure, cholesterol and glucose — because gout signals cardiovascular risk. Where blood pressure treatment is needed anyway, losartan lowers urate as a useful side effect.
Seek urgent in-person assessment — the same day — for:
These may be septic arthritis, which destroys a joint within days and requires joint aspiration and intravenous antibiotics. It looks very like gout, and this is the one situation where a remote consultation is not appropriate — we will direct you to urgent care rather than prescribe.
Call 999 or go to A&E for:
Book a routine consultation for: a first attack, to get the diagnosis right and the urate measured properly afterwards; two or more attacks in a year; any tophi; or if you take allopurinol and are still having attacks — which usually means the dose is too low and the level has never been rechecked.
Worth doing, and not a replacement for treatment:
Gout is one of the few forms of arthritis that can be entirely cured. Not managed — cured. It requires taking a tablet daily and having a blood test a few times until the level is right. A great many people endure years of attacks having never been offered that.
Gout is one of the most treatable conditions in medicine and one of the worst managed — and the gap is almost entirely about long-term treatment rather than the attack itself.
Your NHS GP treats gout free, and allopurinol is one of the cheapest drugs available.
The point worth making is this: most people with recurrent gout are treated only for attacks, when the treatment that changes their life is a daily urate-lowering tablet taken between attacks. Allopurinol titrated properly to a target urate level below 360 µmol/L stops gout happening — not reduces it, stops it — and a great many people have either never been offered it or were started on a low dose that was never increased.
That titration is the whole thing, and it is where care usually fails. It needs a blood test, a dose increase, another blood test, repeated until target is reached.
Where a consultation earns its fee is exactly that — arranging urate and kidney function, starting or optimising allopurinol, and explaining the two things that cause people to abandon it: starting allopurinol can trigger an attack, and stopping it during an attack makes things worse. Neither is a reason to give up.
Free and effective: reducing alcohol, particularly beer, and sugary drinks. The traditional dietary restrictions matter less than either.
NICE NG219, Gout: diagnosis and management, is the governing guideline. It recommends discussing urate-lowering therapy with everyone after a first attack, and offering it to those with recurrent flares, tophi, joint damage, kidney disease or diuretic use.
NG219 recommends a treat-to-target strategy, aiming for a serum urate below 360 µmol/L, or below 300 µmol/L where there are tophi or ongoing flares — the basis for the point above about titration.
NG219 recommends allopurinol or febuxostat as first-line, with low-dose colchicine or an NSAID as flare prophylaxis when starting.
NG219 is explicit that urate-lowering therapy should not be stopped during a flare.
The British Society for Rheumatology guideline on gout aligns with this and covers monitoring, and NICE CKS notes that a normal serum urate during an acute attack does not exclude the diagnosis.
Much less than people think. Around nine in ten people with gout excrete urate poorly through the kidneys, which is largely genetic. Diet contributes at the margin — beer, spirits and sugary drinks most — but dietary change alone rarely lowers urate enough to stop attacks. Decades of dietary advice instead of treatment is a large part of why gout is so poorly controlled.
Not necessarily. Urate frequently falls during an acute attack as crystals precipitate into the joint, so a normal level in the middle of one proves nothing. It should be rechecked four to six weeks after things settle, and that later figure is the one that matters.
No — and this is the single most important question here. Starting allopurinol commonly triggers attacks in the first months as crystals mobilise. That is the drug working, not failing. Taking a low-dose anti-inflammatory or colchicine alongside for the first six months prevents it. Stopping is how people lose the treatment that would have cured them.
Yes, if you want to stay free of gout. Allopurinol keeps urate low so crystals dissolve and do not reform. Stopping means the level rises and the crystals return, usually within a year or two. The trade is a daily tablet against recurring attacks and eventual joint damage.
Effectively, yes — which makes it unusual among arthritis. Keep urate below target for long enough and existing crystals dissolve, tophi disappear and attacks stop. It requires the right dose and blood tests to confirm the target is reached, which is exactly the step most often missed.
No. Vegetable purines do not raise gout risk, despite appearing on every purine-avoidance list. The evidence is clear on this. Beer, spirits, sugary drinks and red meat are where the effect is.
Several reasons: body temperature falls at night and crystals form more readily when cooler; you become mildly dehydrated overnight; and cortisol, which is naturally anti-inflammatory, is at its lowest in the early hours. It is a genuinely characteristic pattern.
Yes, though far less before the menopause — oestrogen helps the kidneys excrete urate. After the menopause the rates converge, and gout in older women is under-diagnosed precisely because it is thought of as a men's condition.
August 23, 2026
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It means the diagnosis can usually be made from your history and photographs, and that treatment can be arranged safely without examining you. Where a condition is not marked treatable online, it is because examination is the diagnosis — listening to a chest, feeling an abdomen, examining an ear or a joint — or because a procedure or device is needed.
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