Gout and High Uric Acid: Treating the Attack and Preventing the Next
Gout is among the most treatable forms of arthritis and among the worst managed. The acute attack is dealt with, the uric acid is never brought down, and the person has attacks for twenty years and eventually joint damage.
What happens
Uric acid is the end product of purine metabolism. When blood levels exceed the saturation point, roughly 6.8 mg/dL, monosodium urate crystals form in joints and tissues. The immune system attacks the crystals, producing intense inflammation.
The first attack classically affects the base of the big toe, called podagra, because it is the coolest and most peripheral joint and crystals form more readily at lower temperature.
The acute attack
Sudden onset, often waking the person in the early hours. The joint becomes exquisitely painful, red, hot and swollen, so tender that bedsheets are unbearable. There may be low fever. It peaks within 12 to 24 hours and settles over days to two weeks even untreated.
Other common sites: ankle, midfoot, knee, wrist, fingers, elbow.
Important: a hot swollen joint can also be a septic joint, which is an emergency. A first attack, a joint with high fever, or an atypical presentation should be examined and often aspirated, with fluid examined for crystals and for infection. Joint aspiration is the definitive test, showing needle-shaped negatively birefringent crystals.
A key diagnostic trap
Uric acid is frequently normal or low during an acute attack, because it shifts into the joints. A normal level does not exclude gout. Measure it two weeks after the attack settles.
Treating the attack
Start treatment as early as possible; effectiveness falls sharply with delay.
- NSAIDs at full dose, where kidneys, stomach and heart allow
- Colchicine, most effective within the first 12 to 24 hours. Modern low-dose regimens work as well as the old high-dose approach with far less diarrhoea. Dose must be reduced in kidney impairment and with certain interacting drugs
- Corticosteroids, oral or injected into the joint, particularly useful in kidney disease where NSAIDs are unsafe
- Rest, elevate, apply ice, keep bedding off the joint
- Do not start or stop urate-lowering therapy during an attack. If already on allopurinol, continue it
Preventing the next attack
This is the part that gets skipped. Urate-lowering therapy is indicated with recurrent attacks, tophi, joint damage on X-ray, kidney stones, or chronic kidney disease.
Allopurinol is first line. Two points determine whether it works:
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- It is titrated to a target, not given at a fixed dose. The target is a uric acid below 6 mg/dL, and below 5 where tophi are present. Starting at 100 mg and never increasing, which is extremely common, achieves nothing
- It is lifelong. Stopping when attacks stop causes them to return
Febuxostat is an alternative where allopurinol is not tolerated.
Starting it can trigger an attack, because falling levels mobilise crystals. This is expected, and prophylaxis with low-dose colchicine or an NSAID for the first three to six months prevents it. People who are not warned about this conclude the drug caused gout and stop it, which is the single most common reason treatment fails.
In some populations, testing for HLA-B*5801 before allopurinol reduces the risk of a severe hypersensitivity reaction.
Diet, in proportion
Diet matters less than most people believe; genetics and kidney excretion dominate. Still, these help:
Reduce:
- Sugar-sweetened drinks and fructose, which raise uric acid substantially and are a bigger factor than most purine foods
- Alcohol, especially beer, which contains purines as well as alcohol
- Organ meats: liver, kidney, brain
- Red meat in quantity
- Shellfish, sardines, anchovies, mackerel
Do not need restricting: most vegetables, including the high-purine ones such as spinach, cauliflower, mushrooms and peas, which do not raise gout risk; dal and legumes in normal amounts; coffee and tea.
Helpful: low-fat dairy, which lowers uric acid; cherries, with modest evidence; coffee; vitamin C in moderate amounts; generous water intake; and weight loss, which has one of the largest effects, though crash dieting can trigger an attack.
Medication review
Several common drugs raise uric acid and should be reviewed: thiazide and loop diuretics, low-dose aspirin, ciclosporin, tacrolimus and some tuberculosis drugs. Losartan and some other agents mildly lower it and may be preferred where a person needs both treatments.
Why it matters beyond the joint
Untreated gout causes:
- Tophi, visible chalky deposits in the fingers, elbows, ears and feet
- Joint destruction and deformity
- Kidney stones and urate nephropathy
Gout is also strongly associated with metabolic syndrome, hypertension, diabetes, obesity, fatty liver and cardiovascular disease, so a diagnosis of gout is a prompt to check blood pressure, lipids, glucose and kidney function.
Asymptomatic hyperuricaemia
A raised uric acid on a routine test without any attacks is common. Routine drug treatment is generally not recommended for this alone; lifestyle measures, review of diuretics and monitoring are usually the right response. The exception is very high levels or specific circumstances discussed with a doctor.
The practical summary
Treat the attack fast. Measure uric acid two weeks later. If attacks recur, start urate-lowering therapy, titrate it to a target below 6, take prophylaxis for the first months, and do not stop it. Done properly, gout essentially disappears.
This is general information. Colchicine and allopurinol dosing depend on kidney function and interactions, and a first hot swollen joint should be examined to exclude infection.