Gout: stopping the acute attack and preventing the next one

What is gout and why does it hurt so much?

Gout is an inflammatory joint disease caused by the crystallisation of uric acid. When uric acid concentration in the blood exceeds the saturation point, it precipitates as needle-shaped monosodium urate crystals inside joint cavities and surrounding tissues. The immune system treats these crystals as foreign invaders and mounts an intense inflammatory response.

The acute attack is famously painful and arrives without warning, most commonly at night or in the early hours of the morning. The classic site is the big toe joint, which becomes swollen, red, warm, and so tender that even the touch of a bedsheet is unbearable. Attacks can also affect the ankle, knee, wrist, and fingers.

Uric acid is a breakdown product of purines, chemical compounds found in food and in the body's own cells as they die and are recycled. When the body produces more uric acid than the kidneys can excrete, it accumulates in the blood. Many people have elevated uric acid, a state called hyperuricemia, without ever developing gout: crystals do not form under every set of conditions and there appears to be an individual threshold.

Gout was historically known as the disease of kings because of its association with rich food and alcohol. Today it is no longer a disease of privilege: the spread of sugary drinks and fructose-sweetened beverages has extended the risk to a much wider population, and in the regional diet these drinks can drive uric acid as much as or more than alcohol.

Who is most at risk in the regional context?

Gout affects men three to four times more often than women, typically in their thirties and forties. Women are largely protected by oestrogen, which helps the kidneys excrete uric acid, until menopause removes that protection. Women who develop gout after menopause or who take diuretic medications are at similar risk to men.

The main risk factors include high blood pressure, obesity, type 2 diabetes, chronic kidney disease which impairs uric acid excretion, and long-term use of thiazide diuretics, which are a common class of blood pressure medication that raises uric acid as a side effect. A family history also plays a genetic role.

In the Middle East and Gulf region, specific dietary patterns contribute significantly. Organ meats including liver, kidney, brain, and offal are high in purines and are traditional components of many regional cuisines. The very high consumption of sugary drinks and fruit-flavoured beverages sweetened with high-fructose corn syrup raises uric acid through a separate mechanism independent of purine content.

A 2025 review in Critical Pathways in Cardiology linked elevated uric acid to an increased risk of cardiovascular disease, making gout management a broader health priority beyond just joint pain relief.

Does a normal uric acid level rule out gout?

This question confuses many doctors and patients. Uric acid can be normal or even below the normal range during an acute attack, and this does not mean the diagnosis is wrong or that gout is not the cause.

The explanation is that the acute attack itself triggers systemic inflammation which causes a temporary redistribution of uric acid from the blood into tissues, while the crystals remain locked in the joint. This is why the American College of Rheumatology and EULAR guidelines recommend measuring uric acid two to four weeks after the flare has settled to get the true resting value.

The gold standard for diagnosis is joint aspiration: a doctor withdraws a small amount of fluid from the inflamed joint with a fine needle and examines it under a polarising light microscope to look for characteristic needle-shaped monosodium urate crystals. This confirms the diagnosis with certainty and, importantly, also rules out septic arthritis, which is a serious bacterial joint infection that can look similar.

Dual-energy CT scanning is a newer imaging technology that can detect urate deposits in joints with high accuracy without aspiration and is available in larger regional centres for cases that are difficult to diagnose conventionally.

How is an acute gout attack treated?

The immediate goal in an acute flare is to extinguish the inflammation as quickly as possible. The three established treatment options are non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin or naproxen, colchicine, and corticosteroids. The doctor's choice depends on kidney function, stomach health, and other conditions.

Colchicine is highly effective when started within the first few hours of a flare. Modern dosing uses lower doses than were historically given, which avoids the severe diarrhoea that used to limit its use. It is not suitable for people with severe kidney failure and may interact with certain other medications, so check with your doctor.

Supporting measures help alongside medication: rest and elevation of the affected limb, ice packs wrapped in a cloth applied for twenty minutes several times a day, and drinking plenty of water. Avoid tight footwear or any pressure on the swollen joint during the attack.

Understanding what triggers flares is important for prevention. Known triggers include alcohol particularly beer, a large meal high in organ meats or shellfish, dehydration, illness or surgery, and abrupt changes in uric acid level from starting or stopping urate-lowering medicines. Recognising your personal triggers helps you anticipate and sometimes prevent attacks.

The biggest mistake: stopping allopurinol during a flare

Allopurinol is the most widely used long-term urate-lowering therapy. It works by inhibiting xanthine oxidase, the enzyme that produces uric acid, and is taken daily as a preventive rather than as an anti-inflammatory for the acute attack itself.

The very common mistake, shared by many patients and unfortunately some practitioners in the region, is stopping allopurinol when a flare begins, on the belief that it caused or is worsening the attack. This is scientifically incorrect: stopping allopurinol mid-flare prolongs the flare and substantially increases the risk of a new flare when the drug is restarted, because of the uric acid level shift this creates.

Both the 2020 American College of Rheumatology guideline and the EULAR recommendations explicitly state to continue urate-lowering therapy during an acute flare and to treat the inflammation separately with colchicine, NSAIDs, or corticosteroids. Following this approach leads to significantly better outcomes.

The reason flares sometimes occur when starting allopurinol or increasing its dose is the sudden shift in uric acid concentration, which destabilises existing crystals and can trigger their movement into the joint space. This is why allopurinol is always started at a low dose and titrated upward slowly, and why colchicine at a low prophylactic dose is often given for the first six months of urate-lowering therapy.

Food and gout: what actually matters and what is myth

A review published in Advances in Chronic Kidney Disease found that dietary changes alone reduce uric acid by only about 1 to 1.5 mg/dL on average. This is less than most people expect and less than medication achieves. Diet matters but it supplements medication rather than replacing it for most people who need urate-lowering therapy.

What is genuinely established to raise uric acid: organ meats including liver, kidney, and brain are very high in purines; oily fish such as sardines and anchovies have a moderate effect; sugary drinks and juices sweetened with high-fructose corn syrup raise uric acid through a fructose-specific metabolic pathway independent of purine content; and alcohol, especially beer, has a double effect through both purine content and competing with uric acid for renal excretion.

What is unfairly blamed in popular belief: vegetables that contain purines, such as spinach, asparagus, mushrooms, and cauliflower, carry a much weaker real-world risk than their purine content suggests, because plant purines are converted to uric acid with much lower efficiency than animal purines. People do not need to avoid these vegetables to manage gout.

The most practical regional dietary advice: cut sugary drinks and sweetened juices dramatically, reduce organ meats and offal which are common in many traditional dishes across the region, and drink enough water daily to keep the kidneys flushing uric acid effectively. Low-fat dairy products actually reduce uric acid slightly and should be encouraged.

What happens if gout is left untreated: tophi and joint damage

Gout that is poorly controlled over years progresses to a form called chronic tophaceous gout, in which crystal deposits accumulate in soft tissues and form firm whitish nodules called tophi (singular: tophus). Tophi appear most often on the outer ear, the back of the hands, around the elbows, and on tendons.

Tophi are painful, can ulcerate and discharge a chalky white substance, impair movement, and cause permanent joint deformity. Urate deposits can also settle in the kidneys, causing recurrent kidney stones and accelerating kidney damage, which in turn makes uric acid harder to excrete and worsens the gout, creating a self-reinforcing cycle.

Recurrent gout alongside hypertension, obesity, and diabetes significantly raises cardiovascular risk, as highlighted by the 2025 review in Critical Pathways in Cardiology. Managing gout is therefore not only about pain relief but about protecting the heart and kidneys over the longer term.

The uric acid target below 6 mg/dL is not a number chosen arbitrarily. At this level, the blood is below the saturation point for monosodium urate, which means existing crystals in the joints begin to dissolve gradually. This is why sustained target achievement, measured by regular blood tests, is the only way to truly reduce flare frequency over time.

Gout and kidney disease: a two-way relationship

Gout and chronic kidney disease feed each other in a cycle. Impaired kidney function reduces the excretion of uric acid, raising its blood level. In turn, urate deposits in the kidney tubules damage them and accelerate further decline. People with both conditions need careful specialist management.

Allopurinol must be dose-reduced in kidney disease to prevent accumulation and toxicity. Febuxostat is an alternative urate-lowering drug that may suit some patients with kidney impairment, but requires caution in those with cardiac disease. Both drugs are dose-adjusted based on kidney function rather than used at standard doses.

Colchicine also requires dose reduction in kidney disease. NSAIDs for the acute flare are potentially harmful to the kidneys and should be avoided or used with extreme caution in anyone with CKD. This means a patient with both gout and kidney disease needs a treatment plan that is specifically tailored rather than the standard protocol applied to someone with healthy kidneys.

The practical message: if you have both gout and kidney disease, make sure your nephrologist and your rheumatologist are both aware of all the medicines you are taking for each condition. Treating one without the other knowing what is prescribed risks interactions and inappropriate dosing that can harm the very organs you are trying to protect.

Sources

• Dalbeth N, Gosling AL, Gaffo A et al: Gout, Lancet, 2021
• FitzGerald JD, Dalbeth N, Mikuls T et al: 2020 American College of Rheumatology Guideline for the Management of Gout, Arthritis care and research, 2020
• Richette P, Doherty M, Pascual E et al: 2016 updated EULAR evidence-based recommendations for the management of gout, Annals of the rheumatic diseases, 2017
• Dalbeth N, Choi HK, Joosten LAB et al: Gout, Nature reviews. Disease primers, 2019
• Kedar E, Simkin PA: A perspective on diet and gout, Advances in chronic kidney disease, 2012
• Vargas-Santos AB, Neogi T: Management of Gout and Hyperuricemia in CKD, American journal of kidney diseases, 2017
• Shubietah A, Awashra A, Milhem F et al: Hyperuricemia and Cardiovascular Risk: Insights and Implications, Critical pathways in cardiology, 2025