Gout

Who gets Gout?

Gout is the commonest inflammatory arthritis in adults and is becoming more common in India. It affects men far more often than women before the menopause, typically from the forties onward. Risk rises with obesity, high blood pressure, chronic kidney disease, diuretic use, alcohol — beer and spirits particularly — and diets high in red meat, organ meat, shellfish and fructose-sweetened drinks. There is a strong hereditary component in how efficiently the kidneys excrete urate.

What are the symptoms of Gout?

Not everyone has every symptom below, and having one does not confirm the diagnosis. These are the features that most often lead to assessment:

• Sudden severe pain in one joint, often overnight, reaching maximum intensity within a few hours
• The joint becomes red, hot, shiny and so tender that bedsheets are unbearable
• Most often the base of the big toe, but also the midfoot, ankle, knee, wrist, elbow or fingers
• Attacks settle over one to two weeks even without treatment, then recur
• Over years, attacks become more frequent, involve more joints and last longer
• Firm white-yellow lumps under the skin over the ears, fingers or elbows (tophi) in long-standing disease
• Kidney stones

How is Gout diagnosed?

Identifying urate crystals in fluid drawn from the joint is the definitive test and separates gout from infection, which can look identical and is an emergency.

A blood uric acid level supports the diagnosis but does not make it — the level is often normal or low during an acute attack, and many people with a high uric acid level never develop gout. A normal uric acid level during an attack is therefore not a reason to exclude gout.

Ultrasound and dual-energy CT can show urate deposits without needing to aspirate. Kidney function is always checked, because it drives both the cause and the treatment choice.

How is Gout treated?

Treatment has two entirely separate parts, and confusing them is the commonest reason gout stays uncontrolled.

The attack is treated with an anti-inflammatory — colchicine, a non-steroidal anti-inflammatory, or a corticosteroid, chosen according to kidney function and other conditions. Started early, this settles an attack within days.

The disease is treated by lowering uric acid, usually with allopurinol or febuxostat, titrated upward until the blood level is below the target — under 6 mg/dL, or under 5 for tophaceous disease. Below that threshold the existing crystal deposits dissolve, and once they are gone the attacks stop.

Urate-lowering treatment is lifelong, and attacks can increase in the first few months as deposits break down, which is why low-dose prophylaxis is given alongside it for the first three to six months. Many patients stop the treatment at this point believing it has failed; continuing through this period is what produces the cure.

Living with Gout

Diet matters, but far less than most patients are led to believe — dietary change alone typically lowers uric acid by about 15 per cent, not enough for someone with recurrent attacks. Limiting beer, spirits, organ meats, shellfish and sugary drinks helps; weight reduction helps more. Neither replaces urate-lowering medication where attacks are recurrent, tophi are present, or there are kidney stones.

When should you see a rheumatologist?

A first attack is worth confirming rather than assuming. Two or more attacks a year, any tophus, kidney stones or chronic kidney disease are firm indications for urate-lowering treatment.

Common questions about Gout

This page is general information to support a consultation. It is not a diagnosis, and it does not replace an assessment by a doctor who has examined you.