Gouty arthritis (gout)

What gout is

Uric acid is a common product of the breakdown of purines, substances found in our cells and in some foods. Normally the body removes uric acid through the kidneys and the gut. When more is produced than is removed (or when the kidneys remove it poorly), its level in the blood rises; this is called hyperuricemia. Above a certain threshold (about 6.8 mg/dl) uric acid starts to crystallize, and the tiny needle-like crystals settle in joints, where they set off strong inflammation.

Not everyone with high uric acid develops gout; many people have hyperuricemia without any attack. But when the crystals trigger attacks, we speak of gout. Without long-term treatment, attacks become more frequent, crystals collect under the skin as hard lumps (tophi), joints are permanently damaged and kidney stones may form.

Gout affects men and postmenopausal women more often, and has a family component. It is closely linked to high blood pressure, overweight, diabetes, and kidney and heart disease, so it calls for an overall health assessment.

Symptoms

A typical attack begins suddenly, often at night, and peaks within 8–12 hours. Its features are:

• very severe pain, often unbearable, even from the weight of a sheet;
• a red, hot, swollen and tender joint;
• most often the big toe (this is what “podagra” originally meant), but also the ankle, knee, wrist or other joints;
• without treatment the attack passes by itself within 1–2 weeks, but returns.

Between attacks the joint is completely normal, so many patients think the disease “has gone away” and neglect further treatment, which is the most common mistake. In repeated disease several joints can be affected at once and tophi appear, usually on the fingers, the Achilles tendon, elbow and ear.

Risk factors and triggers

• diet: red meat and organ meats (liver, kidneys), shellfish, fructose-sweetened drinks and added sugars, and above all alcohol, especially beer and spirits;
• overweight, which raises uric acid production and lowers its removal;
• high blood pressure, kidney disease, diabetes, high cholesterol and heart disease;
• some medicines: diuretics (water tablets, such as thiazides), low-dose aspirin, some blood pressure drugs and drugs taken after transplant;
• family history, age and male sex;
• triggers of an attack: a large meal or heavy alcohol, dehydration, a feverish illness, a recent injury or operation, and starting or changing uric-acid-lowering drugs.

Diagnosis

In a typical attack the diagnosis is made from the clinical picture, but the accurate confirmation is finding urate crystals in joint fluid, taken with a thin needle and examined under a microscope; this is used especially in the first attack or when the diagnosis is unclear, and to rule out infection. Blood uric acid helps, but there is a catch: during an attack it can be falsely normal, and some people with high uric acid never have an attack; so it is better measured 2–4 weeks after an attack.

Joint ultrasound can show crystal deposits on the surface of the cartilage (the “double contour” sign) and tophi, as well as fluid in the joint. X-rays show damage only in late stages. The doctor also checks kidney function, blood pressure, blood glucose and lipids, and rules out diseases that mimic gout: joint infection (an emergency), pseudogout (deposit of other crystals) and rheumatoid arthritis.

Treating an attack

The aim is to calm inflammation as quickly as possible, so an attack is treated as early as possible after it begins. The doctor chooses between:

• anti-inflammatory drugs (NSAIDs), if there are no contraindications (kidney, stomach, heart, anticoagulants);
• colchicine at low doses, which stops the inflammation caused by the crystals; high doses cause diarrhea and are not needed;
• corticosteroids (tablets or a joint injection), when the others cannot be used;
• supportive measures: rest the joint, an ice pack wrapped in cloth for up to 20 minutes, plenty of fluids, avoiding alcohol.

Do not stop long-term uric-acid-lowering drugs during an attack, if you already take them.

Long-term treatment: lowering uric acid

An attack is treated, but the disease is controlled only when uric acid is kept below the threshold for crystallization. Long-term treatment is recommended after repeated attacks, when there are tophi, joint damage on X-ray, kidney stones or chronic kidney disease. It consists of:

• allopurinol (or another drug that lowers uric acid production), started at a low dose and increased slowly, aiming for uric acid below 6 mg/dl (below 5 mg/dl when there are tophi). It is taken every day, even without attacks, and often for life;
• prophylaxis with low-dose colchicine or an anti-inflammatory for some months after starting, because lowering uric acid at first can temporarily trigger attacks;
• lifestyle changes: cutting alcohol (especially beer), sweet drinks and red and organ meats; enough water; gradual weight loss (not harsh diets, which can trigger attacks); control of blood pressure and sugar; care with water tablets.

Diet alone rarely solves the problem: even an exemplary diet lowers uric acid only partly. So do not delay medicines when they are needed, and do not stop them when there are no attacks.

Follow-up

While the dose is being adjusted, uric acid is checked every 2–5 weeks until the target is reached; after that checks are every 6 months to a year, or sooner when the doctor considers it reasonable, along with the kidneys and liver. If attacks continue despite good treatment, or uric acid does not fall, the doctor reviews the plan. This information is educational and does not replace a medical visit.

When to see a doctor

• at the first attack, to confirm the diagnosis;
• when attacks recur, even if they pass on their own;
• when you see hard lumps under the skin or have kidney stones;
• a hot joint with fever: immediately, because infection must be ruled out;
• when you start new blood pressure or heart medicines and have a history of gout.