Gout is a very painful form of inflammatory arthritis that develops in some people who have an elevated blood level of urate (often referred to as uric acid). The symptoms of gout are due to the body’s reaction to the deposition of urate crystals in the joint. Urate crystals can also form in skin and in the kidneys (kidney stones).
Acute gout occurs with sudden onset of severe joint pain with redness and swelling of the joint. The proximal joint of the big toe is often the first joint to be involved. A flare can affect more than one joint.
Acute flares can be triggered by minor trauma such as stubbing the toe or rolling the ankle. Overeating, binges on alcohol or carbonated fizzy drinks can also cause an acute flare.
In people who have persistent high urate levels, urate crystals can accumulate in big clumps and be surrounded by a thick lining of inflammatory tissue. These lumps are called tophi, and can cause permanent damage and deformity to joints.
In the early stages of gout -the best way to make a diagnosis is to put a needle into an inflamed joint and aspirate fluid which can be looked at under the microscope.
To confirm gout the lab will need to be able to see negatively bi-refringent crystals under polarized light (monosodium urate crystals).
The goals of treatment are to treat the acute flare and to prevent further attacks. In patients with tophaceous gout – the aim is to slowly dissolve the tophus.
The treatment of acute gout may involve joint injections with cortisone, anti-inflammatory pain killers, colchicine or prednisone.
Prevention of gout in the long-term relies on reducing urate levels in the blood (to <0.36mmol/L in those without tophi or to <0.30mmol/L in those with tophi). This is best done by using medications that block the enzyme xanthine oxidase. Xanthine oxidase breaks down purines in food into urate. Nearly all food contains some purines. The two currently available medications to block xanthine oxidase in New Zealand are allopurinol and febuxostat. In some patients, we also use medications help the kidneys get rid of urate (called uricosuric medications) – e.g. probenecid and benzbromarone.
Diet has historically played an important role in managing gout. This message has been over emphasized and modification of diet will only make relatively minor changes to serum urate. This is usually not enough to be meaningful in the long-term prevention of gout. On treatment, you should be able to eat most foods in moderation. Reducing overall calories and reducing weight is probably the most important change.
If you want to try some specific dietary changes you can:
Reduce: sugary foods and drinks (including fruit juices), high purine foods (e.g. liver, kidney, sweetbreads, shellfish, red meat, and alcohol)
Increase: water intake, coffee, vitamin c, cherries