Gout

Gout is defined by having sodium urate crystals in your joints. These may be present for years without you knowing they are there, but on occasions they can trigger an attack of gout. Gout is an intensely painful form of arthritis. Attacks of gout usually come on very quickly, often during the night. Doctors describe this sudden development of symptoms as ‘acute’. Gout is the form of arthritis we understand the best, and this has led to a range of therapies to treat acute attacks and control the condition.

Gout is the most common type of inflammatory arthritis, affecting 2.5% of adults in the UK. It affects more men than women and can affect men of any age. Women rarely develop gout before the menopause. It gets more common with increasing age in both men and women, affecting 15% of men and 6% of women over the age of 75. Gout has been getting more common in recent decades in many countries, including the UK. This is mainly because we are living longer, and more people are getting overweight or obese.

At one time it was thought that gout was caused simply by overeating and drinking too much alcohol. While this can make attacks of gout more likely, it’s not the whole story.

Gout is caused by chemical processes that take place in your body. A substance called urate builds up, sometimes because your kidneys aren’t able to get rid of it quickly enough. Over a period of time this leads to urate crystals forming in and around your joints. Once there are a lot of crystals in your joints some of them can trigger a sudden painful episode of severe joint inflammation (an ‘attack’) which usually settles back to appear normal within a week. If untreated these attacks get more common and spread to involve new joints.

Urate crystals cause inflammation, meaning the affected joint becomes intensely painful, red, hot and swollen (see Figure 1). The skin over the joint often appears shiny and may peel. Attacks typically affect the big toe and usually start at night. The symptoms develop quickly and are at their worst within 12-24 hours of first noticing anything is wrong. Any light contact with the affected joint is painful – even the weight of a bedsheet or wearing a sock can be unbearable.

Urate crystals cause inflammation, meaning the affected joint becomes intensely painful, red, hot and swollen (see Figure 1). The skin over the joint often appears shiny and may peel. Attacks typically affect the big toe and usually start at night. The symptoms develop quickly and are at their worst within 12-24 hours of first noticing anything is wrong. Any light contact with the affected joint is painful – even the weight of a bedsheet or wearing a sock can be unbearable.

Although gout most often affects the big toe, other joints may also be affected, including other parts of the feet and ankles, knees, elbows, wrists and fingers. If several joints are inflamed at once this is called polyarticular gout. It’s very rare to have gout in joints towards the centre of the body such as the spine, shoulders or hips.

Urate crystals can also collect outside of the joints and even be seen under the skin, forming small, firm white lumps called tophi (see Figure 2). These aren’t usually painful but can be embarrassing and disfiguring, and can get in the way of clothing. Sometimes they get inflamed, break down and leak pus-like fluid containing gritty white material – the urate crystals themselves.

Gout occurs in people who have levels of urate in their blood that are persistently above a critical level which allows urate crystals to form. About two thirds of the urate in our bodies comes from the breakdown of purines which are naturally present in the cells of our bodies. The other third comes from the breakdown of purines in some foods and drinks.

Having urate in your blood doesn’t mean you’ll definitely develop gout – it’s normal and healthy to have some urate in the bloodstream. When urate levels start to build up, your body usually gets rid of any excess urate through your kidneys into your urine; however, if your body is making too much urate or your kidneys are unable to remove enough urate, then urate levels start to rise. If the level goes above a certain point (the saturation point), it’s possible for urate to form crystals of sodium urate. These crystals mainly form in and around joint tissues, especially joints at the ends of your legs and arms, such as your finger and toe joints.

Figure 3 shows a joint with urate crystals. The crystals gradually build up in your cartilage and other joint tissues over years. You will not know this is happening. When there are a lot of crystals in your joints some of them can spill out into the joint cavity (the space between the bones). This process is called crystal shedding. The hard, needle-shaped crystals touch the soft lining of the joint (the synovium) and make it very inflamed very quickly. The inflammation process breaks down the crystals that have become loose inside the joint, and the attack gradually settles over a few days or weeks, depending on how many crystals spilled out.

Apart from causing sudden attacks of inflammation, a build-up of crystals can eventually lead to tophi forming in and around your joints. These hard tophi can grow and cause pressure damage to your cartilage and bone. This is just like the damage caused by osteoarthritis and can cause more regular, daily pain when you use the affected joints. At this stage the condition is often called chronic tophaceous gout. Some tophi may be seen and easily felt under the skin, but by this time the unseen part of the tophi in your joints and deeper tissues are usually quite extensive.

A diagnosis is often based on your symptoms and an examination of the affected joints, but your doctor may suggest the following tests:

• A blood test: can measure the amount of urate in your blood. The critical serum level of urate (the saturation point) is around 360 μmo/L (equivalent to 6mg/dl). This is within the normal range for men, and for older women, so being informed that your blood test is ‘within normal limits’ is irrelevant – you need to know if it is above or below this critical level. A raised level of urate strongly supports a diagnosis of gout but can’t confirm it – not everyone with a raised level of urate will develop crystals in their joints, and it’s possible for urate levels in the blood to be normal at the time of an acute attack.

• X-rays of joints: will reveal joint damage if you have long-standing and poorly controlled gout. However, x-rays are rarely helpful in confirming the diagnosis because they’re usually normal in the early years of having gout. Ultrasound of joints can be used to detect earlier signs of gout, and can be useful where the diagnosis is uncertain.

• Synovial fluid examinations: involve taking fluid samples from a joint through a needle and examining them under a microscope for urate crystals. This test can confirm the diagnosis but isn’t always practical – it can be difficult and sometimes uncomfortable to draw fluid from a small joint such as the big toe. However, it may be possible to identify a few crystals in a sample taken from your knee, even if you’ve not yet had an attack of gout there. A fine needle inserted into a tophus under your skin can also be used to identify urate crystals.

There are two main parts to treating gout:

• treating the acute attack of inflammation when one or more joints are very inflamed and painful

• ongoing treatment to reduce the level of urate in your blood and get rid of urate crystals

Treatments for acute attacks of gout:

• non-steroidal anti-inflammatory drugs (NSAIDs): Acute attacks of gout are often treated with oral NSAIDs, which can ease pain and possibly reduce some of the inflammation. Examples include ibuprofen, naproxen and etoricoxib. Like all drugs, NSAIDs can sometimes have side-effects, but your doctor will take precautions to reduce the risk of these – for example, by prescribing the lowest effective dose for the shortest possible period of time.

• colchicine: Colchicine is made from the crocus plant. It’s not a painkiller but it’s often very effective at damping down the inflammation caused by the crystals touching the joint lining. As with NSAIDs, colchicine tablets should be taken as close as possible to the beginning of an attack, and certainly within the first 24 hours of the attack starting, otherwise it may not be effective. Your doctor may let you keep a supply so you can start taking them at the first signs.

• steroids: If an acute attack of gout doesn’t improve with NSAIDs or colchicine or if you’re at risk of side-effects from these drugs, your doctor may prescribe a steroid injection into the joint or muscle, or a short course of steroid tablets (usually no more than a few days).

• ice packs: Putting an ice pack on the affected area can reduce some of the swelling, heat and pain. They’re very safe, but make sure that you don’t put the pack directly onto your skin to avoid burning or irritating your skin. You can buy reusable cooling pads from sports shops and chemists, or you can use a pack of frozen peas, wrapped inside a damp towel. You should always use ice packs alongside any drug treatments your doctor has prescribed.

The drugs given to ease an acute attack don’t get rid of the urate crystals in your joints or reduce the level of urate in your blood. Drugs are available that can lower urate levels and get rid of urate crystals in your body. Traditionally, the use of these urate-lowering therapies was reserved for people with more severe gout, for example if they were having frequent attacks, or if they had tophi, kidney stones, evident signs of joint damage or high urate levels.

If you miss doses of your urate-lowering medication, especially in the early stages, this can cause your urate level to go up and down, which can trigger acute attacks. It’s also important to consider other ways of reducing your urate levels.

For example, it’s important:

• to lose weight if you’re overweight

• to avoid foods which are high in purines

• not to drink too much alcohol.

If you have other features of metabolic syndrome (high blood pressure, high lipids, diabetes), good control of these will also help to reduce your urate levels.

Ongoing treatments to reduce urate:

• Allopurinol: Allopurinol is the most commonly used urate-lowering drug. It has been available for many years and is normally effective and very well tolerated if taken correctly. It works by reducing the amount of urate that your body makes and is usually taken once a day.

• Febuxostat: Febuxostat is a more recently introduced drug that also reduces the amount of urate made in the body. However, unlike allopurinol it’s broken down by your liver and is therefore particularly useful if you have kidney problems and can’t take a high enough dose of allopurinol.

• Uricosuric drugs: Uricosuric drugs, which include sulfinpyrazone, benzbromarone and probenecid, work by flushing out more urate than normal through your kidneys. These drugs may not be suitable if you’ve had kidney stones or similar disorders. They’re not widely used in the UK, but they may be a useful alternative if allopurinol isn’t suitable for you.