What is gout?
Gout is an acute inflammatory joint condition and therefore an ‘arthritis’ (which is literally Latin for ‘inflamed joint’). Gout generally begins with an attack of extraordinary pain where the joint becomes red, hot, swollen and obviously in distress to look at. It is caused when elevated levels of uric acid accumulate in the blood. The uric acid then crystallises out of solution as monosodium urate and deposits in joints but also in soft tissues such as tendons. Gout will affect around 1% of the Caucasian population at some point in their lives. It is more common in Africans and Pacific Islanders and less common in Aborigines. The joint that is most commonly affected is the joint at the base of the big toe which accounts for 75% of all first attacks. The reason gout so commonly presents in the foot is due in part to the lower body temperature out at the extremities. Other common sites include other foot joints, elbows and the ear lobe.
What does gout feel like?
If you are reading this, then it is likely that you have recently suffered an episode of gout and you won’t need me to confirm that the pain is extreme. It comes on suddenly, more often then not, overnight. The pain is excruciating and can be worsened by as little pressure as a bed sheet or (according to some) the missus talking too loud. Gout usually only affects one joint at a time and without any intervention will taper off in a week or so. Without preventative treatment, the attacks of gout will usually be repetitive, though there may initially be gaps of months or years between them. Over time. attacks become more frequent and more severe and can spread to involve other joints and tissues. Eventually, a state of continuous joint pain can develop with progressive joint damage known as gouty arthritis or tophaceous gout. The term ‘tophaceous’ means literally the presence of ‘tophi’ which are painless lumps containing the monosodium urate crystals that come to the surface of the skin. When broken they are found to contain white chalky goo with a distinctive granular nature. Gouty arthritis is a very destructive condition where the bone is eroded away giving rise to a very distinctive X-ray appearance.
Why did I get gout?
The basic answer is too much uric acid in your blood which is called hyperuricaemia. This can occur for a number of reasons including diet, family propensity or the kidneys excreting too little urate into the urine. Your doctor may have told you that your uric acid level is too high but this does not guarantee that you will have an attack of gout. Only around 10% of those with hyperuricaemia go on to develop gout. Gout is a disease that mostly affects men and is very rare in younger women. Women become equally prone to developing gout after menopause when it is seen quite often.
Gout is more common in people who:
- Are overweight,
- Consume alcohol
- Have high cholesterol levels.
- Have elevated blood pressure.
- Eat a diet rich in purines (discussed below) sugar, meat and seafood which increase the concentration of uric acid in the blood.
- Eat a diet low in dairy products, vegetables and alternate sources of protein. These are foods that do not elevate (or may lower) uric acid.
- Take certain medications which are known to make gout more likely. These include certain diuretics (fluid tablets), niacin (a B-complex vitamin), regular low dose aspirin, C yclosporine and some forms of chemotherapy. Important DO NOT stop taking medication that appears on this list without consulting your Doctor.
- Have reduced kidney function which reduced urate excretion via the urine.
- Live a sedentary lifestyle.
- Have metabolic syndrome (Syndrome X) being the combination of hypertension, diabetes, dyslipidemia (elevated blood fats such as cholesterol and triglycerides) and truncal obesity (literally too much fat around the trunk / abdomen).
- Suffer from other diseases that make gout more likely including: leukaemia, polycythaemia, obesity, diabetes, Lesch-Nylan syndrome, high blood pressure, kidney disease, haemolytic anaemia and post organ transplant.
- Have been exposed to cytotoxins (poisons) including lead poisoning.
- Have a liver disorder. While the majority of uric acid is excreted by the kidneys, the liver is responsible for about 30% of the elimination.
- Are experiencing starvation or extreme levels of endurance exercise that cause the body to consume its own muscle tissue.
- Are experiencing severe sleep apnoea. In rare cases, the oxygen starvation that comes with sleep apnoea can cause a similar cellular decomposition as occurs in the last example.
How do you treat gout ?
In the acute phase, treatment most commonly involves non-steroidal anti-inflammatory drugs (NSAIDs) which will start to reduce the pain in 4 hours and bring the symptoms under control in as little as 12 to 24 hours. Ibuprofen is used commonly
If more potent treatment is necessary or NSAIDs are not allowable, a steroidal anti-inflammatory (glucocorticoid) can be used orally. Steroid can also be injected directly into the joint although great care is needed to be sure that the diagnosis of gout is correct> If the condition were an infected joint space, steroid injection would be very harmful.
Colchicine is another alternative for those unable to tolerate NSAIDs, although it is often not the first choice as it can reasonably commonly cause gastrointestinal upset.
None of these ‘acute phase’ drugs have any effect on lowering uric acid levels. Rest and elevation of the foot is also important. Apply ice for 20-30 minutes several times per day. (Take appropriate care if you have peripheral neuropathy).
In the longer term, dietary changes and weight loss will almost always be the first line of treatment. Medication called Allopurinol blocks uric acid production and is the most commonly used long term uric acid lowering. Allopurinol is the most used long-term drug in the world and is widely found to be safe and effective. It is usually not started until two weeks after a second episode of gout. Talk to your Doctor about the advisability of preventative medication.
How should I change my diet to reduce my risk of gout?
These foods have higher levels of purines should be restricted or avoided:
- Offal foods like liver, kidneys, sweetbreads, tripe and tongue.
- Large amounts of red meat.
- Shellfish / crustaceans.
- Seafood such as salmon, sardines, and herring.
- Peas. beans and lentils.
Limit the use of fructose – contained in diabetic chocolate and some artificial sweeteners for example.
Bring your body weight into the healthy weight range. Obesity is a strong risk Therefore, a lower fat diet is warranted, though fat is not directly a precipitator of gout
Normalise your blood pressure. Reduce salt intake and talk to your doctor about your current BP status. Is medication required?
Drink plenty of water to make it easier for the kidneys to move the urate into the urine (unless instructed not to in the case of some types of kidney disease).
There is a study that has shown that Vitamin C intake of 1,500 mg per day may decrease the risk of gout by 45%.
Another study suggests coffee (but not tea) will create a lower risk of gout.
What is the test for gout?
Elevated uric acid in the blood is a common feature of gout and it will often be present. Blood tests for gout can show normal or even low levels of uric acid as the crystals forming in the joint will ‘use up’ some of the free uric acid from the blood. This means that the test should be repeated in a couple of weeks to test your normal plasma urate concentration You should also remember from above that only 1 in 10 people who have elevated uric acid will actually succumb to a gout attack. Hyperuricemia is defined by a plasma uric acid level greater than 420 μmol/L (7.0 mg/dL) in males, or 380 μmol/L in females.
Other blood tests are commonly performed including:
- erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) which can be used to consider other forms of arthritis,
- full blood count (especially for white blood cells that may indicate an infection in the joint (symptoms of which can be very similar to gout and can occur after any sort of puncture injury – including vaccinations and acupuncture)
- and electrolytes and creatinine levels to check renal function.
A definitive diagnosis of gout is based upon the identification of monosodium urate crystals within the joint fluid. A small amount of fluid can be removed with a needle at the examination.
Another differential diagnosis is ‘pseudo-gout’ or chondrocalcinosis which is caused by deposition of calcium pyrophosphate rather than uric acid.
Why should I treat my gout?
If you don’t seek treatment during an attack, the pain will continue for days or even weeks. With further episodes, more joints will be affected and the attacks will last longer and come more frequently. If you have gout attacks for many years, you will develop tophi in the tissues, particularly around the toes, fingers and elbows. The affected joints will be destroyed. The elevated urate in the blood can become a problem for the kidneys to process and lead to renal damage and a cyclical worsening of both conditions. In short, if you have had more than one episode of gout, it should not be left untreated.
There is more information on our webpage about diet and gout.