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Friendly Print preview ARTHRITIS
FOUNDATION OF VICTORIA GOUT Gout is one of the most common types of arthritis - one of 150 or more different types. As with many other forms, there is inflammation of the joint, with swelling, warmth, redness and pain. Nowadays, due to advances in medical research, gout can be well controlled. If the correct treatment program is followed, gout need not be a major problem. What is Gout? It is a disease in which there is a build-up of uric acid in the body. A relatively small amount comes directly from the food we eat. It is normally dissolved in the bloodstream and passed out through the kidneys. If the body cannot get rid of enough, the build-up of uric acid will be deposited in joints. The first attack of gout usually involves the big toe or "bunion" joint. The ankle, foot and knee may also be affected. It can occur over the point of the elbow, occasionally in the hand and rarely in other joints. Attacks can occur very quickly, often overnight, unlike most other forms of arthritis, which usually start more gradually. The affected joint rapidly becomes very painful, often to the point that even the weight of a sheet is unbearable. Untreated, each attack lasts approximately a week. After the first attack, which almost always involves only one joint, it is usually months or years before the next one occurs. But without the right management, attacks become more frequent, last longer and may involve other joints. Repeated attacks may accelerate joint damage. Uric acid can also deposit in other tissue. These deposits are called "tophi". They usually occur near affected joints or around the elbow, toes, fingers and even the outer edge of the ear. Tophi usually take many years to be easily seen. Attacks often occur for no obvious reason but can be triggered by:
In some people, excess uric acid can be deposited in the kidney as stones or, less commonly, in the bladder as gravel or multiple stones. The can cause problems with kidney function and sometimes, severe pain. Who gets gout? Almost all people with gout have too much uric acid in their blood, a condition called hyperuricaemia. It usually occurs when the kidneys are unable to get rid of enough uric acid, which the body sometimes overproduces. Hyperuricaemia and gout can be hereditary. Fluid tablets can aggravate the condition because they hamper the kidney's ability to filter uric acid and thereby cause further build-up in the blood. Being overweight, drinking too much alcohol or not drinking enough fluids can all aggravate the condition. About 90% of people with gout are men. The first attack generally occurs between 40 and 50 years of age, but can occur at any age. Women with gout usually develop it after the menopause. It is not, as once thought, a disease of the wealthy, although too much alcohol and over-eating are often associated with its development. About 70,000 Australians have the disease, which affects people from all walks of life. Diagnosis A sudden attack in one joint (usually the big toe) suggests a diagnosis of gout, but some other forms of arthritis can also act like gout, (especially pseudogout and septic arthritis). It is important for a doctor to make a diagnosis. The uric acid level can be measured by a blood test. It is usually raised during an attack but it can also be normal. A raised blood uric acid level does not necessarily indicate gout. To confirm the diagnosis it is sometimes necessary to take fluid from the joint to see if there are gout crystals. Management
While it is important to drink a lot of fluid - at least two litres per day - particularly when there are kidney stones, exercise is also important to keep the joints mobile. Gout can sometimes be associated with hypertension and other vascular disorders (eg. Coronary artery disease) so the blood pressure of people with gout should be checked regularly. Proper diagnosis and management, including weight and diet control, should mean that gout can be totally controlled. For further information about self-management of gout, contact the Arthritis Foundation. Date Last Reviewed by NEVDGP: 20 August, 2006
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