In acute gout, the pain is severe, throbbing and unrelenting and can last longer than a week. The affected joint is swollen, shiny and very tender to touch and often contact with the bed sheath can cause agonising pain.

The initial treatment is an optimal dose of an anti-inflammatory drug. The commonest of these is ibuprofen. Non-steroidal anti-inflammatory drugs (NSAIDs) have side effects and risks to patients but treatment is on a short term basis. Side effects can be reduced by using the slow released formulation of the drug or a suppository. The slow release drug will pass through the stomach intact reducing the risk of nausea and vomiting. If there is a history of gastric bleeding or ulcers, NSAIDs are not recommended.

Colchicine was commonly used before the advent of NSAIDs but it is likely to cause nausea and diarrhoea. The dose is gradually increased until effective or to the limit dictated by side effects.

Azapropazone is a vey useful drug for treating gout.

In large joints the fastest relief is achieved by steroid injection into the synovial space. The commonest manifestation of acute gout is in the big toe. Injection into the joints of this toe is not recommended because the joint is small and very painful.

Phenylbutazone was used extensively in the past, and was first choice in gout treatment but the serious side effect of bone marrow depression on long term treatment has led to the drug withdrawal in most countries.

During treatment of an acute episode of gout, your doctor will not start you on allopurinol. Any attempt to reduce the level of blood uric acid during an acute attack will make your gout worse and the episode last longer.

Dr.Phil Hariram,

Arthritis Guide.

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In gout the uric acid in the blood stream is higher than normal. The circulating level of uric acid in the blood depends on the equilibrium between production and excretion.

Cells in the body are constantly replaced as they get old and these cells die. When this happens, purines are released. Purines are especially found in liver cells. The released purines are gradually broken down until uric acid is formed and ready from disposal. The final stage in the breakdown process relies on an enzyme called xanthine oxidase. This enzyme is found mainly in the liver, bone marrow and cells lining the gut.

In disease such as leukaemia, the bone marrow is overactive and a side effect of this very serious condition is an over production of uric acid.

As uric acid is produced, the constant excretion keeps the level in the blood constant and normal. Two thirds of uric acid excretion from the body is done by the kidneys. So anything that can affect the normal function of the kidneys can affect the uric acid level. Kidney disease and thiazide diuretics will affect the excretion of uric acid and will result in high blood uric acid level (hyperuricaemia).

So drugs and certain illnesses can not only affect the elimination of uric acid but can speed up production. Either way they can cause hyperuricaemia and potentially gout.

In primary gout, however, the production of uric acid is normal but the elimination is slower, leading to an imbalance that can induce an attack of gout.

By understanding how purines are broken down and the role of xanthine oxydase in the final stage of producing uric acid, researchers developed the drug, allopurinol. This drug inhibits xanthine oxydase function and is used as maintenance therapy for gout sufferers.

Dr.Phil Hariram,

Arthritis Guide.

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Gout is a form of inflammatory arthritis. In gout, crystals of uric acid is deposited in and around the joints. For this deposit of urate to occur, the circulating level of uric acid in the blood must be higher than normal.

Gout has been recorded through the centuries. Hippocrates wrote about it and urate crystals were found in the big toe of an Egyptian mummy.

Gout is more prevalent in males and high in affluent societies. This may be a dietary factor. In the old days the rich ate the expensive red meat while the poor could only afford grain. Guess who developed gout?
Acute gout is rare in pre-menopausal women and it is predominantly a male disease up to the age of 50. It usually starts after 30 years of age and more commonly between 40 and 50 in males. In women the first attack is usually between 50-60 years.

The first attack of gout is usually in the big toe and this is called Podagra. 70-90% of first attacks present this way.

Pain often develops at night and within a few hours the pain level can escalate to severe and throbbing. The big toe will become red, hot, swollen and very tender to the touch. This acute attack will resolve spontaneously but can take weeks. Medical intervention often shorten this episode.

After this first attack your doctor is not likely to start you off on long term medication because you may not get another attack for years. On the other hand, you could have another attack in days.

Dr.Phil Hariram,

Arthritis Guide.

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