Gout treatment requires different drugs that reduce the inflammation and the level of uric acid in the body. The following drugs are used in the treatment of gout
- Drugs that control the inflammation
Drugs that lower the level of uric acid in bloodAllopurinolProbenecid
- steroids such as prednisolone, betamethasone
- Non steroidal anti-inflammatory drugs such as ibuprofen, diclofenac
Steroids have a strong anti-inflammatory effect and they control the symptoms of the disease effectively and quickly. Initially they are given in high doses which are then gradually tapered and stopped after symptoms have resolved and other medications to reduce the blood levels of uric acid have started. They can also be injected directly into the involved joint.
Non steroidal anti-inflammatory drugs are also effective in controlling the symptoms of gout. Their main side effect in gastric irritation and gastro-intestinal bleeding.
Colchicine is a alkaloid that was isolated from the plant Colchicum autumnale in the year 1820. It is a very effective drug for acute gout treatment. It acts by inhibiting the chemical mediators of inflammation in gout and migration of white blood cells to the inflammatory site. It rapidly reduces the inflammation. Its recommended dose is 1.2mg every 6 to 8 hourly till resolution of symptoms occurs.
It can also be by intravenous route. Main side effect is vomiting and diarrhoea when it is given by the oral route. It should be stopped when these symptoms manifest. Toxicity and sudden death have been see with the intravenous route, when the dose has exceeded 4mg per day.
Definitive gout treatment is directed at the reduction of the blood uric acid levels to the normal range which is ideally less than 6mg/decilitre or 360micromole/litre. This prevents the repeated attacks of gout and causes resolution of the crystal deposits in the tissues and the joints.
General measures to reduce the uric acid blood levels include
- loss of excess weight
- reduction of dietary purine intake
- adequate hydration of the tissues by drinking water
- avoiding alcohol, diuretic drugs, levodopa and nicotinic acid
- control of increased blood pressure
If after adopting the above measures the uric acid level does not reduce to the normal levels then uric acid lowering drugs are started.
These drugs are started from the very beginning when the uric acid levels are above 9mg/decilitre or 535micromole/litre or if there is established gouty arthritis, crystal deposits or uric acid renal stones.
Probenecid is a fat soluble acid that blocks active transport of compounds in the renal tubules. Thus it prevents the re-absorption of uric acid from the renal tubules. Usual starting dose is 250mg twice daily and can be increased to 3 gram per day. Main side effect is gastric disturbances. It is not effective it the renal function is compromised and the level of creatinine in blood is above 2mg/decilitre. Creatinine level is a marker for renal function. Normal level is 0.8 to 1.2mg/decilitre.
Allopurinol is a drug that inhibits the enzyme xanthine oxidase. This enzyme is directly responsible for the synthesis of uric acid from xanthine and hypoxanthine. So now instead of uric acid only now hypoxanthine and xanthine are also present in the blood. Hypoxanthine and xanthine are more soluble than uric acid and are more easily excreted from the kidney. This results in a decrease in the level of uric acid in the blood. Therapy is started with a dose of 300mg/day and can be increased to 800mg/day. Dose has to be reduced in renal insufficiency. Side effects are rare but serious and include
- Skin rash and necrosis
- Liver damage
- Bone marrow depression
Febuxostat is also a drug that inhibits the enzyme xanthine oxidase. It is metabolised in the liver and so can be given in patients whose renal function is compromised with out any dose alteration. Its usual dose is 80 to 120mg per day. Side effects are similar to that of allopurinol.
Before initiating therapy with blood uric acid lowering drugs prophylaxis should be given with colchicine, NSAIDs or steroids to prevent a acute attack.
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This page was updated on 9th January 2011
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