Gout is a common disorder in which a build-up of uric acid crystals causes an acutely painful arthritis, most often affecting joints in the hands and feet, however other joints and the kidneys may be involved. ‘Attacks’ of gout tend to be intermittent. Gout is most common in men over 40 years.
An acute attack of gout often follows minor trauma to the affected area and typically awakens the person with severe pain and a red, hot and tender joint. Untreated, gout attacks become more frequent and more prolonged, ultimately resulting in erosion of joints - with chronic pain and deformity, ‘tophi’ – white deposits of uric acid in soft tissues, and kidney stones and kidney damage from uric acid deposits within the kidney. Kidney damage causes a marked increase in the incidence of high blood pressure and heart disease.
Uric acid is the end product of purine metabolism – purines being an essential component of cell structures. High levels of uric acid in the system result from any of :
- excessive dietary intake of purines – yeasts, organ meats, shellfish etc. (a separate diet sheet is available)
- excessive production of purines within the body – obesity, metabolic syndromes, high tissue turnover (e.g. with tumours, chemotherapy or radiotherapy)
- *reduced excretion of uric acid by the kidney
- alcohol – more than 10 grams per day – especially beer
- *thiazide diuretics – used a lot for hypertension
- kidney disease
TREATMENT
Acute Attack
- non steroidal anti-inflammatory medications are very effective, alternates when these can’t be used are:
- colchicine which has its use limited by the diarrhoea it may cause (dose has to be reduced in renal impairment)
- steroids
Long Term Prevention
- modify lifestyle factors : reduce weight, reduce alcohol intake and address other dietary factors
- avoid thiazide diuretics
- exclude other medical conditions – check blood pressure, cholesterol, blood sugar, thyroid and kidney function
- preventive medication – long term
Allopurinol (Zyloprim) is the most effective medication in gout prevention – it works by preventing xanthine (the immediate chemical precursor) being converted to uric acid in the body. Xanthine is much more soluble than uric acid and is readily excreted in the urine.
*Allopurinol should not be commenced during an acute attack of gout as it will make the symptoms much worse.
*During the first month of allopurinol therapy it must be combined with an anti-inflammatory medication or colchicine to prevent an acute gout flare up while uric acid deposits are dissolving from the joints.
The dose of allopurinol should be reduced in the presence of impaired renal function and the drug avoided in renal failure.
Allopurinol should not be taken with azathioprine.
Rarely a generalised itch and rash can develop from allopurinol use and the medication needs to be ceased. (Han-Chinese are at particular risk of developing severe skin reactions).
Colchicine in low dose can be used to prevent gout symptoms, however it does not reduce uric acid levels. Although relatively contraindicated, colchicine is often used in low dose to control gout symptoms in renal failure.
Probenecid is an alternate medication which works by increasing uric acid excretion by the kidneys. However it also reduces the kidneys ability to excrete a wide range of other medications with potentially serious consequences. Aspirin prevents probenecid from working and it is ineffective in renal failure. *Probenecid markedly increases the toxicity of methotrexate.
Losartan (Cozaar) – non PBS – and amlodipine (Norvasc, Amlo) are blood pressure medications which also reduce uric acid levels.
Click here to view Gout Diet Sheet
PSEUDO-GOUT presents similarly to gout but is due to the build-up of another crystal (calcium pyrophosphate) in joints. The crystals deposit in joint cartilage – usually in larger peripheral joints e.g. ankle.
Pseudogout may follow trauma, including joint surgery and is particularly associated with haemochromatosis, hypothyroidism, hyperparathyroidism, gout, amyloidosis and Wilson’s Disease.
Acute episodes are treated with anti-inflammatory medications or colchicine. Allopurinol is ineffective as a preventive treatment.
An acute attack of gout often follows minor trauma to the affected area and typically awakens the person with severe pain and a red, hot and tender joint. Untreated, gout attacks become more frequent and more prolonged, ultimately resulting in erosion of joints - with chronic pain and deformity, ‘tophi’ – white deposits of uric acid in soft tissues, and kidney stones and kidney damage from uric acid deposits within the kidney. Kidney damage causes a marked increase in the incidence of high blood pressure and heart disease.
Uric acid is the end product of purine metabolism – purines being an essential component of cell structures. High levels of uric acid in the system result from any of :
- excessive dietary intake of purines – yeasts, organ meats, shellfish etc. (a separate diet sheet is available)
- excessive production of purines within the body – obesity, metabolic syndromes, high tissue turnover (e.g. with tumours, chemotherapy or radiotherapy)
- *reduced excretion of uric acid by the kidney
- alcohol – more than 10 grams per day – especially beer
- *thiazide diuretics – used a lot for hypertension
- kidney disease
TREATMENT
Acute Attack
- non steroidal anti-inflammatory medications are very effective, alternates when these can’t be used are:
- colchicine which has its use limited by the diarrhoea it may cause (dose has to be reduced in renal impairment)
- steroids
Long Term Prevention
- modify lifestyle factors : reduce weight, reduce alcohol intake and address other dietary factors
- avoid thiazide diuretics
- exclude other medical conditions – check blood pressure, cholesterol, blood sugar, thyroid and kidney function
- preventive medication – long term
Allopurinol (Zyloprim) is the most effective medication in gout prevention – it works by preventing xanthine (the immediate chemical precursor) being converted to uric acid in the body. Xanthine is much more soluble than uric acid and is readily excreted in the urine.
*Allopurinol should not be commenced during an acute attack of gout as it will make the symptoms much worse.
*During the first month of allopurinol therapy it must be combined with an anti-inflammatory medication or colchicine to prevent an acute gout flare up while uric acid deposits are dissolving from the joints.
The dose of allopurinol should be reduced in the presence of impaired renal function and the drug avoided in renal failure.
Allopurinol should not be taken with azathioprine.
Rarely a generalised itch and rash can develop from allopurinol use and the medication needs to be ceased. (Han-Chinese are at particular risk of developing severe skin reactions).
Colchicine in low dose can be used to prevent gout symptoms, however it does not reduce uric acid levels. Although relatively contraindicated, colchicine is often used in low dose to control gout symptoms in renal failure.
Probenecid is an alternate medication which works by increasing uric acid excretion by the kidneys. However it also reduces the kidneys ability to excrete a wide range of other medications with potentially serious consequences. Aspirin prevents probenecid from working and it is ineffective in renal failure. *Probenecid markedly increases the toxicity of methotrexate.
Losartan (Cozaar) – non PBS – and amlodipine (Norvasc, Amlo) are blood pressure medications which also reduce uric acid levels.
Click here to view Gout Diet Sheet
PSEUDO-GOUT presents similarly to gout but is due to the build-up of another crystal (calcium pyrophosphate) in joints. The crystals deposit in joint cartilage – usually in larger peripheral joints e.g. ankle.
Pseudogout may follow trauma, including joint surgery and is particularly associated with haemochromatosis, hypothyroidism, hyperparathyroidism, gout, amyloidosis and Wilson’s Disease.
Acute episodes are treated with anti-inflammatory medications or colchicine. Allopurinol is ineffective as a preventive treatment.
