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Gout is a metabolic disorder that may be inherited. It is characterized by recurrent acute joint inflammation (gouty arthritis) usually in the extremities, caused by crystals that are deposited in and around the joints. These crystals come from blood that contains markedly high concentrations of uric acid (urate), a waste product of digestion that is normally excreted in the urine.
Symptoms include heat, red and shiny skin, and extreme tenderness and pain in the affected joints. It tends to affect the peripheral joints, most often those in the big toe, but can also affect the knees, elbows, thumbs or fingers.
The arthritis may become chronic and cause joint deformity. Tophi – small, hard lumps of urate deposits – may also form around the ankles, hands, tips of the elbows and earlobes. The tophi may erupt, causing a discharge.
Collection of urate crystals in the kidneys can lead to kidney stones.
Not all persons with high urate levels in their blood (hyperuricaemia) develop gout, but the greater the degree and duration of hyperuricaemia, the greater the risk of crystal deposition and acute gout attacks. Gout is a common disease and one of the oldest in medical literature. One of the oldest drugs in therapeutics, colchicine, is used for the acute attack of gout.
Urate is normally steadily excreted in the urine. In some people the mechanism to excrete the uric acid is defective. These people are known as under-excretors, and constitute the majority of gout sufferers. This is aggravated by certain medications, especially diuretics and kidney disease. It occurs commonly in the setting of people with heart disease, obesity and diabetes and commonly in women who are post-menopausal who use diuretics.
Hyperuricaemia may also be caused by blood conditions such as lymphoma, leukaemia and haemolytic anaemia (where blood cells are destroyed), and by other cancers or psoriasis. In this situation the problem is over-production and the patients are called over-producers.
If urate levels in the blood rise too high (hyperuricaemia) the urate starts to crystallise as needle-like crystals in the joint fluid (synovial fluid) and joint lining (synovial lining). It forms deposits where the temperature is lower, as it is in the extremities, particularly around the big toe.
Some foods may contribute to high blood levels of urate. Marked rises in urate often follow overindulgence in high protein foods, especially if alcoholic beverages are also consumed. In most cases alcohol does not contain uric acid, but further prevents the excretion of uric acid via the kidneys.
Urate can also form small, plate-like crystals in the kidneys, where they may aggregate to form gravel or stones.
Intense joint inflammation occurs when white blood cells engulf the crystals.
In order for this to occur there is often a precipitating event. Known precipitating factors for gout attacks include acute infection, emotional upset, the use of diuretic drugs such as Furosemide or Lasix, surgery and trauma. In fact any “change” in the daily routine of a patient can precipitate an attack. This includes a food or alcohol binge. But even a new (especially high protein) reducing diet can aggravate the onset of an attack.
Risk factors
• Genetic predisposition for an abnormality in handling urate accounts for approximately half of all cases. A family history of gout can be a risk factor.
• Male sex in middle age
• High blood pressure
• Drugs: thiazide diuretics, aspirin, tuberculosis medication (pyrazinamide and ethambutol)
• Obesity or excessive weight gain, especially in youth
• Moderate to heavy alcohol intake
• Abnormal kidney function
• A western lifestyle
• Underlying diseases with a high turnover of cells (cancers – especially blood cancers and haemolytic anaemia)
The following conditions can trigger gout:
• Recent surgery
• Dehydration
• Joint injury
• Excessive dining
• Heavy alcohol intake
• Stress
• Change in diet
• Foods with a high protein content such as red meat, shell fish, legumes and soya
Symptoms include heat, red and shiny skin, and extreme tenderness and pain in the affected joints. It tends to affect the peripheral joints, most often those in the big toe, but can also affect the knees, elbows, thumbs or fingers.
The arthritis may become chronic and cause joint deformity. Tophi – small, hard lumps of urate deposits – may also form around the ankles, hands, tips of the elbows and earlobes. The tophi may erupt, causing a discharge.
Collection of urate crystals in the kidneys can lead to kidney stones.
Not all persons with high urate levels in their blood (hyperuricaemia) develop gout, but the greater the degree and duration of hyperuricaemia, the greater the risk of crystal deposition and acute gout attacks. Gout is a common disease and one of the oldest in medical literature. One of the oldest drugs in therapeutics, colchicine, is used for the acute attack of gout.
Urate is normally steadily excreted in the urine. In some people the mechanism to excrete the uric acid is defective. These people are known as under-excretors, and constitute the majority of gout sufferers. This is aggravated by certain medications, especially diuretics and kidney disease. It occurs commonly in the setting of people with heart disease, obesity and diabetes and commonly in women who are post-menopausal who use diuretics.
Hyperuricaemia may also be caused by blood conditions such as lymphoma, leukaemia and haemolytic anaemia (where blood cells are destroyed), and by other cancers or psoriasis. In this situation the problem is over-production and the patients are called over-producers.
If urate levels in the blood rise too high (hyperuricaemia) the urate starts to crystallise as needle-like crystals in the joint fluid (synovial fluid) and joint lining (synovial lining). It forms deposits where the temperature is lower, as it is in the extremities, particularly around the big toe.
Some foods may contribute to high blood levels of urate. Marked rises in urate often follow overindulgence in high protein foods, especially if alcoholic beverages are also consumed. In most cases alcohol does not contain uric acid, but further prevents the excretion of uric acid via the kidneys.
Urate can also form small, plate-like crystals in the kidneys, where they may aggregate to form gravel or stones.
Intense joint inflammation occurs when white blood cells engulf the crystals.
In order for this to occur there is often a precipitating event. Known precipitating factors for gout attacks include acute infection, emotional upset, the use of diuretic drugs such as Furosemide or Lasix, surgery and trauma. In fact any “change” in the daily routine of a patient can precipitate an attack. This includes a food or alcohol binge. But even a new (especially high protein) reducing diet can aggravate the onset of an attack.
Risk factors
• Genetic predisposition for an abnormality in handling urate accounts for approximately half of all cases. A family history of gout can be a risk factor.
• Male sex in middle age
• High blood pressure
• Drugs: thiazide diuretics, aspirin, tuberculosis medication (pyrazinamide and ethambutol)
• Obesity or excessive weight gain, especially in youth
• Moderate to heavy alcohol intake
• Abnormal kidney function
• A western lifestyle
• Underlying diseases with a high turnover of cells (cancers – especially blood cancers and haemolytic anaemia)
The following conditions can trigger gout:
• Recent surgery
• Dehydration
• Joint injury
• Excessive dining
• Heavy alcohol intake
• Stress
• Change in diet
• Foods with a high protein content such as red meat, shell fish, legumes and soya
