The Herald (Harare)
15 March 2008
Gout is one of those diseases which raises a nervous laugh, because it is so
painful, and, also, because it most commonly affects the people (mostly men) we
are normally scared of laughing at for their pompous behaviour or because of
their position or place in society.
Gout is caused by an excess in the body of uric acid and its salts a breakdown product of a food substance known as purine.
It is relatively insoluble so large amounts crystallise in the extremities of the body and are also concentrated in kidneys.
If you have ever seen uric acid crystals, which are triangular shaped with sharp edges and pointed ends, you will realise that they cant crystallise in kidneys without doing a lot of damage.
Dogs and horses, don't metabolise purine to uric or urates, instead they manufacture hipp uric acid which is very much more soluble.
It stands to reason therefore that dogs and horses and a lot of other animals don't get gout.
Gouty people can often be diagnosed clinically by looking at the external ear because deposits of urates occur and they are called tophi, which are very sensitive too.
The aim of treatment is to reduce the amount of uric acid and its salt (called urates) in the serum.
The older one gets the more likely an acute attack of gout is likely to strike. Surprisingly, it is not only the traditional old age, lazy, man, who drinks too much, is overweight and exercises mostly in bed.
Some therapies, such thiazide treatment (HCT) for high blood pressure, can precipitate an attack, as well as diabetes and kidney disease can bring on gout as a complication.
Recently, a diet produced by the UK Gout Society is available, free, and can be obtained at www.ukgoutsociety.org.
Purine-rich foods, such as beer and spirits, red meat, and a history of renal stone should alert the health worker, if not the patient, to the possibility of a high uric acid level in the blood.
I have found that inadequate hydration i.e. the reduction of intake of water or other fluids -- is an important factor in the first episode of a clinical gout attack.
Traditionally, this affects the left big toe, and the pain is so severe that everybody knows about it, from the yells and groans of the patient.
It is very likely to afflict men, and it is well-known that adult males cannot recall when he last saw a doctor, and, paradoxically, the treatment, if introduced too enthusiastically can result in further episodes of acute gout.
The prevention of further attacks should include an NSAID, such as Brufen, or colchicines (the active ingredient in several corms, notably the autumn corm), to avoid further attacks while gradually reducing the serum urate level.
This can effectively be done, without recourse to sophisticated laboratory tests by initiating allopurinol one month after the presenting acute attack.
If laboratory facilities are available, the aim should be to reduce the serum urate concentration -- the objective 'goal standard' of effective treatment -- to about 360µmol/1 or below.
The patient's confidence in his health adviser must be secure, because, even with appropriate treatment and proper diet, as well as maybe modifying his other therapy, attacks of gout are likely to be provoked by treatment.
The mutual understanding of this scenario should be clearly understood by both the patient and the doctor.
Recently, the contribution of soft drinks and fruit juices as a result any form of sweetening, but particularly fructose derived from corn starch and fructose rich fruits and fruit drinks has been associated with an increased risk of gout.
Perhaps there is some truth, after all, in the old wives' tale that tomatoes cause gout.
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