Gout is a syndrome
caused by an inflammatory response to the formation of monosodium urate monohydrate
crystals which develop secondary to hyperuricemia. Acute and chronic forms are recognized.
Hyperuricemia may be due to environmental and/or genetic factors.
Most commonly affects middle-aged males. It is an acute and
usually relapsing self-limiting arthritis. A Chronic form associated with collections of
crystals - tophus formation occurs, and bone and joint destruction can occur.
commonly associated with
Heavy alcohol intake
It especially involves the first metatarsophalangeal joints
especially the big toe, heels, ankles and knees.
Gout has been called the disease of kings. The term
gout, is derived from Latin gutter (a drop) which reflects
the notion that gout resulted from a local instillation of malevolent humour. These
concepts are well illustrated in paintings of persons afflicted with gout. It is also seen
as a "disease of plenty - which is an incorrect generalization.
Hyperuricemia has been defined as a serum or plasma urate
concentration greater than
7.0mg/dl (0.42mmol/l) in males
6.0mg/dl (0.36 mmol/l) in females
It is important to recognize the clear distinction between
hyperuricemia and gout.
Hyperuricemia is clearly a risk factor for the development of gout,
the risk increasing with a higher urate concentration. However, many years of
hyperuricemia have usually elapsed before the development of acute gouty arthritis, and in
some hyperuricemic people gout may never develop.
Acute gout is
characterized rapid onset of pain, There is pain and the swelling, with associated
redness of the affected joint. The pain may be excruciating. In
over half of the initial attacks, the onset is in the first metatarsophalangeal joint
(MTP), and in time, this joint is affected in some 90% of patients with gout.
Almost any joint can be affected. However, the lower limbs are
involved more often than upper limbs.
Mild attacks may resolve within one to two days. More severe attacks
exhibit rapidly increasing pain reaching its peak usually within a few hours, remaining at
this level for some one to three days, then slowly remitting, such that the attack has
often subsided within seven to ten days. It may take several weeks before very severe
attacks settle completely.
Several factors have been recognized as precipitants of acute
attacks of gout.
Alcohol (especially beer and wines)
Drugs that either increase or decrease the plasma urate
concentration. ..especially diuretics
A radical change in diet or food
Patients who develop
gout usually are those whose hyperuricemia is not controlled.
Tophi appearing within the first two years of gout are extremely
rare and patients have usually suffered from gout for at least 10 years before tophi
develop. The tophi are
collections of crystals that form deposits in soft tissue, joint, bone and tendons. They
cause erosion and destruction of the bone, and cause damage that may lead to
crippling. Such crippling is I feel a tragedy, as this situation is completely
controllable, and preventable. To be crippled from gout is "completely unnecessary,
Acute gout - swelling
redness and heat in the joint
Chronic joint involvement with crystal
accumulation - tophus
accumulation at the elbow - tophus
Neglected chronic gout with tophi
Therapy for Gout
Therapy in gout is directed towards:
1. the management of acute attacks
2. The prevention of further attacks and the complications of
It is important when considering therapy for gout to distinguish
between therapy for reducing inflammation and that for managing hyperuricemia.
The decision to introduce drugs to normalize hyperuricemia depends
in part :
1. on the number of previous attacks of acute gout
2. The degree of hyperuricemia
3. The presence or otherwise of reversible factors
4. The presence of tophi.
Urate lowering drugs will not normally be used after just a
single attack of gout. but should be considered after the second or third attacks.
Furthermore, they should virtually always be used for tophaceous gout.
The patient needs to be informed that the decision to commence
antihyperuricemic therapy usually implies life-long treatment and the patient, needs to be
committed to this policy.
Therapy is aimed at controlling the
acute attack - completely, and then if indicated, controlling the uric acid level at source or
by increasing it's removal from the body. Introduction of these second line drugs must
never be during the actual acute attack, as they will potentially aggravate the acute
episode and prolong it.
Both increases and decreases in plasma urate concentrations may
precipitate or prolong an attack of gout. Therefore, therapy aimed at reducing urate
concentrations should be delayed until after the complete resolution of all signs of
inflammation. It must be noted that one of the commonest cause of difficulty in
controlling an attack, is the simultaneous administration or withdrawal of drugs that
alter the plasma urate concentration.
Colchicine and Nonsteroidal anti-inflammatory drugs (NSAIDs) are
effective in the treatment of acute gout and are much superior to paracetamol or aspirin.
In addition, NSAIDs are superior to colchicine in terms of speed of onset of action. Thus,
despite having been used for centuries, colchicine is usually reserved for patients in
whom NSAIDs are contraindicated. Oral corticosteroids
such as prednisone is useful in resistant gout and we use this for 10 days
to 2 weeks, during and after treatment of the acute episode, whilst
instituting second line therapy to prevent recurrence in patients who are
difficult to control.
Intra-articular administration of Corticosteroids is a particularly
effective means of terminating an attack of gout.
Resolution is typically complete within
Cortisone is of particular value in some patients with
renal impairment and other conditions where the use of full doses of other drugs may be
Despite the use of effective prophylaxis, only correction of the
hyperuricemia can alter the underlying tendency to gout.
Drugs to correct hyperuricemia
act either by
Promoting the renal excretion of urate - (uricosuric agents) or by
Decreasing urate production - by inhibiting
xanthine oxidase (allopurinol)
Unfortunately allergy to
allopurinol is possible. Hypertension also can occur with allopurinol, so
your doctor should check your blood pressure after starting it.
If allopurinol is not tolerated
because of allergy, probenecid can be used.
It cannot be stressed too much that antihyperuricemic drugs should
not be commenced until an attack of gout has settled completely. In addition, I use
prophylactic doses of colchicine or NSAID's or even low
dose cortisone to minimize the risk of inducing an
attack of acute gout, whilst introducing the second line - preventative drugs..
The principle of treatment of tophi is to lower the plasma urate
concentration to such a degree, as to allow urate to be resorbed from the surface of the
tophi. The uric acid therefore is slowly excreted at the kidney, and production is
lower than excretion, resulting in net loss of uric acid.
(In this phase, I use citrosoda 10ml twice a day to prevent
deposition of crystal in the kidney, and prevent kidney stone developement.)
It is therefore aimed at maintaining the urate concentration
within the middle of the optimal range.
This requires the long-term use of urate-lowering drugs over many
Colchicine and most NSAIDs, while controlling acute attacks, will
not prevent the formation of tophi and may, by preventing the inflammatory response,
actually increase the development of tophi unless hyperuricemia is controlled at the same
Gout and diet
General Guidelines for Gout prevention
Avoid purine-rich foods (see Diet sheet chart - below )
The higher the purine content, the more uric acid will be produced
in the body.
If you are overweight, try and achieve your ideal weight through
slow, controlled weight loss (maximum 500 g per week).
Rapid / sudden fasting is not recommended as this can raise uric
acid levels and aggravate gout.
Avoid heavy, rich meals with high fat and protein content.
Alcohol should be avoided, particularly wine since it interferes
with uric acid excretion.
I generally require patients to comply strictly with diet whilst
starting them on second line medication therapy for gout, but liberalize the diet after
approximately six weeks, once stable.
Very high purine content.
Herring, herring roe, meat extracts, mussels,
Sardines, yeast (brewers and bakers).
Alcohol : Alcohol contains no purine but interferes with uric acid
High purine content - not more than one item once a week.
Anchovies, bacon, chicken soup, Beef, mutton leg, mutton chop,
pheasant, salmon, sausage, trout, turkey, veal, venison, lobster, crab.
Moderate purine content-not more than one item 4 times a week.
Asparagus, bass, bouillon, brains, cauliflower, chicken, duck,
halibut, ham, kidney beans, lentils, Lima beans, liverwurst, mushrooms, oysters, peas,
plaice, pork, rabbit, roe, shad, spinach, tongue, tripe, tuna, wholegrain cereals and
Low or no purine content - as often as desired.
Beverages -tea, coffee, cocoa, chocolate
Carbonated soft drinks
Vegetables : (except those under BE CAREFUL)
Vegetables and cream soups (no meat stock)
Butter, fats of all kinds (in moderation)
Bread (except wholegrain)
Cereals (except wholegrain)
Cheese : all kinds (in moderation)
Milk - buttermilk, condensed, malted
Nuts - all kinds, peanut butter
Drink plenty of water (2-3 litres per day) to help flush uric
acid through the kidneys. Please note - if you have cardiac or kidney disease, your doctor
may actually require fluid restriction - and you should consult him regarding fluid intake
Keep dietary fat to a minimum.
Be careful not to damage the joint.
Take your prescribed medication regularly.