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.

Clinical features

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. It is commonly associated with 
Obesity
Heavy alcohol intake
Hypertension
Renal impairment
Diuretic use.

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.
These include:
Acute illness
Trauma
Surgery
Alcohol (especially beer and wines)
Drugs that either increase or decrease the plasma urate concentration. ..especially diuretics

Patients who develop chronic 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, and tragic".

Acute gout - swelling redness and heat in the joint	Chronic joint involvement with crystal accumulation - tophus
Early crystal 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 chronic gout.

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.

Acute Gout
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 12–24 hours.
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 relatively contraindicated.

Recurrent Gout
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..
Tophaceous Gout
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 years.
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 time.

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.

Diet sheet

Forbidden
Very high purine content.
Herring, herring roe, meat extracts, mussels,
Sardines, yeast (brewer’s and baker’s).
Alcohol : Alcohol contains no purine but interferes with uric acid excretion.
Liver

Avoid
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.

Moderation
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 bread.

Acceptable
Low or no purine content - as often as desired.
Beverages  -tea, coffee, cocoa, chocolate
Carbonated soft drinks
Fruit juices
Sugar, sweets
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)
Eggs
Fruit
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 allowance.
Keep dietary fat to a minimum.

Be careful not to damage the joint.

Take your prescribed medication regularly.