Gout and Hyperuricaemia: Features, Diagnosis and Treatment

In this article we will discuss about the Gout and Hyperuricaemia:- 1. Meaning of Gout and Hyperuricaemia 2. Clinical Features of Gout and Hyperuricaemia 3. Complications 4. Diagnosis 5. Treatment.

Contents:

1. Meaning of Gout and Hyperuricaemia
2. Clinical Features of Gout and Hyperuricaemia
3. Complications of Gout and Hyperuricaemia
4. Diagnosis of Gout and Hyperuricaemia
5. Treatment of Gout and Hyperuricaemia

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1. Meaning of Gout and Hyperuricaemia:

Gout is a characteristic arthritis which affects sin­gle joints, often the big toe giving pains that last only a few days but are liable to recur. Middle aged men are chiefly affected. It is caused by the deposi­tion of urate crystals in the joint. The increased concentration of urate in the plasma causes hype­ruricaemia.

Hyperuricaemia may be asymptomatic. Such individuals carry a greatly increased chance of the clinical complications, gouty arthritis or uric acid stones in the urinary tract. Those who have recur­rent gout and hyperuricemia over long time are li­able to develop tophi, accumulations of urate in tendons or cartilage.

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2. Clinical Features of Gout and Hyperuricaemia:

(a) The patient has suddenly stabbing pain in one joint. The big toe is easily stubbed or injured by an ill-fitting shoe. The wrists, ankles and knees are much less common sites. The spine is practically immune.

(b) The joint is swollen and exquisitely ten­der; pain is aggravated by the least move­ment.

(c) The overlying skin is tense, red and shiny with distended veins and may later show oedema.

(d) Fever, malaise, loss of appetite, gastro­intestinal upset and scanty highly col­oured urine are common.

(e) The patient may be very irritable.

(f) Blood E.S.R. rate is raised.

(g) As the inflammation subsides the skin over the joint becomes scaly and itches. The joints recover completely.

(h) If the hyperuricaemia is high and not regu­lated, attacks tend to occur with increas­ing frequency and to last longer. Eventu­ally a stage may be reached where there is chronic persistent though generally less painful arthritis of several joints.

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3. Complications of Gout and Hyperuricaemia:

People with hyperuricaemia have a greatly in­creased liability to form uric acid stone in the uri­nary tract. These can present with renal colic and are one cause of the chronic renal disease that is an important late complication in gout.

In gout, the kidneys may receive decreased amounts of glutamine because more has been diverted into purine synthesis. Degenerative renal disease occurs in patients with chronic gout, and hypertension itself appears to reduce uric acid clearance. Raised plasma urates have also been found in patients with cerebral vas­cular disease.

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4. Diagnosis of Gout and Hyperuricaemia:

(a) When the big toe is affected, clinical di­agnosis is confirmed by a raised plasma urate.

(b) There is another type of arthritis caused by deposition of crystals of calcium pyro­phosphate in joints, sometimes called pseudo-gout.

(c) Large joints are usually involved, espe­cially the knees, which show calcification of articular cartilage. It does not respond to colchicine and the plasma urate is nor­mal.

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5. Treatment of Gout and Hyperuricaemia:

i. Drug:

(a) There are drugs which relieve the acute arthritis, but do not affect plasma urate concentrations. The oldest effective remedy for acute gout is colchicine. It acts by in­hibiting the polymorph response to urate crystals and thus breaks the vicious cycle. The dose is 1 mg two hourly until relief is obtained or diarrhoea supervenes.

If the response with colchicine is too slow or diarrhoea too troublesome, it may be re­placed by a short course of phenylbutazone or of corticotrophin or one of the adrenocorticosteroids. During the acute attack the patient gets little rest from pain which is always worse at night. He should be in bed and the joint made as comfort­able as possible by supporting it on pil­lows and protecting it from pressure and knocks.

The second group of drug is Probenecid which impairs the reabsorption of uric acid by the renal tubules and so increases uric acid excretion in the urine by 30 to 50 per cent. As its administration is continued, plasma urate falls and later the frequency of arthritis decreases and tophi regress.

When there is gross overproduction of uric acid, the newer drug allopurinol is the best for treatment. It inhibits xanthine oxidase so that uric acid production is reduced and the patient excretes instead xanthine and hypoxanthine which are more soluble.

Allopurinol has no direct effect on gouty arthritis and prophylactic doses of colchi­cine 0.5 mg three times a day should be given for the first two or three months. Other adverse effects are unusual with these drugs.

ii. Diet:

(a) If the patient is overweight, he should be advised to bring his weight down by a gen­tle dietary regimen.

(b) Fasting should be avoided. Heavy, rich meals high in purines or fat are likely to raise the plasma urate and may be followed by an acute attack.

(c) Excessive alcohol precipitates gout. The patient should be advised not to drink al­cohol at all.

(d) It is always better to avoid foods rich in purine, e.g., liver, kidneys, sweet breads, fish and meat extracts.

(e) The patient should be advised to drink water before going to bed. Coffee and tea—although contain methylxanthines such as caffeine can be drunk because caf­feine is not converted into uric acid in the body.

(f) Lastly, it is wise to check fasting plasma lipids and treat hyperlipemia if present and to give some-advise to gouty patients on diets which may reduce the risk of coro­nary heart disease.