Management of gout in primary care: challenges and potential solutions by 98.4

Reminder from 98.4 Online Pharmacy that gout is a common inflammatory arthritis that is increasing in prevalence. It is caused by the deposition of urate crystals. Gout results from a raised total body uric acid concentration with consequent deposition of crystals in joints and occasionally elsewhere. Unlike most mammals, humans lack the enzyme capable of degrading uric acid. Humans tend to have far higher urate concentrations and these are linked to a constellation of clinical conditions, most notably gout.

There are two important factors that influence uric acid concentrations in the body. These are the amount of uric acid produced and the clearance of uric acid from the body. Approximately two-thirds is removed by renal clearance and one-third by intestinal clearance.

Clinical features

Monosodium urate crystals typically form in relatively cooler parts of the body including the metatarsophalangeal joint of the big toe, the joints of the feet, knees, elbows and hands. The crystals may also deposit in the soft tissues around joints and form tophi which can also occur on the cartilage of the ears.


Gout usually presents as a painful monoarthritis that spontaneously resolves over a few days to one to two weeks. It occurs more commonly in males after puberty, and in females after menopause. Gout is characterised by recurrent flares of severe joint inflammation, but most patients are asymptomatic between attacks.


For a definitive diagnosis of gout, urate crystals must be demonstrated in synovial fluid or in the tophus. Synovial fluid should be analysed by polarised light microscopy. Once the definitive diagnosis has been made, repeat attacks do not require diagnostic aspiration unless there is a suspicion of joint sepsis. A normal or low serum urate does not exclude the diagnosis of acute gout, because the concentration may not be elevated during an acute attack.

First metatarsophalangeal joint involvement, local erythema, maximal inflammation within 24 hours and hyperuricaemia are suggestive of gouty arthritis, however a response to colchicine and the presence of tophi have a higher diagnostic usefulness.Some imaging modalities such as ultrasound and dual-energy CT scan may be helpful if the diagnosis is uncertain.

Several drugs used for treatment of comorbid conditions can alter serum urate concentrations. Losartan, atorvastatin, fenofibrate and calcium channel blockers all have weak urate-lowering properties. Low-dose aspirin and diuretics, particularly thiazide diuretics, increase serum urate. If possible, thiazide diuretics should not be used to treat hypertension in people with gout.

It is important not to overlook other causes of hyperuricaemia. These include renal diseases and myeloproliferative disorders.

Treatment of acute attacks

Non-steroidal anti-inflammatory drugs, colchicine and corticosteroids are options for the management of acute gout. They are equally efficacious and comorbidities guide the best choice.

Allopurinol is an effective treatment for reducing concentrations of uric acid. Renal function guides the starting dose of allopurinol and the baseline serum uric acid concentration guides the maintenance dose.

Febuxostat ( is another xanthine oxidase inhibitor. It is clinically equivalent to allopurinol.

Uricosuric drugs, such as probenecid, increase uric acid excretion. New drugs in this class will soon become available and are likely to have a role in the treatment of patients who do not respond to other drugs.

The burden of gout is growing worldwide, due to the increasing number of people with conditions that predispose them to hyperuricaemia such as hypertension, obesity, diabetes, chronic kidney disease and the use of diuretics. 984degree focusing on providing guidance for the effective management of gout.