Treatment of gout 

Summary points   What is gout   Treatment of gout   Indications for Uric acid lowering therapy   Lifestyle interventions   Pharmacists have a key role in the care of people with gout   Prevalence and impact of gout   References   Issue 8 Contents

---

Indications for uric acid lowering therapy^6-8

All patients with any one of the following should receive long-term uric acid lowering therapy:

• Recurrent gout attacks (≥2 attacks/year)
• Tophi
• Gouty arthropathy
• Radiographic damage

  “Early treatment of gout, before onset of tophi and erosive disease, is recommended”

• Early onset, family history and serum uric acid >0.60 mmol/L

It should be noted that although effective treatment of gout can lead to regression of tophi, management is far more difficult once tophi develop, due to the high total body urate load.

Hitting the target in gout: aim for a serum uric acid concentration of <0.36 mmol/L

Several recent studies have emphasised the importance of excellent long-term control of serum uric acid in order to suppress gout attacks and achieve regression of tophi. These studies have identified a serum uric acid level of <0.36 mmol/L as the target required for dissolution of monosodium urate crystals within the joints and subcutaneous tissues.^9–11 This target has been endorsed in the recent European League Against Rheumatism (EULAR) guidelines for management of gout.⁷

“Patients with gout should be encouraged to think of their uric acid level in the same way that patients with diabetes think of their HbA1c”

Reduction of the serum uric acid level requires both pharmacological and non-pharmacological management. Allopurinol is the first choice urate-lowering drug unless there is a history of allopurinol allergy/intolerance.

Allopurinol prescribing: a how-to guide

1. Wait for at least two weeks after an acute gout attack before starting allopurinol
2. ‘Start low and go slow’. Start with allopurinol 100 mg daily, and increase by 100 mg every two weeks until the serum uric acid level is <0.36 mmol/L. For most patients with normal renal function, a dose of 300 mg daily is needed to achieve this target. Patients with renal impairment may require less allopurinol to achieve this target. Sudden changes in the serum uric acid level are likely to precipitate gout attacks. Gradually increasing the dose of allopurinol is less likely to trigger a gout attack
3. Use prophylaxis against acute attacks. Prophylaxis with colchicine (0.5 mg daily to twice daily) or NSAIDs for the first three months of starting allopurinol (or until serum uric acid <0.36 mmol/L) should be prescribed to reduce the risk of gout attacks.¹⁴ Ensure the patient knows that in this situation the colchicine is for gout prevention and the dose should not be altered without medical advice if an acute episode occurs.
4. Monitor serum uric acid levels on a monthly basis while establishing allopurinol. Once serum uric acid is <0.36 mmol/L, monitor uric acid and renal function on a three-monthly basis.
5. Allopurinol should be continued as life-long therapy for management of gout, except in the case of allopurinol intolerance. Do not stop taking allopurinol during an acute attack of gout.

Other urate-lowering drugs

The uricosuric agent probenecid is an effective urate-lowering drug in patients with normal renal function and urate under-excretion. This agent is particularly useful in combination with allopurinol if there is persistent hyperuricaemia despite therapeutic doses of allopurinol, or in allopurinol intolerance.¹⁵ A typical dose is 250 mg twice daily for two weeks, then 500 mg twice daily thereafter.

Probenecid is contraindicated in patients with a history of renal stones. Patients should be advised regarding the importance of high fluid intake while taking probenecid, around eight glasses of water per day.

	Urate Cam Kyle and Stephen Du Toit Chemical Pathologists About one third of body urate comes from the diet, two thirds from endogenous tissue catabolism. Under excretion of urate by the kidneys is the cause of high serum levels in over 80% of adult patients. Insulin resistance (metabolic syndrome) is associated with increased urate resorption and higher serum urate levels. About 20% of males have a serum urate above 0.42 mmol/L, but this has been chosen as the upper end of the male range because at that level urate becomes supersaturated in body fluids at 37°C, resulting in increased crystal deposition in tissues. Above this level the 5–year risk of gout rises fifty-fold from about 0.1% below 0.42 mmol/L to 5% above 0.54 mmol/L. Above 0.60 mmol/L the 5–year prevalence of gout is about 30%. An upper limit of 0.36 mmol/L is used for women because their levels before menopause average 0.06 mmol/L lower than men. After menopause, levels in women approach those in men and the risk of gout increases, being similar to men over age 60. Serum urate is the most important predisposing risk factor for gout, but is not used alone to make the diagnosis. Most patients with high urate levels do not develop gout and, conversely, serum urate may be normal, especially during acute attacks. Visual identification of crystals from joint fluid or tophi is the gold standard. For patients with clinical gout on long-term treatment, a target urate level of 0.36 mmol/L has been recommended by some international bodies. The long-term risk of gout recurrence is much lower when levels are maintained below this threshold and it also favours the slow dissolution of chronic tophi, being well below the solubility constant of urate. D-News, Diagnostic Medlab, August 2007 Available from: http://www.dml.co.nz/

Submit a comment about this article

View comments about this article

Page  1 | 2 | 3 | 4 | 5 | 6 | 7 | 8

Page 4