1 | Optimal treatment of gout requires both non-pharmacological and pharmacological modalities and should be tailored according to: | | | | |
| (a) specific risk factors (levels of serum urate, previous attacks, radiographic signs) | | | | |
| (b) clinical phase (acute/recurrent gout, intercritical gout, and chronic tophaceous gout) | | | | |
| (c) general risk factors (age, sex, obesity, alcohol consumption, urate raising drugs, drug interactions, and comorbidity) | | 96 (93 to 98) | | 100 |
2 | Patient education and appropriate lifestyle advice regarding weight loss if obese, diet, and reduced alcohol (especially beer) are core aspects of management | | 95 (91 to 99) | | 100 |
3 | Associated comorbidity and risk factors such as hyperlipidaemia, hypertension, hyperglycaemia, obesity, and smoking should be addressed as an important part of the management of gout | | 91 (86 to 97) | | 94 |
4 | Oral colchicine and/or NSAID are first line agents for systemic treatment of acute attacks; in the absence of contraindications, an NSAID is a convenient and well accepted option | | 94 (91 to 98) | | 100 |
5 | High doses of colchicines lead to side effects, and low doses (for example, 0.5 mg three times daily) may be sufficient for some patients with acute gout | | 83 (74 to 92) | | 82 |
6 | Intra-articular aspiration and injection of long acting steroid is an effective and safe treatment for an acute attack | | 80 (73 to 87) | | 88 |
7 | Urate lowering therapy is indicated in patients with recurrent acute attacks, arthropathy, tophi, or radiographic changes of gout. | | 97 (95 to 99) | | 100 |
8 | The therapeutic goal of urate lowering therapy is to promote crystal dissolution and prevent crystal formation; this is achieved by maintaining the serum uric acid below the saturation point for monosodium urate (⩽360 μmol/l) | | 91 (86 to 96) | | 100 |
9 | Allopurinol is an appropriate long term urate lowering drug; it should be started at a low dose (for example, 100 mg daily) and increased by 100 mg every 2–4 weeks if required; the dose must be adjusted in patients with renal impairment; if allopurinol toxicity occurs, options include other xanthine oxidase inhibitors, a uricosuric agent, or allopurinol desensitisation (the latter only in cases of mild rash) | | 91 (88 to 95) | | 100 |
10 | Uricosuric agents such as probenecid and sulphinpyrazone can be used as an alternative to allopurinol in patients with normal renal function but are relatively contraindicated in patients with urolithiasis; benzbromarone can be used in patients with mild to moderate renal insufficiency on a named patient basis but carries a small risk of hepatotoxicity | | 87 (81 to 92) | | 94 |
11 | Prophylaxis against acute attacks during the first months of urate lowering therapy can be achieved by colchicine (0.5–1 mg daily) and/or an NSAID (with gastro-protection if indicated) | | 90 (86 to 95) | | 100 |
12 | When gout associates with diuretic therapy, stop the diuretic if possible; for hypertension and hyperlipidaemia consider use of losartan and fenofibrate, respectively (both have modest uricosuric effects) | | 88 (82 to 94) | | 100 |