SP0155 Eular Gout Treatment
Authors: E. Pascual Gomez
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> Gout is a urate crystal deposit disease; crystal deposit is present at the time of the first attack – that signals the presence of a urate deposit – and if hyperuricemia persists, it grows and expands to other sites. Urate crystals are recognized by the innate immune system triggering inflammation that results in gout attacks and also during intercritical periods in persistent subclinical chronic inflammation linked to the crystals. Crystal deposition is far from innocuous and gout – through the acute and subclinical inflammation –associates to a higher risk of cardiovascular disease and other arteriosclerotic consequences. Most important, reduction to normal values results in dissolution and final disappearance of the crystals. So, gout is currently taken as a curable disease. The main aim of gout treatment is to fully dissolve the urate crystals. Secondary aims include to avoid the attacks, treat them if they occur and recognize and treat associated conditions. <i>Crystal dissolution</i> is achieved by reducing urate crystals to normal values; lower values result in faster dissolution and earlier disappearance of the crystals. New EULAR guidelines take this in account and suggest lower values when crystal deposits are heavy as in long standing gout having affected several joints or in tophaceous gout. Maintained values below 3 mg/dl are not recommended because possible association with Parkinson disease. The xantine oxidase (XO) inhibitor Alopurinol is the mainstay of gout treatment. Since severe toxicity has been linked to the starting dose, it is appropriate to start with a 50 or 100 mg/d to escalate to the necessary dose; frequently under dosed at a fixed 300 mg/dl it can escalated and given up to 800 mg/d, in occasional patients with severe gout. This escalation also reduces the flares that occur at the start of serum uric acid lowering treatment. Febuxostat – also a XO inhibitor – is highly effective and particularly indicated in patients with intolerance to allopurinol or those with renal failure in whom achieving a particularly low uricemia appears appropriate. Uricosurics combined with XO inhibitors are useful in difficult to treat patients in whom XO inhibitors in full dose are insufficient. Pegloticase/rasburicase result in very low uricemia and rapid dissolution of the crystals though only a limited number of doses can be given; they may have a role in the initiation of treatment of very severe and difficult gout. <i>Prophylaxis (prevention) of attacks</i> is especially necessary at the initiation of serum uric acid reducing treatment that commonly triggers attacks as a result of the drop in uricemia. Prophylaxis is achieved by reducing the subclinical inflammation linked to the urate crystals making it more stable. Colchicine 0.5–1 mg/d is the usual approach. If not tolerated NSAID9s can be tried (as 500–1000 mg/d of naproxen). If inappropriate because of the frequent gout comorbidities, a small dose of prednisone 5 to 15 mg/d at least until stable target uricemia is achieved can be given. A single dose of Canakinumab lasting up to three months offers an alternative. <i>Treatment of gout attacks</i> - that are the usual reason of seeking medical attention – should be started as early as possible. Effective drugs include colchicine at doses of 1.2 to 1.6 mg the first 24 hours, followed by 1–1.2 mg/day. Most NSAID9s at full dose are effective, but are less desirable in patients that frequently suffer from comorbidities. Corticosteroids are frequently used; a short course of oral prednisone (as 30 mg initially to be tapered in 4 to 6 days) is an option mostly free of side effects. If accompanied by colchicine in prophylactic doses (0.5–1 mg/d) from the start, the gout rebounds that accompanied too short treatment schedules are usually avoided. A Intraarticular corticosteroid – especially if accompanied by a local anesthetic – often offers prompt resolution of the symptoms. Finally the anti IL1 drugs – especially anakinra – is increasingly utilized in this context. Gout management should include evaluation – and treatment if required – of its frequent comorbidities. Life style modification and patient information should not be forgotten. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6315