GOUT: PREVENTION AND TREATMENT Wilf Treasure 11/8/13 INTRODUCTION Gout is inflammation of one of your joints caused by the

formation of uric acid crystals in it. The higher the level of uric acid in your blood stream, the greater the chance of crystals forming in a joint and the greater the chance of an episode of gout. TREATMENT During an episode of gout, treatment can be given with one of, or a combination of, the following: steroid injection into the joint this is only occasionally possible; steroid tablets (prednisolone); nonsteroidal anti-inflammatory drugs (such as ibuprofen, naproxen, indometacin); or colchicine (Khanna, Khanna, et al. 2012). A likely regime would be colchicine in fixed dose and non-steroidal antiinflammatory drugs (usually ibuprofen or naproxen) as needed. Of 10 patients taking colchicine 1mg (two tablets) immediately then 0.5mg (one tablet) an hour later, 4 get pain relief (compared with 2 given placebo/dummy), 2 have tolerable diarrhoea (same as placebo/dummy) and 3 take non-steroidal anti-inflammatory tablets (Terkeltaub et al. 2010). PREVENTION After an episode of gout, the likelihood of a further episode during the course of a year rises from odds of 1:9 (probability of 10%) when your blood uric acid level is 0.3 mmol/L to odds of 9:1 (probability of 90%) when your blood uric acid level is 0.6 mmol/L ) (Shoji et al. 2004). You might be able to reduce the risk of gout by changing your diet and lifestyle: aim for ideal body weight without starving yourself, limit your intake of protein, purine, red meat, liver, kidneys, seafood and alcohol (Khanna, Fitzgerald, et al. 2012) (NICE 2012), and avoid sugar-sweetened soft drinks (Choi & Curhan 2008). Youll probably get no benefit from taking Vitamin C: this reduces blood uric acid levels but not enough to reduce the chances of getting gout (Juraschek et al. 2011). You might be prescribed allopurinol. This lowers the level of uric acid in your blood stream, reduces the tendency for crystals to form in a joint and so lowers the risk of another episode of gout. Allopurinol usually causes no side-effects but like all drugs can occasionally cause harm. Its started at a dose of no more than 100 mg a day. The dose can then be increased every 2-5 weeks until your blood uric acid level is below 0.3 mmol/L. If you get itch or rash you should stop the drug straight away because these symptoms might herald a dangerous reaction. Of 10000 people who take allopurinol ten have a dangerous reaction and two die. These reactions tend to occur, if theyre going to, in the first few months of treatment, so thats the time to be particularly cautious (Khanna, Fitzgerald, et al. 2012). If you stop allopurinol you increase the chances of getting further episodes of gout. How quickly this happens depends on the level of uric acid in your blood when you stopped the allopurinol. Whatever the level when you stopped the allopurinol, by 5 years the odds of having an episode of gout are 4:1 (probability of 80%) (Perez-Ruiz 2009). If you have gout you have a higher risk of developing vascular disease such as heart attack or stroke. Thats not because gout or uric acid cause vascular disease but for some other underlying reason that isnt clear to medical science. So if you have gout its sensible to have your vascular risk assessed by a doctor or nurse (Ruilope 2012) (Janssens et al. 2003).

REFERENCES Choi, H.K. & Curhan, G., 2008. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ, 336(7639), pp.309312. Janssens, H. et al., 2003. Gout, just a nasty event or a cardiovascular signal? A study from primary care. Family Practice, 20(4), pp.413416. Juraschek, S.P., Miller, E.R., 3rd & Gelber, A.C., 2011. Effect of oral vitamin C supplementation on serum uric acid: a meta-analysis of randomized controlled trials. Arthritis care & research, 63(9), pp.12951306. Khanna, D., Fitzgerald, J.D., et al., 2012. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis care & research, 64(10), pp.14311446. Khanna, D., Khanna, P.P., et al., 2012. 2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis care & research, 64(10), pp.14471461. NICE, 2012. Gout, National Institute for Health and Care Excellence. Available at: http://cks.nice.org.uk/gout#!scenariorecommendation:10. Perez-Ruiz, F., 2009. Treating to target: a strategy to cure gout. Rheumatology, 48(suppl 2), pp.ii9 ii14. Ruilope, L.M., 2012. Antihypertensives in people with gout or asymptomatic hyperuricaemia. BMJ (Clinical Research Ed.), 344, p.d7961. Shoji, A., Yamanaka, H. & Kamatani, N., 2004. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis and rheumatism, 51(3), pp.321325. Terkeltaub, R.A. et al., 2010. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebocontrolled, parallel-group, dose-comparison colchicine study. Arthritis and rheumatism, 62(4), pp.10601068.