Is There A Role For Primary Prevention For Patients With Asymptomatic Hyperuricaemia?

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Is there a role for primary prevention for patients with asymptomatic hyperuricaemia?
Indrajeet Mandal
Gout is a very common disease in the UK, with 1 in 40 adults being affected by the condition (The Gout Society UK 2014). The prevalence of the condition has increased in the past few decades, and there is a greater disease burden in the more economically-developed countries (Kuo et al. 2015).
Uric Acid & Gout: Physiology
Gout is an arthropathy that involves the deposition of urate crystals into a joint. An acute gout attack involves deposition of joints into a joint, resulting in a painful, swollen joint that classically affects the first metatarsophalangeal joint, although can involve other joints as well. Figure 1: the natural
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2011), and these have been shown to be independent risk factors (Lin et al. 2000).
Hyperuricaemia is associated with higher all-cause mortality
The classical hypothesis is that high uric acid levels lead to increased chance of crystals forming, which then deposit in the joints. However, recent evidence has started to suggest that hyperuricaemia itself is a risk factor for increased mortality from causes other than gout. A study carried out on Japanese men has shown that high serum uric acid has been linked with an increased relative risk of mortality from all causes in a study carried out on Japanese male workers (Tomita et al. 2000). An increased mortality raises the question of whether we should routinely prescribe primary prevention interventions in patients who are in the stage of asymptomatic hyperuricaemia.
Early studies have shown that there is no significant increase in mortality from renal failure. A prospective study followed a cohort of 2046 initially healthy men and measured urate levels and the incidence of a raised serum creatinine (Campion et al. 1987). They concluded that there wasn’t a significant rise in the creatinine level, and that there was no significant renal impairment caused hyperuricaemia, supporting a conservative treatment regimen.
However, it is worth nothing that this measurement was done by correlation urate levels and creatine levels – as the baseline creatinine varies from person to person, it could be argued that this is not

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