The finding of hyperlipidaemia in patients with hyperuricaemia and gout is common. The usual abnormality is hypertriglyceridaemia (type IV hyperlipoproteinaemia),1 ,2 being reported in between 25% and 60% of patients with gout.3 ,4 This finding has been related to reports of an increased frequency of coronary artery disease in some patients with gout and has contributed to the suggestion that the urate concentration might be an indicator of coronary risk. Now that gouty arthritis itself is so treatable, an associated disorder that might reduce the life span becomes even more important in the management of a patient with gout.

However, our understanding of the mechanism of any association between hypertriglyceridaemia and hyperuricaemia is far from complete and this becomes increasingly important when determining the factors that contribute to the development of hyperuricaemia and gout in a particular person. No longer can it be assumed that there is a common aetiology for the hyperuricaemia in patients who present with an acute urate crystal arthropathy and refer to it as “primary gout”. Similarly, it is no longer expected that each patient with gout would have inherited a “gouty diathesis”, unless you regard this concept as meaning a relatively poor renal clearance of urate in the presence of otherwise normal renal function.5 Hyperuricaemia in most patients is found to have multiple causes, some genetic and others environmental, with many of the latter being able to be modified, potentially correcting the contribution of that cause to the hyperuricaemia.6 ,7

In such an assessment, …