• normouricaemia
• gout

Gouty attacks usually occur in patients with hyperuricaemia, but patients with gout who have normouricaemia are believed to be in the minority.^1,2 This is a common conception about gout because monosodium urate crystals are formed at blood concentrations of uric acid over 420 μmol/l at a body temperature of 37°C.³ Recently, two studies showed that the incidence of gouty attacks in normouricaemia was as high as 39–43%,^4,5 which is much higher than our traditional view.^1–3 However, few data on normouricaemia in gout have been reported so far.^6–8 The prevalence of patients with gout who have normouricaemia at diagnosis has not yet been determined, and even their clinical characteristics and laboratory findings have not been reported.

We designed this study to determine the prevalence of normouricaemia in patients with gout at diagnosis, and to determine the natural course of normouricaemic gout and the differences between the clinical characteristics of patients with normouricaemic and hyperuricaemic gout at diagnosis.

We retrospectively reviewed 226 Korean patients who were newly diagnosed as having gout at the Severance Hospital, Yonsei University College of Medicine, Seoul, Korea, between January 1996 and May 2000. The diagnosis of gout was made during an acute attack of gouty arthritis and confirmed by either the presence of negatively birefringent needle shaped crystals or by satisfaction of the American College of Rheumatology criteria for gout.⁹ Normouricaemia is defined as serum uric acid below 420 μmol/l in men and 360 μmol/l in women.¹⁰ Patients taking urate lowering agents (allopurinol, probenecid) were excluded. Serum uric acid was determined in samples drawn when a gouty attack occurred at diagnosis by the uricase enzyme method.

Among the 226 gouty patients, 27 (12%) male patients showed normouricaemia at diagnosis. Table 1 summarises the clinical characteristics of the patients. Twenty one of 27 gouty patients with normouricaemia were followed up; among these patients, 17 patients (81%) developed hyperuricaemia at a median of one month after diagnosis (range: one week to 24 months) (fig 1), and only four patients (19%) still showed normouricaemia. These four patients were followed up at 11, 25, 28, and 34 months respectively, but showed no more gouty attacks. All these patients had gout proved by the presence of crystals and also had normouricaemia before diagnosis.

The mean age at diagnosis was higher in gouty patients with normouricaemia than in patients with hyperuricaemia, whereas the duration from the first symptom to diagnosis, and the prevalence of documented tophi, was higher in gouty patients with hyperuricaemia. Serum uric acid, blood urea nitrogen, and creatinine levels were lower in gouty patients with normouricaemia (table 1).

We found that 27/226 (12%) of gouty patients at diagnosis had normouricaemia, which was a lower incidence than found in the two reports mentioned previously.^4,5 The discrepancy between our results and the results of those studies may be because the previous studies analysed the incidence of gouty patients with normouricaemia at the time of any acute attack,^4,5 whereas we analysed the incidence at the time of diagnosis.

Seventeen of 21 (81%) gouty patients with normouricaemia at diagnosis subsequently became hyperuricaemic. The median time for progression from normouricaemia to hyperuricaemia was one month. Our results corresponded with those of previous reports which showed that serum uric acid usually fell during an acute attack and rose during the interim.^4,5 Only four gouty patients with normouricaemia at diagnosis continued to have normouricaemia. This “genuine” normouricaemic gout was present in only a small proportion, and these patients followed a mild disease course without secondary attack.

These observations may help a doctor to decide whether a diagnosis of gout can be made when normouricaemia is present and may help in predicting the disease course of normouricaemic gout at diagnosis.

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Figure 1

Time from the diagnosis of gout to the development of hyperuricaemia.