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Epidemiology of gout

 

Clinical bottom line.

In 1999 the prevalence of gout and hyperuricaemia in the USA was 41 per 1000, and in the UK the prevalence of gout diagnosis was 14 per 1000. There are signs that incident and prevalent gout rates began to decline in the late 1990s.


References


KL Wallace et al. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. Journal of Rheumatology 2004 31: 1582-1587.

TR Mikuls et al. Gout epidemiology: results for the UK General Practice Research Database, 1990-1999. Annals of the Rheumatic Diseases 2005 64: 267-272.

Studies

Two large studies have examined trends in gout prevalence and incidence in the decade of the 1990s in the USA and in the UK. They have similar results.

USA

The study population was eight million persons enrolled commercially in healthcare plans in various states throughout the USA, over the years 1990 to 1999. Databases had coded diagnoses, and incorporated pharmacy claims. Gout or hyperuricaemia were defined as a diagnosis, or pharmacy claim for gout or serum urate lowering medicines, though excluding some associated with certain types of cancer treatment. Prevalence was reported as per 1000 persons in a given year, by age and by sex.

Result

Annual prevalence rates of gout or hyperuricaemia increased over the period, mainly in older persons (Figure 1). This increase was similar in men and women. Men had three times higher prevalence of gout than women. The overall prevalence of gout and hyperuricaemia was 41 per 1000 in 1999.

Figure 1: Age-specific prevalence of gout or hyperuricaemia in the USA over 1990-1999

UK

The study population was about 1.7 million persons in practices forming part of the UK General Practice Research Database over the 10 years between 1990 and 1999. Here cases had to have a coded diagnosis of gout, and with a minimum of 12 months data before gout diagnosis. As well as information about patient and medical history, information about gout-related medicines was also obtained. Similar information was abstracted for patients with a diagnosis of osteoarthritis.

Result

Annual incidence rates of gout increased from about 12 cases per 1000 in 1990 to about 18 cases per 1000 in 1994, but then fell over succeeding years to 1990 levels (13 cases per 1000) by 1999. Incidence cases in men and women by age, and overall, are shown in Figure 2.

Figure 2: Age- and sex specific incidence of gout in the UK in 1999

The overall prevalence of gout diagnosis was 1.4%, or 14 per 1000, in 1999. The male:female ratio was 3.6:1.

Comparing 63,000 patients with gout with 157,000 patients with osteoarthritis (and excluding those with dual diagnosis), those with gout were younger (60 vs 67 on average), and were more likely to be male (80% vs 34%). Gout patients had higher rates of comorbidities like coronary artery disease, hypertension, diabetes and renal problems. They were no more likely to be taking diuretics (33% in each group).

Over the period 1990-1999, use of glucocorticoids (5%), allopurinol (25%), colchicine (2%) and uricosuric drugs (1%) remained constant. Use of NSAIDs declined from 67% in 1990 to 41% in 1999. Use of NSAIDs was higher, at 88%, in incident cases. The decreased use of NSAIDs in prevalent cases was mirrored by a similar fall in NSAID use in prevalent cases of osteoarthritis, from 67% to 39% over the period.

Comment

These are useful studies, even if they apparently provide slightly different pictures. Reduced gout incidence in the UK from a mid-90s peak may be presaging a similar change in the US, where gout or hyperuricaemic prevalence was beginning to fall in the later 1990s. Of course, the two studies are measuring slightly different things, a diagnosis of gout in the UK study, and gout plus hyperuricaemia in the USA. The two figures are different, with UK prevalence of gout of 14 per 1000 in 1999, compared with 41 per 1000 of gout plus hyperuricaemia in the US in the same year. This suggests that hyperuricaemia without gout is more common, and that successful treatment may be preventing or delaying the onset of clinical gout.