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This Atlas presents information on gout by district health board (DHB), including gout prevalence, prevalence by ethnicity, and treatment. The goal is to identify any areas of wide variation between DHBs and opportunities for quality improvement.

Update 2016

This Atlas has been updated with data from 2012–14.

Key messages

  • The prevalence of identified gout has increased by almost 1 percent of the total population since 2011. Men, Māori and Pacific peoples are most affected.
  • Less than half of people with gout regularly received allopurinol to prevent gout attacks. The data do not allow us to infer whether or not treatment is clinically indicated.
  • Although Māori and Pacific peoples were more affected, they were less likely to regularly receive allopurinol.
  • Over half of those with gout were dispensed non-steroidal anti-inflammatory drugs (NSAIDs) in 2014. This may indicate the need for more preventive treatment and suggest more research and debate into the use of these drugs is needed. Māori and Pacific peoples with gout were dispensed more NSAIDs than other ethnic groups.
  • Only one-third of those dispensed allopurinol had a serum urate test within 6 months of allopurinol being dispensed. Achieving a serum urate target of <0.36 mmol/L is essential for effective long-term treatment of gout.
  • Māori and Pacific peoples had at least five times as many admissions due to gout than those of European/Other ethnicities.

Key findings 2014

The number of people identified as having gout is increasing. Men, Māori and Pacific people are most affected.

  • In 2014 on average, 5 percent of the population aged 20 and over were identified as having gout (161,600 people). This has increased from 4.3 percent in 2012 (136,100 people).
  • Gout prevalence varied 2.7-fold between DHBs, ranging from 3.2 percent in Canterbury to 8.1 percent in Tairawhiti DHB, reflecting different ethnicity and age structures between DHBs.
  • Men had over three times the gout prevalence of women.
  • Māori and Pacific peoples had at least twice the gout prevalence of European/Other and Asian populations.
  • Gout prevalence increased significantly with age.

Table 1: Population identified as having gout, by age, ethnicity and gender, 2014

  20–44 years (%) 45–64 years (%) 65 years and over (%) Total (%) Total (%)
Female Male Female Male Female Male Female Male
Māori 0.7 4.2 4.8 17.8 19.6 36.7 3.9 11.8 7.6
Pacific peoples 1.5 10.1 8.4 31.0 24.7 46.0 6.0 19.8 12.7
European/Other 0.2 1.2 1.2 6.5 6.1 16.5 1.9 6.3 4.0
Total 0.4 2.3 1.9 8.9 7.4 18.4 2.4 7.7 4.9

Māori and Pacific peoples were less likely to receive allopurinol regularly

  • On average, 41 percent of people identified with gout regularly received allopurinol.
  • There was variation between ethnic groups. Pacific peoples received significantly less allopurinol – 33 percent, followed by Māori – 39 percent. Forty-three percent of people identifying as European/Other group received allopurinol regularly.
  • This inequity needs to be addressed.

NSAIDs were dispensed to 55 percent of those identified as having gout. Māori and Pacific peoples were dispensed more NSAIDs

  • Over a one-year period, on average, 55 percent of people identified as having gout were dispensed an NSAID compared with 26 percent for the resident population aged 20 years and over.
  • There was limited regional variation.
  • People identifying as European/Other used significantly fewer NSAIDs – 54 percent of those with gout, compared with 60 percent of Māori.

Seven percent of people identified as having gout received colchicine in a year without any allopurinol. Pacific peoples received significantly more colchicine

  • On average, 7 percent of people with gout received colchicine and no allopurinol over the course of a year.
  • This varied 2.5-fold between DHBs, with some DHBs having consistently high rates.
  • Pacific peoples received significantly more colchicine at 8 percent, compared with 6.7 percent for Māori and 6.4 percent for European/Other.
  • Younger people received significantly more colchicine.

An NSAID without any allopurinol was dispensed in 21 percent of people identified as having gout

  • On average, 21 percent of people with gout received an NSAID in a year without any allopurinol being dispensed.
  • Rates did not vary widely by ethnicity, but did decrease significantly with age.

Serum urate was tested in the six months following allopurinol dispensing in 33 percent of people identified as having gout

  • On average, 1 in 3 people identified with gout received a serum urate test within 6 months after allopurinol dispensing.
  • Achieving a serum urate target of <0.36 mmol/L is essential for the effective long-term treatment of gout.
  • This varied 1.7-fold between DHBs.
  • Rates of testing increased significantly with age.

Note: This indicator differs from that reported for gout in the Equity Explorer. The indicator above looks at serum urate testing following any dispensing of allopurinol in a year, whereas the equity indicator measures serum urate testing in those regularly receiving allopurinol (those dispensed allopurinol in three or four quarters in a year). This is a subset of those dispensed allopurinol. 

Māori and Pacific peoples had five times as many hospital admissions for gout

  • Māori and Pacific peoples had more than five times as many hospital admissions as European/Other groups due to gout.

Background

Gout is the most common form of inflammatory arthritis. It is caused by an inflammatory response to monosodium urate (MSU) crystals, which form in the presence of high urate concentrations. Patients typically present initially with recurrent flares of severe joint inflammation. Over time, in the presence of elevated serum urate concentrations (hyperuricaemia), gouty tophi, chronic arthritis and joint damage can occur.

Gout is estimated to affect approximately 3.75 percent of adult New Zealanders.[1] Rates of gout are particularly high in men Māori and Pacific peoples, affecting up to one-third of those aged over 65 years.[1] Acute attacks of gout are extremely painful, and disrupt work and home life. Tophaceous gout causes bone and joint damage and musculoskeletal disability.[2–4]

Long-term urate-lowering therapy is recommended for patients with recurrent gout flares (>1/year), chronic gouty arthritis and joint damage. Allopurinol is the first-choice urate-lowering therapy drug in New Zealand. A target serum urate of <0.36mmol/L is required to achieve dissolution of MSU crystals, suppression of gout flares and regression of tophi. Two other medications – benzbromarone and febuxostat are also funded to treat chronic gout. Due to the very low number of people dispensed these medicines in 2014 the EAG opted to focus on data of allopurinol dispensing, as it remains the first line agent. The use of these medicines may be included in future updates. Acute gout flares can be treated with NSAIDs, colchicine or corticosteroids.
Other indicators of the quality of gout management include the frequency of serum urate monitoring,[5] the use of NSAIDs and the rate of hospital admissions with gout as the primary diagnosis.

For each of the indicators, it was not possible to assess whether medicine was clinically indicated, whether the dose was optimal or whether the dose was taken. Read the methodology used.

Find My Patients query and clinical audit template

Find My Patients allows you to run a query using your patient management system (PMS) to identify patients who have not had a recent serum uric acid test. You can also use the query as part of a clinical audit. GPs who complete the audit are entitled to Maintenance of Professional Standards (MOPS) credits from the Royal New Zealand College of General Practitioners (RNZCGP).

Download the Find My Patients query and clinical audit template.

Links

Auckland Regional Clinical Pathway for Acute Gout

Auckland Regional Clinical Pathway for Gout Prevention

BPAC guidance: The medical management of gout revisited


References

  1. Winnard D, Wright C, Taylor W, et al. 2012. National prevalence of gout derived from administrative health data in Aotearoa New Zealand. Rheumatology 51(5): 901–9.
  2. Lindsay K, Gow P, Vanderpyl J, et al. 2011. The experience and impact of living with gout: a study of men with chronic gout using a qualitative grounded theory approach. J Clin Rheumatol 17(1): 1–6.
  3. Martini N, Bryant L, Te Karu L, et al. 2012. Living with gout in New Zealand: an exploratory study into people's knowledge about the disease and its treatment. J Clin Rheumatol 18(3): 125–9.
  4. Dalbeth N, House ME, Horne A, et al. 2013. The experience and impact of gout in Maori and Pacific people: a prospective observational study. Clin Rheumatol 32(2): 247–51.
  5. Dalbeth N, Winnard D, Gow PJ, et al. 2015. Urate testing in gout: why, when and how. NZMJ 128(1420): 65–8.

Last updated 12/02/2018