Single map PHO analysis Consumer summary (133KB, pdf)

This Atlas domain presents information on gout by district health board (DHB) including prevalence, prevalence by ethnicity and treatment. It identifies areas of wide variation between different parts of the country and opportunities for quality improvement.

Updated 2021

This domain has been updated with data from 2012–19.

Key messages

  • Gout is estimated to affect around 6 percent of the total population aged 20 years and over. People aged 65 years and over, men, Māori and Pacific peoples are most affected. For those aged 20–44 years, the prevalence of identified gout for Māori and Pacific peoples is three and seven times that of non-Māori, non-Pacific populations.
  • While Māori and Pacific peoples were more likely to receive some urate-lowering therapy in a year, they were less likely to receive it regularly. This is important because urate-lowering therapy needs to be used continuously long-term for people to benefit from it.
  • Although the dispensing rates of non-steroidal anti-inflammatory drugs (NSAIDs) for New Zealanders with gout have reduced since 2012, Māori and Pacific peoples with gout are dispensed NSAIDs at higher rates than other ethnic groups. There is a concerning relationship between NSAID use and kidney damage. Since kidney disease is more common in Māori and Pacific peoples, more debate into the use of these drugs to treat gout is needed.
  • Māori and Pacific peoples with gout were more likely to receive colchicine, prednisone or NSAIDs than other ethnic groups.
  • People identified with gout have been admitted to hospital for gout at decreasing rates since 2012. However, hospital admission rates have remained substantially higher for Māori and Pacific peoples than other ethnic groups.

Key findings

Infographic gout Mar 2021

Gout: key findings 2019 (click to download full size (716KB, pdf))

The number and prevalence of people identified as having gout has increased.[1] Men, Māori, Pacific peoples and people aged 65 years and over were most affected.

  • In 2019, on average, 5.7 percent of the population aged 20 years and over were identified as having gout (208,000 people). This increased from 4.5 percent in 2012 (146,000 people).
  • Gout prevalence varied 2.3-fold between DHBs, ranging from 3.9 percent in Canterbury DHB to 9.1 percent in Hauora Tairāwhiti; this is likely to reflect the different ethnicity and age structures between DHBs.
  • Gout prevalence increased significantly with age.
  • Men had over three times the gout prevalence of women.
  • Māori and Pacific peoples had 2‒3 times the gout prevalence of non-Māori, non-Pacific populations. For those aged 20–44 years, the prevalence of identified gout for Māori and Pacific peoples was three and seven times that of non-Māori, non-Pacific populations. In men aged 65 years and over, gout is estimated to affect 18 percent of those identifying as non-Māori, non-Pacific, 35 percent of Māori and 50 percent of Pacific peoples.
  • Even these very high percentages for Māori and Pacific men are thought to underestimate the burden of gout in Māori and Pacific communities. Qualitative studies suggest younger men with gout in particular found it hard to access care[1] and a previous data linkage study[2] suggested the method used here underestimated total prevalence by approximately 20 percent.

Table 1: Percentage of population identified as having gout, by age, ethnicity and gender, Aotearoa New Zealand 2019

Ethnicity Age and gender (%)
20–44 years 45–64 years 65+ years All age groups
Female Male Female Male Female Male Female Male
Māori 1.0 5.6 5.1 18.9 18.0 35.4 4.3 13.1
Pacific peoples 1.9 12.5 9.7 34.4 26.1 49.6 7.0 22.8
Non-Māori, non-Pacific 0.3 1.8 1.4 7.8 6.1 17.5 2.1 7.4
All ethnic groups 0.5 3.2 2.3 10.5 7.5 19.6 2.7 9.0

The difference between any dispensing and regular dispensing of urate-lowering therapy is greater for Māori and Pacific peoples than non-Māori, non-Pacific populations with gout.

  • People experience urate-lowering benefits when therapy is used continuously long-term. Any dispensing was defined as people dispensed medicine at least once in a year. Regular dispensing was defined as people dispensed medicine in three or four quarters in a year. Regular dispensing indicates medicine persistence, that is, the availability of medicine to a person over the year.
  • While Māori and Pacific peoples were more likely to receive urate-lowering therapy in 2019 (60 percent) than non-Māori, non-Pacific populations (56 percent), they were less likely to receive it regularly. Māori (39 percent) and Pacific peoples (36 percent) regularly received urate-lowering therapy compared with non-Māori, non-Pacific populations (43 percent).
  • The same treatment levels for different populations does not necessarily mean equitable treatment. In this instance, gout in Māori and Pacific peoples has a different clinical profile from other groups (with earlier onset and more severe disease), so to achieve equitable care would require higher levels of urate-lowering therapy for Māori and Pacific peoples.
  • Rate of regular use increased significantly with age.

Table 2: Percentage of people identified as having gout, who were dispensed a urate-lowering therapy regularly in a year, by age and ethnicity, Aotearoa New Zealand 2019

Dispensing type Age and ethnicity (%)
20–44 years 45–64 years 65+ years All age groups
Māori Pacific peoples Non-Māori, non Pacific Māori Pacific peoples Non-Māori, non Pacific Māori Pacific peoples Non-Māori, non Pacific Māori Pacific peoples Non-Māori, non Pacific
Any dispensing 48 53 45 60 61 54 68 64 59 60 59 56
Regular dispensing 16 18 21 38 38 39 56 53 50 39 36 43
  • The difference between ethnic groups was especially visible for those aged 20–44 years, where there is a much higher burden of identified gout in Māori and Pacific peoples, particularly for men.
  • There were differences in the occurrence of gout across all age groups. The inequity in persistence of use of urate-lowering therapy when considering all age groups raises questions about how to address it.

NSAIDs were dispensed to 38 percent of those identified as having gout. Māori and Pacific peoples were dispensed NSAIDs at higher rates.

  • In 2019, 38 percent of people identified as having gout were dispensed an NSAID compared with 24 percent for the resident population aged 20 years and over.
  • Overall, NSAID dispensing has reduced over time, across all age groups and ethnicities.
  • There was limited regional variation.
  • People identifying as non-Māori, non-Pacific had statistically lower rates of NSAID dispensing – 35 percent, compared with 46 percent of Pacific peoples and 41 percent of Māori.
  • Younger people, particularly Māori and Pacific peoples, were dispensed NSAIDs at significantly higher rates. These findings should be taken in the context of the inequity in regular urate-lowering therapy in younger Māori and Pacific peoples.

An NSAID without any urate-lowering therapy was dispensed in 15 percent of people identified as having gout.

  • On average, 15 percent of people with gout received an NSAID in a year without any urate-lowering therapy being dispensed.
  • Since 2012, rates for Māori and Pacific peoples have consistently decreased, while rates for non-Māori, non-Pacific populations have not changed. In 2019, these rates were almost the same across all ethnicities.
  • Rates also consistently decreased with age.

Māori and Pacific peoples with gout were more likely to receive colchicine, prednisone or NSAIDs but less likely to receive them without any urate-lowering therapy.

  • In 2019, on average, 55 percent of those with gout received either colchicine, prednisone or an NSAID. Only 22 percent received one of these but not urate-lowering therapy.
  • For all age groups, Pacific peoples with gout were more likely to receive colchicine, prednisone or an NSAID (62 percent), followed by Māori (59 percent). This dropped to 52 percent for those identifying as non-Māori, non-Pacific.

Serum urate was tested in the six months following urate-lowering therapy dispensing in 56 percent of people identified as having gout.

  • On average, three in five people identified as having gout received a serum urate test within six months of being dispensed urate-lowering therapy.
  • For gout to be treated effectively long term, there is a serum urate target of < 0.36 mmol/L.
  • There was 1.7-fold variation between DHBs for this indicator.
  • Rates of testing did not vary widely by ethnicity but increased with age.

Note: The Equity Explorer (www.hqsc.govt.nz/atlas/equity-explorer) reports on people with gout whose serum urate was tested in the six months following allopurinol dispensing. The indicator in this Atlas domain is not the same. It does not include point-of-care testing because only laboratory data on testing is available.

Māori and Pacific peoples identified with gout had three times as many hospital admissions for gout.

  • People identified with gout have been admitted to hospital for gout at decreasing rates since 2012.
  • However, they are still three times as high for Māori and Pacific peoples as non-Māori, non-Pacific populations identified with gout.
  • Admissions for people with gout are also twice as high for people aged 20–44 years as for any other age group.
  • Admissions for the general population for gout are reducing over time, especially for Pacific peoples. However, the admission rates are still five times higher for Māori and 10 times higher for Pacific peoples than for non-Māori, non-Pacific populations.

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), tophi, chronic arthritis and joint damage can occur.

Gout is estimated to affect approximately 6 percent of adult New Zealanders. Rates of gout are particularly high in Māori and Pacific men, affecting approximately half of Pacific men aged 65 years and over. There is a potential relationship between the method of identifying people with gout and the increasing prevalence. As appropriate dispensing of urate-lowering therapy has increased in line with best practice, and dispensing of urate-lowering therapy is used in the algorithm to identify people with gout, this will contribute to the apparent increase in prevalence, alongside a real increase in prevalence. Gout flares are extremely painful and disrupt work and home life. Tophaceous gout causes bone and joint damage and musculoskeletal disability.[3–5]

Long-term urate-lowering therapy is recommended for patients with recurrent gout flares (two or more per year), chronic gouty arthritis and joint damage. Allopurinol is the first-line urate-lowering therapy drug in Aotearoa New Zealand, but probenecid, benzbromarone and febuxostat are also effective. You need a target serum urate of < 0.36 mmol/L to dissolve MSU crystals, suppress gout flares and for tophi to regress. 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[6], the use of NSAIDs and the rate of hospital admissions with gout as the primary diagnosis.

For each of the indicators in this Atlas domain, it was not possible to assess whether medicine was clinically indicated, whether the dose was optimal (including the recommended starting and maintenance dose of urate-lowering therapy), whether anti-inflammatory prophylaxis was prescribed at the time of starting urate-lowering therapy, or whether the medicine was taken. Download the methodology (238KB, pdf).

Clinical experience raises questions about the cause for the trends in hospitalisation data – whether at least some of the changes represent differences in the way hospitals are triaging, managing and recording acute severe gout presentations. This is warrants further exploration.

Since the rates for Asian populations were similar to those of the European/Other population, and in some DHBs Asian populations were small, we combined these into a non-Māori, non-Pacific group.

Recent research has found that genetics were significantly more likely than unhealthy foods to lead to higher urate levels.[7]

Links

Health Navigator regional pathways
BPAC: Managing gout in primary care, part 1
BPAC: Managing gout in primary care, part 2
BPAC guidance: An update on the management of gout
Atlas of Healthcare Variation: Health service access

Recommended reading

Dalbeth N, Dowell A, Gerard C, et al. 2018. Gout in Aotearoa New Zealand: the equity crisis continues in plain sight. NZMJ 131(1485): 8–12.
Dalbeth N, Gerard C, Gow P, et al. 2016. Gout in Aotearoa New Zealand: are we going to ignore this for another 3 years? NZMJ 129(1429): 10–13.
Jackson G, Dalbeth N, Te Karu L, et al. 2014. Variation in gout care in Aotearoa New Zealand: a national analysis of quality markers. NZMJ 127(1404): 37-47.
Lawrence A, Scott S, Saparelli F, et al. 2019. Facilitating equitable prevention and management of gout for Māori in Northland, New Zealand, through a collaborative primary care approach. J Prim H C 11(2): 117–27.
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.

In the media

Te Karere (TVNZ): Research suggests equity issues around gout treatment.
E-Tangata. The shameful treatment of gout in New Zealand.
Waatea News: Māori and Pacific peoples more likely to suffer from gout, less likely to be treated.
Health Quality & Safety Commission: South Auckland providers responding to gout.

References and notes

  1. Te Karu L, Kenealy T, Bryant L, et al. 2020. I just kind of wanted to close myself off and die. The long shadow of inequity for Māori with gout. MAIJournal. 9(2): 152–65.
  2. Jackson G, Wright C, Thornley S, et al. 2012. Potential unmet need for gout diagnosis and treatment: capture-recapture analysis of a national administrative dataset. Rheumatology 51: 1820–4.
  3. 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.
  4. 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.
  5. 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.
  6. Dalbeth N, Winnard D, Gow PJ, et al. 2015. Urate testing in gout: why, when and how. NZMJ 128(1420): 65–8.
  7. Major TJ, Topless RK, Dalbeth N, et al. 2018. Evaluation of the diet wide contribution to serum urate levels: Meta-analysis of population based cohorts. BMJ 2018; 363:k3951. URL: https://www.bmj.com/content/363/bmj.k3951 (accessed 6 November 2018).

Last updated 19/03/2021