Hyperuricaemia in Māori : to treat or not to treat? : exploring the reality of gout in Māori and whether there is rationale to treat hyperuricaemia before the onset of gout

Abstract

Background: Māori have the poorest health outcomes in New Zealand. Māori suffer disproportionately from gout and from cardiovascular disease (CVD). Gout typically manifests after many years of a hyperuricaemic state. Hyperuricaemia is associated with cardiovascular disease. Objective: The ultimate objective of this research is to give consideration and subsequent projection that if hyperuricaemia is an independent predictor of cardiovascular disease, then there is rationale to treat hyperuricaemia before it leads to gout. In particular this research aims to investigate this consideration, specifically for Māori. Method: The method for this thesis incorporated three aspects of investigation. Firstly a literature review was undertaken to ascertain whether population demographics could explain the differences in findings between those studies endorsing an independent association of hyperuricaemia with cardiovascular disease and those that do not. Secondly a qualitative study was undertaken in Māori, who have gout, to investigate experiences and beliefs around the condition itself and the treatment they received. This section is premised on the knowledge that to have gout requires hyperuricaemia and any recommendation to treat hyperuricaemia in the absence of gout requires an understanding of the current use of urate lowering therapy. Māori are the indigenous peoples of New Zealand and reflected in societal groups of whānau (family), hapū (sub-tribe) and iwi (tribe). Lastly a cross-sectional study was undertaken to explore the associations between ethnicity (Māori vs. other ethnic groups), hyperuricaemia or gout, and cardiovascular disease in a primary health population. Results: In populations of increased risk of cardiovascular disease, there is consensus amongst the literature that hyperuricaemia is independently associated with cardiovascular disease. There is little research however assessing the effect of treating hyperuricaemia on cardiovascular disease. The qualitative section of this thesis identified that Māori do not receive best practice treatment for gout according to international guidelines. For Māori men the average length of time from onset of acute symptoms of gout to successful allopurinol commencement was more than 22 years. Associated with this were themes of immense suffering and impact on all aspects of life from relationships to employment. In addition there was a gap in understanding of the aetiology and disease process of gout for Māori that health professionals do not address in totality or understand from a patient prospective. Gout is associated with pre-existing cardiovascular disease in Māori, after controlling for other known risk factors. The quantitative component of the thesis demonstrated an odds ratio of 1.52 (C.I.1.03 to 2.23) for existing CVD in Māori with a serum uric acid level above 0.35mmol/L, after adjusting for other CVD risk factors. Māori were the only ethnicity to show a greater odds ratio that was significant. Māori were also less likely to be tested for known risk factors of CVD as well as serum urate concentrations when compared to other ethnicities in this cross-sectional study. Conclusion: It is reasonable to further investigate whether treating hyperuricaemia in Māori would reduce risk of cardiovascular disease through a randomised controlled trial. Given the suboptimal practice of current urate lowering therapy use, evidenced in this thesis, a paradigm shift needs to occur along with a substantive education programme for both health professionals and communities. This would support improved health outcomes currently for gout and for any future use of urate lowering therapy, should treatment of asymptomatic hyperuricaemia demonstrate health benefits.