AIMS
The aim of this study was to estimate adherence to urate-lowering therapy (ULT), predominately allopurinol, from Australia's Pharmaceutical Benefits Scheme (PBS) claims database in association with (1) patient-reported doses and (2) World Health Organization's (WHO) defined daily doses (DDD), namely, allopurinol (400 mg/day) or febuxostat (80 mg/day).


METHODS
Proportion of days covered (PDC) was calculated in 108 Gout App (Gout APP) trial participants with at least two recorded ULT dispensings in an approximately 12-month period before provision of intervention or control apps. Adherence was defined as PDC ≥80%. We measured the correlation between the two methods of calculating PDC using a Wilcoxon signed rank test. Agreement between ULT-taking status (self-reports) and ULT-dispensed status (PBS records) was tested with Cohen's kappa (κ), and positive and negative percent agreement.


RESULTS
Allopurinol was prescribed in 93.5% of participants taking ULT. Their self-reported mean daily dose (SD) was 291 (167) mg/day. Mean PDC (SD) for allopurinol was 83% (21%) calculated using self-reported dose, and 63% (24%) using WHO's DDD. Sixty-three percent of allopurinol users were identified as adherent (PDC ≥80%) using self-reported dose. There was good agreement between self-reported ULT use and PBS dispensing claims (κ = 0.708, P < .001; positive percent agreement = 90%, negative percent agreement = 82%).


CONCLUSIONS
Participant-reported allopurinol daily doses, in addition to PBS dispensing claims, may enhance confidence in estimating PDC and adherence compared to using DDD. This approach improves adherence estimations from pharmaceutical claims datasets for medications where daily doses vary between individuals or where there is a wide therapeutic dose range.

Estimation of adherence to urate-lowering therapy in people living with gout using Australia's Pharmaceutical Benefits Scheme and patient-reported dosing.

Gout is a chronic disease of monosodium urate crystal deposition in the setting of hyperuricemia that typically presents with recurrent flares of acute inflammatory arthritis that occur due to innate immune response to deposited crystals. The molecular mechanism of the progression from hyperuricemia to clinical gout is poorly understood. Here we provide insights into this progression from a genetic study of 2.6 million people, including 120,282 people with gout. We detected 376 loci and 410 genetically independent signals (148 new loci in urate and gout). We identified 1,768 candidate genes with subsequent pathway analysis revealing urate metabolism, type 2 diabetes, and chromatin modification and structure as top pathways in gout. Genes located within or statistically linked to significant GWAS loci were prioitized for their potential to control the progression from hyperuricemia to gout. This identified strong candidate immune genes involved in epigenetic remodelling, cell osmolarity, and regulation of NLRP3-inflammasome activity. The genetic association signal at XDH, encoding the urate-producing enzyme xanthine oxidoreductase (XOR), co-localizes with genetic control of XDH expression, but only in the prostate. We demonstrate XOR activity and urate production in the mouse prostate, and use single-cell RNA sequence data to propose a model of urate reuptake, synthesis, and secretion by the prostate. The gout-associated loci were over-represented for genes implicated in clonal hematopoeiesis of indeterminate potential (CHIP) and Mendelian randomization analysis provided evidence for a causal role of CHIP in gout. In concert with implication of epigenomic regulators, this provides support for epigenomic remodelling as causal in gout. We provide new insights into the molecular pathogenesis of gout and identify an array of candidate genes for a role in the inflammatory process of gout.

A genome-wide association analysis of 2,622,830 individuals reveals new pathogenic pathways in gout.

Abstract Objectives There is limited research on the burden of rheumatologic disease affecting First Nations people in Australia. We sought to characterise public hospital utilisation by First Nations people for a 6‐year period (2014–2019) for gout, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), osteoarthritis (OA) and osteoporosis (OP) in Western Sydney, New South Wales. Design A cross‐sectional medical records review. Setting All patients who presented to the emergency departments (EDs) of, or who were admitted to, any of the four Western Sydney Local Health District hospitals with a primary diagnosis of gout, SLE, RA, OA or OP between 1 January 2014 and 31 December 2019. Main outcome measures Description of ED presentations and hospital admissions for the five conditions among First Nations and non‐First Nations people. The hospital utilization rate was calculated for both First Nations and non‐First Nations people. Results There was a higher likelihood of First Nations people accessing public hospital healthcare for gout compared to the non‐First Nations population (73.3% vs 62.4%, P &lt; 0.030). The public hospital utilisation rate for First Nations people with rheumatological conditions was almost three times that of the non‐First Nations population for those aged ≥45 years (13.1 per 1000 people vs 5.0 per 1000 people respectively). Conclusions This study suggests First Nations people living in Western Sydney access public hospital care for rheumatological conditions at a higher rate than the general population. 

Higher frequency of public hospital utilisation for rheumatological conditions by First Nations people in Western Sydney

OBJECTIVE
To determine the healthcare burden of gout in Western Sydney.


METHODS
We characterised patients managed in the Emergency Departments (ED) of the 4 Western Sydney Local Health District (WSLHD) hospitals and those admitted for gout as the primary or secondary diagnosis from January 1, 2017 to December 31, 2018.


RESULTS
There were 472 patients managed in ED on 552 occasions at a direct cost to the LHD of AUD367 835. Those of Māori or Pacific Islander ethnicity comprised 25.2% (n=119/472) of these, while half of those (n=39/80) managed in ED for gout on two or more occasions were of Māori or Pacific Islander ethnicity. Overall, 310 patients were admitted with gout as the principal diagnosis on 413 occasions at a cost of AUD1.73 million. Seventy-five of the 310 patients (24.2%) were of Māori or Pacific Islander heritage. A total of 584 WSLHD inpatients had gout as a secondary diagnosis. This was associated with 714 admissions.


CONCLUSIONS
The disproportionately large healthcare burden of gout in Western Sydney from the relatively small Māori and Pacific Islander population needs attention. Urgent culturally-appropriate interventions to address gout are required to address this inequality. This article is protected by copyright. All rights reserved.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/imj.15831

The Disproportionately Large Contribution of the Māori and Pacific Islander Community to the Healthcare Burden of Gout in Western Sydney.

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The Disproportionately Large Contribution of the Māori and Pacific Islander Community to the Healthcare Burden of Gout in Western Sydney.