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Māori and NZEuropean individuals with gout report different understandings and education preferences around personal triggers of gout, treatment options, and ways of receiving information about gout. Further research is required to develop ethnicity-specific gout education resources internationally.

INTRODUCTION Gout is a common form of arthritis that is typically managed in primary care. Gout management guidelines emphasise patient education for successful treatment outcomes, but there is limited literature about the educational experiences of people living with gout in New Zealand, particularly for Māori, who have higher gout prevalence and worse gout outcomes than Pākehā. AIM To explore gout patient education in primary care from the perspectives of Māori and Pākehā people with gout. METHODS In total, 69 people with gout were recruited through primary care providers in three locations across New Zealand. Nine semi-structured focus groups were run with Māori and Pākehā participants in separate groups. RESULTS Thematic analysis yielded two themes in relation to gout education: (i) ‘Multiple sources of gout education’; and (ii) ‘Gaps in gout knowledge’. Participants received education from general practitioners, educational resources, family and friends, and their own experiences. Māori participants preferred information to be kanohi-ki-te-kanohi (face-to-face) and with significant others present where necessary. Participants disclosed gaps in gout’s epidemiology and management. Pākehā and Māori participants reported limited understanding of the genetic basis of gout or the biological underpinnings of the condition and its treatments, but learned treatment adherence through experience. DISCUSSION Despite improved gout patient education, knowledge gaps remain and may contribute to poor medication adherence. Gout patient education interventions need to be tailored to culture and incorporate suitable methods of disseminating information about gout management.

Objectives TNF-α inhibitors are widely used in rheumatoid arthritis (RA) with varying success. Response to TNF-α inhibition may reflect the evolution of rheumatoid inflammation through fluctuating stages of TNF-α dependence. Our aim was to assess plasma concentrations of Th-17-related cytokines and the presence of circulating effector T-cells to identify predictors of response to TNF-α inhibitors. Methods Ninety-three people with RA were seen prior to and 4–6 months after commencing etanercept or adalimumab. Plasma concentrations of Th17-related cytokines, circulating effector T-cells, their production of relevant transcription factors and intracellular cytokines were measured at baseline. EULAR response criteria were used to define poor (ΔDAS28 ≤ 1.2 and/or DAS28 > 3.2) and good (ΔDAS28 > 1.2 and DAS28 ≤ 3.2) responders. Multivariate logistic regression was used to identify predictors of response. Results Participants with plasma IL-23 present at baseline were more likely to be poor responders [15/20 (75%) of IL-23+ versus 36/73 (49.3%) of IL-23−; p = 0.041]. While frequencies of Th1, Th17, ex-Th17 and Treg cell populations were similar between good and poor responders to anti-TNF therapy, IL-17A+IFNγ+ ex-Th17 cells were more prevalent in good responders (0.83% of ex-TH17 cells) compared to poor responders (0.24% of ex-Th17 cells), p = 0.023. Both plasma IL-23 cytokine status (OR = 0.17 (95% CI 0.04–0.73)) and IL-17A+IFNγ+ ex-Th17 cell frequency (OR = 1.64 (95% CI 1.06 to 2.54)) were independently associated with a good response to anti-TNF therapy. Receiver operator characteristic (ROC) analysis, including both parameters, demonstrated an area under the ROC curve (AUC) of 0.70 (95% CI 0.60–0.82; p = 0.001). Conclusions Plasma IL-23 and circulating IL-17A+IFNγ+ ex-Th17 cells are independently associated with response to anti-TNF therapy. In combination, plasma IL-23 and circulating IL-17A+IFNγ+ ex-Th17 cells provide additive value to the prediction of response to anti-TNF therapy in RA.

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