Background: The ABCG2 Q141K (rs2231142) and rs10011796 variants associate with hyperuricaemia (HU). The effect size of ABCG2 rs2231142 on urate is~60% that of SLC2A9, yet the effect size on gout is greater. We tested the hypothesis that ABCG2 plays a role in the progression from HU to gout by testing for association of ABCG2 rs2231142 and rs10011796 with gout using HU controls. Methods: We analysed 1699 European gout cases and 14,350 normouricemic (NU) and HU controls, and 912 New Zealand (NZ) Polynesian (divided into Eastern and Western Polynesian) gout cases and 696 controls. Association testing was performed using logistic and linear regression with multivariate adjusting for confounding variables. Results: In Europeans and Polynesians, the ABCG2 141K (T) allele was associated with gout using HU controls (OR = 1.85, P = 3.8E − 21 and OR meta = 1.85, P = 1.3E − 03 , respectively). There was evidence for an effect of 141K in determining HU in European (OR = 1.56, P = 1.7E − 18 ) but not in Polynesian (OR meta = 1.49, P = 0.057). For SLC2A9 rs11942223, the T allele associated with gout in the presence of HU in European (OR = 1.37, P = 4.7E − 06 ), however significantly weaker than ABCG2 rs2231142 141K (P Het = 0.0023). In Western Polynesian and European, there was epistatic interaction between ABCG2 rs2231142 and rs10011796. Combining the presence of the 141K allele with the rs10011796 CC-genotype increased gout risk, in the presence of HU, 21.5-fold in Western Polynesian (P = 0.009) and 2.6-fold in European (P = 9.9E − 06 ). The 141K allele of ABCG2 associated with increased gout flare frequency in Polynesian (P meta = 2.5E − 03 ). Conclusion: These data are consistent with a role for ABCG2 141K in gout in the presence of established HU.

Objective To assess changes in presentations to EDs during the COVID‐19 pandemic lockdown in the Southern Region of New Zealand. Methods We conducted a retrospective audit of patients attending EDs in the Southern District Health Board (SDHB), from 1 March to 13 May 2020. We made comparisons with attendances during the same period in 2019. The 2020 study period included ‘pre‐lockdown’ (1 March–25 March), ‘level 4 (strict) lockdown’ (26 March–27 April) and ‘level 3 (eased) lockdown’ (28 April–13 May). Results Patient volumes reduced in all SDHB EDs during levels 4 and 3, mostly representing a loss of low acuity patients (Australasian Triage Scale 3, 4 and 5), although high‐acuity presentations also declined. Average patient age increased by 5 years; however, the proportions of sexes and ethnicities did not change. Presentations of cerebrovascular accidents and appendicitis did not change significantly. Trauma, mental health, acute coronary syndrome and infectious respiratory presentations decreased significantly during level 4, and infectious respiratory presentations decreased further in level 3. Conclusions Within the SDHB, patient volumes reduced during levels 4 and 3 of our lockdown, with reduced low‐acuity presentations. High‐acuity patient numbers also declined. Trauma, mental health, alcohol‐related, infectious respiratory and acute coronary syndrome presentations declined while cerebrovascular accident and appendicitis numbers showed little to no change.

Background The ABCG2 Q141K ( rs2231142 ) and rs10011796 variants associate with hyperuricaemia (HU). The effect size of ABCG2 rs2231142 on urate is ~60% that of SLC2A9, yet the effect size on gout is greater. We tested the hypothesis that ABCG2 plays a role in the progression from HU to gout by testing for association of ABCG2 rs2231142 and rs10011796 with gout using HU controls. Methods We analysed 1,699 European gout cases and 14,350 normourciemic (NU) and HU controls, and 912 New Zealand (NZ) Polynesian (divided into Eastern and Western Polynesian) gout cases and 696 controls. Association testing was performed using logistic and linear regression with multivariate adjusting for confounding variables. Results In Europeans and Polynesians, the ABCG2 141K (T) allele was associated with gout using HU controls (OR=1.85, P =3.8E -21 and OR meta =1.85, P =1.3E -03 , respectively). There was evidence for an effect of 141K in determining HU in European (OR=1.56, P =1.7E -18 ) but not in Polynesian (OR meta =1.49, P =0.057). For SLC2A9 rs11942223, the T allele associated with gout in the presence of HU in European (OR=1.37, P =4.7E -06 ), however significantly weaker than ABCG2 rs2231142 141K ( P Het =0.0023). In Western Polynesian and European, there was epistatic interaction between ABCG2 rs2231142 and rs10011796 . Combining the presence of the 141K allele with the rs10011796 CC-genotype increased gout risk, in the presence of HU, 21.5-fold in Western Polynesian ( P =0.009) and 2.6-fold in European ( P =9.9E -06 ). The 141K allele of ABCG2 associated with increased gout flare frequency in Polynesian ( P meta = 2.5E -03 ). Conclusion These data are consistent with a role for ABCG2 141K in gout in the presence of established HU.

This is the first study to investigate attitudes and practices of NZ paediatricians regarding GAT for severely disabled children. Results indicate a range of views but suggest that family requests for GAT do occur and that the majority of paediatricians are not opposed to GAT in the appropriate ethical and clinical context. The development of practice guidelines for GAT may lead to a more informed decision-making process about GAT for families and paediatricians.

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