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Objectives: This study aims to estimate the annual medical costs of systemic lupus erythematosus (SLE) in New Zealand (NZ)., Methods: SLE patients were linked to the Australia and New Zealand Dialysis and Transplant Registry, Pharmaceutical Collection, National Minimum Dataset, National Non-Admitted Patients Collection and Mortality Collection. National direct medical costs of SLE in 2006-2021 and annual costs per patient were estimated. Generalized linear model was used to examine the impact of various factors on medical costs, including ethnicity, gender, age, socioeconomic status and presence of end-stage kidney disease (ESKD)., Results: The annual national costs of SLE were stable over time, around NZ$12 million. The average costs were NZ$8,324 (US$5,277, €5,011) per patient per year, with the costs for patients with ESKD being nine times higher than patients without ESKD (NZ$47,143 vs NZ$5,091). The costs per patient for Māori and Pacific were both around twice the costs for European/Others (NZ$13,124 and NZ$11,842 vs NZ$6,153), but the difference attenuated after adjustment for ESKD and other factors. Among patients without ESKD, Asian, males and patients living in the most deprived areas were associated with higher costs. For patients with ESKD, Māori and patients living in the most deprived areas had higher costs., Conclusions: The annual national costs of SLE were stable over time. The increase in pharmaceutical costs were offset by decrease in hospitalisation costs. Costs for patients with ESKD were nine times higher than costs for patients without ESKD. Interventions for slowing the disease progression and preventing ESKD can reduce medical costs., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Objectives: This study aims to explore the treatment pattern of systemic lupus erythematosus (SLE) in Aotearoa/New Zealand., Methods: SLE patients were linked to the pharmaceutical dispensing data. The use of publicly funded anti-malarials, immunomodulators, biologics, glucocorticoids and bisphosphonates were compared by gender, ethnicity, age group, socioeconomic status and year of SLE identification. Adherence to hydroxychloroquine was examined using the medication possession ratio (MPR), with a MPR of ≥0.8 considered as high adherence., Results: Of the 2631 SLE patients, 73.8% used hydroxychloroquine, 64.1% used immunomodulators/biologics and 68.0% used 5 mg or more prednisone daily for at least 90 days. Women were more likely to use hydroxychloroquine than men. Asian patients had a different treatment pattern than other ethnic groups, and Māori were less likely to use hydroxychloroquine. The proportions of patients using different treatments decreased with age. Of the patients using hydroxychloroquine, 54.5% had high adherence. For patients over 40 years old and on long term prednisone, 47.3% had bisphosphonates and this figure was 17.8% for patients under the age of 40 years old. Patients with better socioeconomic status had a higher probability of using bisphosphonates than patients with lower socioeconomic status., Conclusions: Adherence to hydroxychloroquine in these patients varied and was lower in men and in Māori. Prednisone is commonly prescribed and used long term. Half of those over the age of 40 years old co-administered bisphosphonate. Further research is needed to identify the reasons for these discrepancies on SLE treatments by gender, ethnicity, age and socioeconomic status., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Genetic and environmental factors appear to contribute to the pathogenesis of systemic lupus erythematosus (SLE). Viral infections have been reported to be associated with the disease. A number of exogenous viruses have been linked to the pathogenesis of SLE, of which Epstein-Barr virus (EBV) has the most evidence of an aetiological candidate. In addition, human endogenous retroviruses (HERV), HRES-1, ERV-3, HERV-E 4-1, HERV-K10 and HERV-K18 have also been implicated in SLE. HERVs are incorporated into human DNA, and thus can be inherited. HERVs may trigger an autoimmune reaction through molecular mimicry, since homology of amino acid sequences between HERV proteins and SLE autoantigens has been demonstrated. These viruses can also be influenced by oestrogen, DNA hypomethylation, and ultraviolet light (UVB) exposure which have been shown to enhance HERV activation or expression. Viral infection, or other environmental factors, could induce defective apoptosis, resulting in loss of immune tolerance. Further studies in SLE and other autoimmune diseases are needed to elucidate the contribution of both exogenous and endogenous viruses in the development of autoimmunity. If key peptide sequences could be identified as molecular mimics between viruses and autoantigens, then this might offer the possibility of the development of blocking peptides or antibodies as therapeutic agents in SLE and other autoimmune conditions.