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. 2023 Aug 26;63(6):1560–1567. doi: 10.1093/rheumatology/kead427

Mortality and causes of death in systemic lupus erythematosus in New Zealand: a population-based study

Chunhuan Lao 1,, Douglas White 2, Kannaiyan Rabindranath 3, Philippa Van Dantzig 4, Donna Foxall 5, Ross Lawrenson 6,7
PMCID: PMC11147544  PMID: 37632770

Abstract

Objectives

This study aims to assess the mortality of systemic lupus erythematosus (SLE) patients and examine whether there are variations by subgroup.

Methods

SLE patients from 2005 to 2021 were identified from the national administrative datasets. The underlying causes of death were examined. Standardized mortality ratio (SMR) was estimated to compare the relative rate of observed deaths in SLE patients with expected deaths in the general population. The hazard ratios (HR) and 95% confidence intervals (CI) of all-cause mortality and SLE specific mortality by ethnicity were estimated after adjustment for age using a Cox proportional hazards model.

Results

Of the 2802 patients included for analysis, 699 (24.9%) died with 209 (29.9%) SLE deaths. The age-standardized mortality rate of SLE was 0.29 per 100 000 for women and 0.05 for men. The mean age at death was 65.3 (17.1) years. Younger patients were more likely to have SLE as the underlying cause of death, from 78.9% for those under 20 years old to 18.7% for those aged 70–79 years. Compared with the general population, SLE patients were four times more likely to die (SMR: 4.0; 95% CI: 3.7, 4.3). Young patients had higher SMRs than older patients. Māori had worse all-cause mortality (HR: 1.72; 95% CI: 1.10, 2.67) and SLE specific mortality (HR: 2.60; 95% CI: 1.29, 5.24) than others.

Conclusions

The outcomes of SLE in New Zealand were still very poor compared with the general population. Māori with SLE had worse survival than others. Further research is needed to identify the reasons for this disparity.

Keywords: SLE, lupus, mortality, underlying cause of death, ethnic difference


Rheumatology key messages.

  • Compared with the general population, SLE patients were four times more likely to die.

  • Among SLE patients, SLE is the leading underlying cause of death.

  • Māori with SLE had worse survival than other ethnic groups.

Introduction

SLE is a chronic autoimmune disease that can lead to severe clinical outcomes [1]. It affects millions of people worldwide [2], and the epidemiology varies by age, gender and ethnicity. Most SLE patients are women, and the reported gender ratio of women to men ranged from 2:1 to 15:1 [3]. Most of the SLE cases were between the ages of 15 and 45 years [4]. The prevalence differs by ethnicity—SLE is more common and of greater severity in Australian Aboriginal, Asian, Polynesian and African American patients [5]. A New Zealand study in 1983 reported that the age-adjusted prevalence rates was 14.6 per 100 000 people for New Zealand Europeans, 50.6 for Polynesians and 19.1 for others [6]. While the incidence of SLE has been relatively stable over time, the prevalence was reported to be increasing [7, 8].

The outcome of SLE is highly variable, ranging from permanent remission to death [9]. Previous studies showed that patients with SLE are three times more likely to die over a 10-year period than age-matched people in the general population [10, 11]. Approximately 85% of SLE patients survive 10 years from diagnosis and 75% survive 20 years [12, 13]. Long-term outcomes in SLE have been dramatically improved over the past decades due to earlier diagnosis and treatment advancements [14]. The 5-year survival of patients with SLE has improved from 50% in the 1950s to over 90% since the 1990s [15–19]. Cardiovascular disease, cancer and SLE itself are reported to be the major causes of death for SLE patients [9, 16, 19]. SLE patients had a 2.7 times increased risk of cardiovascular events than the general population [20].

The main determinants of long-term outcomes in SLE were reported to be age, sex, race/ethnicity, genetic profile, environmental factors, disease activity, major organ involvement including lupus nephritis and CNS involvement, comorbidities, coexistence with antiphospholipid syndrome, treatment adherence, socio-economic factors, and access to care [21]. For example, juvenile SLE patients suffered from more severe disease presentation and had a higher mortality rate compared with adult SLE patients [22]. Some studies also reported that men with SLE had worse survival than women with SLE [16, 21, 23]. African, Hispanic and Asian patients with SLE tend to develop more severe clinical features and have inferior outcomes than Europeans [24, 25]. Outcomes of SLE in New Zealand have rarely been reported. However, updated knowledge in SLE outcomes is crucial for guiding preventive and therapeutic strategies and for improving survival of SLE patients in New Zealand. This study aims to assess the mortality of SLE patients in New Zealand, determine the cause of death and examine whether there are variations by subgroup.

Methods

We first identified the SLE cases between 1 January 2005 and 31 December 2021 using the ICD-10 code ‘M32’ from the National Minimum Dataset (NMDS) and the Mortality Collection (coded death records) and using the key words ‘systemic lupus erythematosus’ from the Death Certificates (uncoded death records). The first date in the NMDS for an inpatient event with an ICD-10 code of ‘M32’ or the first date from the National Non-admitted Patient Collection (NNAPC) for an outpatient event in the Rheumatology department or Renal Service, whichever date was earlier, was considered as the date of first identification of SLE. The NMDS records inpatient and day patient discharges from all public hospitals and over 90% of private hospitals. The NNAPC includes event-based purchase units that relate to medical and surgical outpatient events and emergency department events from both public and private hospitals. The Mortality Collection and Death Certificates contain information about all deaths (including date and cause of deaths) registered in New Zealand, and the Death Certificates collect more up-to-date death records not yet included in the Mortality Collection. The NMDS and the NNAPC started collecting data from 2005, and the NNAPC does not include ICD codes. These datasets were linked together through their National Health Index (NHI) number. NHI is a unique identifier assigned to every person who uses health and disability services in New Zealand. It can accurately identify people and link them with the right health records.

To validate our methods for identifying SLE patients and date of SLE identification using the national administrative datasets, we compared the data from national administrative datasets with the medical records using patients in the Waikato region. For these patients we examined their medical records in the Clinical Workstation in Waikato hospital to confirm the diagnosis of SLE and to identify the first date of SLE identification. The date of SLE identification in the clinical records was compared with the date from the national administrative datasets.

The last date of follow-up for mortality was 31 December 2022, and patients who were still alive by this date were censored. The mean age at death and standard deviation were calculated by gender (women and men), ethnicity (Māori, Pacific, Asian and European/other) and socioeconomic deprivation. Ethnicity is self-identified in New Zealand. Socioeconomic deprivation was defined using the New Zealand Index of Deprivation 2018 (NZDep 2018) analysed as quintiles, from 1 (least deprived) to 5 (most deprived) [26]. The NZDep is an area-based measure of socioeconomic deprivation in Aotearoa/New Zealand. It measures the level of deprivation for people in each small area. The differences in mean age at death by subgroup were examined with an independent sample Student’s t-test and one-way ANOVA, with a P-value of <0.05 considered significant.

The underlying cause of death is indicated and coded with ICD-10 code in the Mortality Collection but was not indicated in the Death Certificates. The Death Certificates contains up to seven causes of deaths. Two of the authors (C.L. and P.D.) examined the Death Certificates to identify the underlying cause of deaths. The underlying cause of death is defined by the world Health Organization (WHO) as (i) ‘the disease or injury which initiated the train of events leading directly to death’, or (ii) ‘the circumstances of the accident or violence which produced the fatal injury’ [27]. The underlying causes of death were categorized into eight groups: (i) SLE, (ii) cardiovascular and cerebrovascular disease, (iii) cancer, (iv) respiratory, (v) other rheumatological disease, (vi) infectious disease, (vii) renal failure, and (viii) others. The proportions of patients in different groups were compared by gender, age group (<20, 20–29, 30–39, 40–49, 50–59, 60–69, 70–79 and 80+ years) and ethnicity. A logistic regression model was used to examine the characteristics associated with SLE as the underlying cause of death in patients with SLE. The odds ratios by subgroup and the 95% confidence interval (95% CI) were estimated, after adjustment for gender, age, ethnicity, comorbidity and deprivation. Comorbidity was examined with the Charlson Comorbidity Index (CCI). Comorbidities recorded in the NMDS before or on the date of SLE identification were included in the CCI score calculation, and SLE was not included in the CCI score calculation.

The standardized mortality ratio (SMR) was estimated to compare the relative rate of observed deaths in SLE patients with expected deaths in the general population. The gender, age and year specific mortality rates for the general population were from Statistics New Zealand. The mortality probability was assigned to each patient each year since the SLE identification based on the age, gender and calendar year, and these were summed to yield expected deaths. SMR was estimated by dividing the actual (observed) deaths by the expected deaths. Subgroup analyses on SMR was performed by gender, age, ethnicity and deprivation quintile. SMRs were calculated and compared between all patients and patients identified in 2010–2021. For patients identified in 2010–2021, the dates of SLE identification were more accurate than those for patients in earlier years, with 78.4% of patients identified in 2010–2021 having an accurate date of first SLE identification and 11.4% of patients having a gap of 1–5 years between the two dates.

The WHO age-standardized mortality rate of SLE and 95% CI was calculated separately for men and women in 2010–2021. Survival curves of all-cause survival and SLE specific survival were produced to compare the difference by ethnicity after adjustment for age at diagnosis for patients in 2010–2021 using a Cox proportional hazards model. The hazard ratios of all-cause mortality and SLE specific mortality by ethnic group were estimated, before and after adjustment for age. All data analyses were performed in IBM SPSS Statistics v. 29 (IBM Corp., Armonk, NY, USA), except SMR calculation, which was performed in Microsoft Excel (Microsoft Corp., Redmond, WA, USA). Ethics approval for the study was granted through the Northern B Health and Disability Ethics Committee (reference: 2022 EXP 13741). Consent to participate and for publication is not applicable.

Results

During the study period, we identified 2837 patients with SLE. Thirty-five patients were excluded because of unknown date of first identification of SLE. Overall, 2802 patients were included in this study, comprising 2422 women and 380 men (Table 1). Of these 2802 patients, 699 (24.9%) died during the follow-up period. The mean (s.d.) age at death was 65.3 (17.1) years. The mean age at death for men was 3 years older than for women (68 vs 64.7 years). The mean age at death for European/other (70.2 (14.1) years) was 20 years older than for Pacific (50.3 (19.6) years), 15 years older than for Māori (54.7 (17.0) years) and 12 years older than for Asian (58.5 (17.4) years) patients. Patients living in the most deprived areas had the youngest mean age at death (59.7 years), while patients living in the less deprived areas had the oldest mean age at death (67.7 and 70.8 years for those in the deprivation quintile 5 and 4, respectively).

Table 1.

Mean age at death of all SLE patients by subgroup

Subgroup Number of patients Number of deaths Age at death, mean (s.d.), years P-value
Gender
 Women 2422 573 64.7 (17.3) 0.049
 Men 380 126 68.0 (16.1)
Ethnicity
 Māori 430 90 54.7 (17.0) <0.001
 Pacific 431 74 50.3 (19.6)
 Asian 416 45 58.5 (17.4)
 European/other 1525 490 70.2 (14.1)
Deprivation quintile
 1 (least deprived) 408 82 67.7 (14.8) <0.001
 2 481 117 70.8 (15.7)
 3 489 125 65.3 (17.5)
 4 649 185 66.7 (16.4)
 5 (most deprived) 746 186 59.7 (17.8)
 Unknown 29 4 52.0 (15.8)
Total 2802 699 65.3 (17.1)

Of the 699 patients who died, 209 (29.9%) died of SLE (Table 2). There was a slightly higher proportion of women having SLE as the underlying cause of death than men (30.9% vs 25.4%, P = 0.223). Māori, Pacific and Asian patients were more likely to have SLE as the underlying cause of death than Europeans/others (43.3%, 44.6% and 40.0% vs 24.3%, respectively, P < 0.001). Among patients who passed away, younger patients were more likely to die of SLE than older patients, from 78.9% for those under 20 years old to 18.7% for those aged 70–79 years. In contrast, the proportion of patients dying from cardiovascular and cerebrovascular disease increased with age, from 10.5% for those under 20 years old to 31.9% for those aged 80 years or older. Only 16 (2.3%) patients had infectious disease as the underlying cause of death. After adjustment for age, ethnicity, comorbidity and deprivation, women and men had similar risk of having SLE as the underlying cause of death (Table 3). Compared with patients aged 60–69 years old, patients aged under 20 years old had almost 13 times, patients aged 20–29 years had more than eight times and patients aged 30–59 years had more than twice the risk of dying of SLE than from other causes. After adjustment for other factors, the ethnic difference in underlying cause of death attenuated. Comorbidity and deprivation did not affect the probability of having SLE as the underlying cause of death.

Table 2.

Underlying cause of death of all patients by subgroup

Subgroup SLE Cardiovascular and cerebrovascular disease Cancer Respiratory Other rheumatological disease Infectious disease Renal failure Others Total
Gender
 Women 177 (30.9) 130 (22.7) 105 (18.3) 36 (6.3) 17 (3.0) 13 (2.3) 6 (1.0) 89 (15.5) 573
 Men 32 (25.4) 30 (23.8) 29 (23.0) 11 (8.7) 3 (2.4) 3 (2.4) 4 (3.2) 14 (11.1) 126
Age group, years
 <20 15 (78.9) 2 (10.5) 0 0 0 0 0 2 (10.5) 19
 20–29 23 (69.7) 5 (15.2) 1 (3.0) 0 0 0 0 4 (12.1) 33
 30–39 22 (40.0) 9 (16.4) 6 (10.9) 1 (1.8) 4 (7.3) 2 (3.6) 2 (3.6) 9 (16.4) 55
 40–49 30 (40.0) 13 (17.3) 14 (18.7) 4 (5.3) 1 (1.3) 2 (2.7) 2 (2.7) 9 (12.0) 75
 50–59 45 (34.9) 22 (17.1) 27 (20.9) 10 (7.8) 2 (1.6) 0 3 (2.3) 20 (15.5) 129
 60–69 29 (17.7) 44 (26.8) 44 (26.8) 14 (8.5) 6 (3.7) 6 (3.7) 1 (0.6) 20 (12.2) 164
 70–79 29 (18.7) 43 (27.7) 31 (20.0) 11 (7.1) 5 (3.2) 5 (3.2) 2 (1.3) 29 (18.7) 155
 80+ 16 (23.2) 22 (31.9) 11 (15.9) 7 (10.1) 2 (2.9) 1 (1.4) 0 10 (14.5) 69
Ethnicity
 Māori 39 (43.3) 17 (18.9) 14 (15.6) 6 (6.7) 1 (1.1) 1 (1.1) 2 (2.2) 10 (11.1) 90
 Pacific 33 (44.6) 13 (17.6) 6 (8.1) 4 (5.4) 2 (2.7) 1 (1.4) 1 (1.4) 14 (18.9) 74
 Asian 18 (40.0) 6 (13.3) 11 (24.4) 1 (2.2) 1 (2.2) 0 3 (6.7) 5 (11.1) 45
 European/other 119 (24.3) 124 (25.3) 103 (21.0) 36 (7.3) 16 (3.3) 14 (2.9) 4 (0.8) 74 (15.1) 490
Total 209 (29.9) 160 (22.9) 134 (19.2) 47 (6.7) 20 (2.9) 16 (2.3) 10 (1.4) 103 (14.7) 699

Data are presented as n (%).

Table 3.

Adjusted odds ratio of having SLE as the underlying cause of death by subgroup

Subgroup Adjusted odds ratio (95% CI) P-value
Gender
 Women Reference
 Men 0.93 (0.58, 1.48) 0.749
Age group, years
 <20 12.96 (3.83, 43.92) <0.001
 20–29 8.64 (3.53, 21.15) <0.001
 30–39 2.64 (1.32, 5.28) 0.006
 40–49 2.82 (1.50, 5.29) 0.001
 50–59 2.43 (1.40, 4.21) 0.002
 60–69 Reference
 70–79 1.14 (0.64, 2.03) 0.662
 80+ 1.54 (0.76, 3.15) 0.233
Ethnicity
 Māori 1.46 (0.84, 2.53) 0.179
 Pacific 1.23 (0.66, 2.29) 0.509
 Asian 1.26 (0.64, 2.50) 0.507
 European/other Reference
Charlson comorbidity index score
 0 Reference
 1 0.85 (0.55, 1.32) 0.474
 2 0.48 (0.25, 0.92) 0.027
 3 0.89 (0.37, 2.16) 0.801
 4+ 0.78 (0.29, 2.09) 0.621
Deprivation quintile
 1 Reference
 2 1.43 (0.72, 2.85) 0.306
 3 1.18 (0.60, 2.33) 0.625
 4 1.02 (0.54, 1.94) 0.957
 5 1.42 (0.74, 2.72) 0.297
 Unknown 0.86 (0.08, 9.44) 0.898

When comparing all 2802 SLE patients with the general population, SLE patients were four times more likely to die (SMR: 4.0; 95% CI: 3.7, 4.3; Table 4). The SMR was higher for women than men (4.2 vs 3.5). The SMR decreased with increasing age, from 13.3 for patients under 20 years old to 2.6 for patients aged 80 years or older. Māori and Pacific people had a higher SMR than Asian and European/other (SMR: 6.3, 5.8, 3.5 and 3.7, respectively). These SMRs were close to those estimated using only patients identified in 2010–2021 with an overall SMR of 4.2 (95% CI: 3.6, 4.8), except for a wider gap between ethnic groups. The average age-standardized mortality rate of SLE in 2010–2021 was 0.29 (95% CI: 0.10, 0.48) per 100 000 people for women and 0.05 (95% CI: 0.02, 0.08) for men (Supplementary Table S1, available at Rheumatology online). The mortality rate was stable over time.

Table 4.

Standardized mortality ratios of SLE patients compared with the general population

All patients
Only patients in 2010–2021
Subgroup Deaths Expected deaths SMR (95% CI) Deaths Expected deaths SMR (95% CI)
Gender
 Women 573 137.4 4.2 (3.8, 4.5) 139 32.4 4.3 (3.6, 5.0)
 Men 126 35.8 3.5 (2.9, 4.2) 38 10.2 3.7 (2.6, 5.0)
Age group
 <20 19 1.4 13.3 (8.0, 20.0) 7 0.5 13.4 (5.3, 25.2)
 20–29 33 2.7 12.2 (8.4, 16.7) 7 0.6 12.2 (4.8, 22.9)
 30–39 55 8.2 6.7 (5.1, 8.6) 10 1.4 7.3 (3.5, 12.6)
 40–49 75 15.9 4.7 (3.7, 5.8) 15 2.7 5.5 (3.1, 8.7)
 50–59 129 26.5 4.9 (4.1, 5.7) 25 4.9 5.1 (3.3, 7.3)
 60–69 164 44.5 3.7 (3.1, 4.3) 42 8.8 4.8 (3.5, 6.4)
 70–79 155 47.3 3.3 (2.8, 3.8) 38 10.9 3.5 (2.5, 4.7)
 80+ 69 26.6 2.6 (2.0, 3.2) 33 12.8 2.6 (1.8, 3.5)
Ethnicity
 Māori 90 14.3 6.3 (5.1, 7.7) 14 5.1 9.5 (6.3, 13.5)
 Pacific 74 12.9 5.8 (4.5, 7.1) 116 32.1 7.8 (4.8, 11.6)
 Asian 45 12.9 3.5 (2.5, 4.6) 27 2.8 2.8 (1.5, 4.4)
 European/other 490 133.1 3.7 (3.4, 4.0) 20 2.6 3.6 (3.0, 4.3)
Deprivation quintile
 1 (least deprived) 82 21.5 3.8 (3.0, 4.7) 28 4.9 5.7 (3.8, 8.1)
 2 117 38.1 3.1 (2.5, 3.7) 26 9.1 2.9 (1.9, 4.1)
 3 125 33.9 3.7 (3.1, 4.4) 37 10.6 3.5 (2.5, 4.7)
 4 185 46.7 4.0 (3.4, 4.6) 43 10.1 4.3 (3.1, 5.6)
 5 (most deprived) 186 31.4 5.9 (5.1, 6.8) 41 7.6 5.4 (3.9, 7.2)
 Unknown 4 1.6 2.6 (0.7, 5.7) 2 0.3 7.5 (0.7, 21.4)
Total 699 173.2 4.0 (3.7, 4.3) 177 42.6 4.2 (3.6, 4.8)

SMR: standardized mortality ratio.

Supplementary Table S2 (available at Rheumatology online) shows the number of deaths and death rate by age group and ethnic group among patients in 2010–2021. The death rate was highest for Europeans/others (22.3%), but only a small proportion of deaths were in the younger age groups (4.3% in patients aged <40 years). In contrast, Māori, Pacific and Asian patients had a lower death rate (15.4%, 9.3% and 6.0%, respectively), but a higher proportion of deaths was in the younger age groups (25.9%, 40.0% and 28.6%, respectively, in patients aged <40 years). After adjustment for age, Māori were more likely to die than European/other patients for both all-cause mortality (hazard ratio: 1.72; 95% CI: 1.10, 2.67) and SLE specific mortality (hazard ratio: 2.60; 95% CI: 1.29, 5.24, Table 5). The age-adjusted survival curves (Fig. 1) show similar results with Māori patients having the worst all-cause survival and SLE specific survival.

Table 5.

Adjusted hazard ratio of SLE specific mortality among patients in 2010–2021

Factors All-cause mortality
SLE specific mortality
Adjusted hazard ratio (95% CI) P-value Adjusted hazard ratio (95% CI) P-value
Ethnicity
 Māori 1.72 (1.10, 2.67) 0.016 2.60 (1.29, 5.24) 0.008
 Pacific 1.32 (0.80, 2.18) 0.287 1.17 (0.46, 2.96) 0.745
 Asian 0.66 (0.38, 1.17) 0.154 0.94 (0.38, 2.34) 0.895
 European/other Reference Reference
Age (continuous) 1.07 (1.06, 1.08) <0.001 1.05 (1.03, 1.07) <0.001

Figure 1.

Figure 1.

SLE specific survival and all-cause survival curve by ethnicity after adjustment for age. (A) All-cause survival. (B) SLE specific survival

Discussion

Though the outcome for SLE patients has been improving over time, the survival of SLE patients is still very poor compared with the general population. The life expectancy in New Zealand was 80.0 years for men and 83.5 years for women in 2017–2019 [28], while the mean age at death for SLE patients was 68.0 years for men and 64.7 years for women. The SLE mortality in New Zealand is comparable to other countries, with our estimated SMR (4.0) being consistent with the published SMRs (2.2–5.3). The poor survival and high risk of dying from SLE indicated unmet needs of SLE patients. Actions will be needed to improve disease management and to improve survival of SLE patients.

In our study, SLE was the leading cause of death among SLE patients, followed by cardiovascular disease. This is consistent with what was found in a French study [29] including 1593 deaths with 637 (40%) deaths due to SLE and 341 (21%) due to cardiovascular disease. However, these are contradictory to some other studies [16, 19, 30], which showed that cardiovascular disease was the leading cause of death for SLE patients. It was shown that patients with SLE have 2–10 times increased risk of cardiovascular disease compared with the general population [31]. Around 2% of the deaths were due to infectious disease in our study, which was also found in a population-based study in California [30], but another American study using a National Inpatient Sample found that infections accounted for 37% of deaths [32]. The big differences are explained by the data limitation of the National Inpatient Sample, which includes repeated records and missing information from death certificates [30, 32].

Young patients with SLE had a higher mortality compared with the general population matched with age and gender. However, compared with older patients, younger patients with SLE still had better survival. This is not consistent with what has been found in other studies showing that juvenile SLE patients suffered from more severe disease presentation and had a higher mortality rate compared with adult SLE patients [22]. Younger patients were more likely to have SLE as the underlying cause of death than older patients. In contrast, the proportion of patients dying from cardiovascular and cerebrovascular disease increased with age. Higher mortality was observed in women than men, which was contradictory to some other studies [16, 21, 23]. A study conducted in Finland in 2000–2008 [19] reported the mean age at death was 67.8 years for women and 62.3 years for men, while the mean age at death in our study was 64.7 years for women and 68.0 years for men. Patients with the worst socioeconomic status had the worst outcomes.

Māori and Pacific patients had much higher SMR and younger mean age at death than Europeans, but lower mortality rate than Europeans. This is because a greater proportion of deaths of Māori and Pacific patients was in the younger patients who had higher SMR but lower mortality rate as described in the last paragraph. After adjustment for age, Pacific patients had similar mortality compared with Europeans, while Māori had higher SLE specific mortality and all-cause mortality than Europeans. Other studies have demonstrated different outcomes in SLE patients by ethnic groups [24, 25]. For example, African, Hispanic and Asian patients with SLE were found to develop more severe clinical features and had inferior outcomes than Europeans [24, 25]. Ethnic difference in underlying cause of death was also found in other studies [30]. African American patients with SLE were more likely to have cardiovascular disease as the underlying cause of death than European descendants (39% vs 28%) [30]. In our study, before adjustment for age, Māori, Pacific and Asian patients were more likely to have SLE as the cause of death than Europeans/others. However, the difference disappeared after adjustment for age.

This is a population-based study including 699 deaths related to SLE. The number of deaths in this study is relatively large compared with other published studies [16, 19, 30, 33, 34], which makes our results more robust. Linking with other national administrative datasets, we had complete data on patients’ characteristics, except for 29 patients with missing socioeconomic status. These complete data enabled us to make a more accurate estimation of the impact of the characteristics on SLE outcomes and underlying cause of death. However, this study has some limitations. From our data validation with the Waikato patient cohort, we found that around 80% of the dates of SLE diagnosis in our dataset were the same as or close to the accurate dates of diagnosis. There were still around 20% of patients who had a wrong date of SLE diagnosis, but we did not have other sources to correct that. This would have slightly biased the results of impact of age on SLE outcomes. We did not have data on disease severity, and therefore we could not assess its impact on outcomes. It is known that the life expectancy in New Zealand varies by ethnicity [35], which may partly explain the difference in SMRs by ethnicity. However, ethnicity specific mortality rates are not available in New Zealand to calculate the expected deaths.

Conclusions

The outcomes of SLE in New Zealand were still very poor compared with the general population. SLE is the leading cause of death among SLE patients. Young patients with SLE were more likely to die of SLE than older patients. Māori with SLE had worse survival than other ethnic groups. Further research is needed to identify the reasons for this disparity. Better management of SLE is needed to improve the outcomes and to reduce ethnic differences.

Supplementary Material

kead427_Supplementary_Data

Acknowledgements

We would like to acknowledge the Ministry of Health for providing the detailed data.

Contributor Information

Chunhuan Lao, Medical Research Centre, The University of Waikato, Hamilton, New Zealand.

Douglas White, Rheumatology Department, Waikato Hospital, Hamilton, New Zealand.

Kannaiyan Rabindranath, Renal Unit, Waikato Hospital, Hamilton, New Zealand.

Philippa Van Dantzig, Rheumatology Department, Waikato Hospital, Hamilton, New Zealand.

Donna Foxall, Te Huataki Waiora—School of Health, The University of Waikato, Hamilton, New Zealand.

Ross Lawrenson, Medical Research Centre, The University of Waikato, Hamilton, New Zealand; Strategy and Funding, Waikato Hospital, Hamilton, New Zealand.

Supplementary material

Supplementary material is available at Rheumatology online.

Data availability

The data underlying this article cannot be shared publicly due to the ethics for patinet privacy. The data will be shared on reasonable request to the corresponding author.

Funding

This study was funded by Arthritis New Zealand (Lupus-SLE Postdoctoral Fellowship for C.L.).

Disclosure statement: The authors declare that they have no conflict of interest.

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Associated Data

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Supplementary Materials

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Data Availability Statement

The data underlying this article cannot be shared publicly due to the ethics for patinet privacy. The data will be shared on reasonable request to the corresponding author.


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