• systemic lupus erythematosus
• epidemiology
• cardiovascular disease

It was with great interest that we read the correspondence of Abud-Mendoza1 on our recent paper in which we described a decreased risk of developing systemic lupus erythematosus (SLE) in statin users who continued their therapy for >1 year.2

We agree that prevention of cardiovascular disease in rheumatic diseases is of great importance.3 Whether statins decrease disease activity in SLE is, however, controversial since a recent meta-analysis of five controlled trials did not suggest any significant effect of statin therapy on Systemic Lupus Erythematosus Disease Activity Index.4

Unfortunately, in the UK’s Clinical Practice Research Datalink (CPRD)—an ongoing primary care database of anonymised medical records from general practitioners that was used in our study—no measurements for SLE activity before or after initiating statin therapy are available.2 We, however, do not think that statin therapy is superior to hydroxychloroquine (HCQ) as therapy to reduce relapses and thrombotic events in SLE. HCQ does not only prevent relapses in SLE but also has anti-atherogenic effects and is, in contrast to statins, associated with a reduced risk of development of diabetes mellitus.5–7

Abud-Mendoza wondered whether inclusion of patients <40 years changed our findings.1 When we included these patients and excluded patients with SLE before the index date, we identified 539 431 statin users and 539 431 non-users after using a matched random sampling approach (1:1). The index date (‘baseline’) was defined as the date of the first prescription of a statin; that is, ‘statin user’. Each statin user was matched to one control (‘non-user’) based on age, sex and general practice at index date, with the index date of the control being the same as that of the statin user. The characteristics at baseline are presented in table 1 and are in line with the characteristics that have been shown in Table 1 in our paper.2 Statin users and non-users had similar distributions of age (statin users: mean age, 62.7 years; and non-users: 61.9 years) and sex (statin users and non-users: 47.7% women). In our study population aged ≥16 years, the incidence rate was the same as the incidence rate in our recent study,2 0.7 cases per 10 000 person-years.

Compared with our previous findings, we found similar associations between statin use and the risk of SLE, only slightly attenuated. Among patients aged ≥16 years, current statin users had a risk of developing SLE which was comparable to that of non-users (HR_adjusted, 0.81; 95% CI 0.57 to 1.15). Moreover, current statin users who continued therapy for >1 year had a 34% decreased risk of developing SLE (HR_adjusted, 0.66; 95% CI 0.44 to 0.98) (table 2).

Finally, Abud-Mendoza wondered whether we had information regarding adverse events related to statins.1 Since our study objective was to assess the association between the statin use and the risk of SLE, we had no access to other study outcomes than SLE. However, several population-based studies using CPRD data have found adverse events of statins such as rhabdomyolysis and cataract.8 9

We conclude that statins are probably safe in SLE but that more research is needed to assess the benefit/risk profile of statins in other autoimmune rheumatic diseases such as polymyalgia rheumatica.10