Statins exert no effect on systemic lupus risk
Current statin use does not contribute to an increased risk of developing systemic lupus erythematosus (SLE) in individuals aged 40 years or above, according to a population-based cohort study. There is rather a signal of protection against the risk among long-term statin users.
Using data from the UK Clinical Practice Research Datalink, researchers identified 519,847 statin users and similar number of nonusers aged ≥40 years. The mean age was 63.1 years among users and 62.9 among nonusers. Follow-up in the group of statin users was divided into periods of current, recent and past exposure, with patients moving among these three exposure categories over time. Current statin users were also stratified according to duration of exposure: ≤1 year or >1 year. Analysis was performed using time-dependent Cox models.
Compared with nonusers, current statin users were not at high risk of developing SLE (adjusted hazard ratio [aHR], 0.75; 95 percent CI, 0.53 to 1.07). Furthermore, current statin use of >1 year was associated with a 38-percent lower risk of developing SLE (aHR, 0.62; 0.42 to 0.93), although this particular association was not observed when more specific definitions for SLE were used.
Statins are used to reduce the risk of cardiovascular morbidity and mortality in patients with hyperlipidaemia, hypertension or diabetes. The drugs demonstrate cholesterol-lowering activity, have anti-inflammatory and immunomodulatory properties, and possibly suppress the expression of ongoing autoimmune responses. A number of previous studies have shown that statins reduce the proinflammatory biomarkers and/or disease activity scores in patients with SLE. [J Rheumatol 2006;33:2361–3; Rheumatology 2007;46:1560–5; Clin Exp Rheumatol 2014;32:162–7]
The mechanisms by which statins may influence the risk of developing rheumatic autoimmune diseases are unknown, but the drugs have been shown to potentially promote regulatory T cell (Treg) differentiation in the periphery while blocking T helper (Th) 17 cell differentiation, which may be protective against SLE. Conversely, statins may also promote a shift in Th1/Th2 balance or lead to unstable peripheral Tregs, thus inducing autoimmunity. [Arthritis Res Ther 2010;12:R53; J Eur Acad Dermatol Venereol 2007;21:17–24; Nat Immunol 2009;10:1000–7]