Statin exposure associated with idiopathic inflammatory myositis

Association of Statin Exposure With Histologically Confirmed Idiopathic Inflammatory Myositis in an Australian Population

Literature - Caughey GE, Gabb GM, Ronson S et al. - JAMA Intern Med. 2018; published online ahead of print

Introduction and methods

Statins decrease LDL-c levels, reduce CV risk, and cause musculoskeletal adverse events in some patients, which usually resolve after discontinuation [1]. Case reports and a small case-control study related statin therapy with idiopathic inflammatory myositis (IIM). This is a group of rare, autoimmune muscular disorders, including polymyositis, inclusion body myositis, dermatomyositis, and necrotizing myositis, which may lead to permanent disability and death [2,3].

This retrospective, population-based, case-control study assessed the association between current exposure to statins and histologically confirmed IIM. Moreover, the prevalence of specific types of IIM and temporal changes in the proportion of IIM cases exposed to statins was evaluated.

For this purpose, patients aged ≥40 years with histologically confirmed IIM were identified in the South Australian Myositis Database [4] between 1990 and 2014. Statin use was self-reported or reported by the treating rheumatologist. Population-based controls obtained from the North West Adelaide Health Study [5] between 2004 and 2006 were randomly matched by age, gender and comorbidity index in a 3:1 ratio of controls to cases.

Main results

A total of 221 IIM cases were identified. Statin exposure at the time of IIM diagnosis was 30.8% of cases (95%CI: 24.7-36.9) and 21.5% (95%CI: 18.3-24.6; P = 0.005) in matched controls.
Polymyositis, the most common subtype of IIM, was diagnosed in 40.3% of cases, out of whom 30.3% were exposed to a statin.
29.9% had inclusion body myositis, out of whom 30.3% were exposed to a statin.
50% had dermatomyositis, out of whom 17.4% were exposed to a statin (P=0.02)
10.9% had necrotizing myositis, out of whom 50.0% were exposed to a statin (P=0.02).
Patients with IIM had an almost two-fold increased likelihood of statin exposure compared with controls (ORadj: 1.79; 95%CI: 1.23-2.60; P = 0.001).
The total number of cases of IIM varied over time, with an increase seen over the periods 2000-2002, 2003-2005 and 2006-2008 (up to about 52%), followed by a drop in 2009-2011 (~32%) and another increase up to about 44% in 2012-2014). Statins dispensed in Australia increased over this period, but stabilized between 2009-2011 and 2012-2014. The proportion of IIM patients who were exposed to statins varied across periods.

Conclusion

Statin exposure was significantly associated with histologically confirmed IIM. Although IIM is rare, and statin-associated autoimmune myopathy even rare, considering the severity of the condition and the increasing use of statins, awareness and early recognition of the disease is important. Causality of the relationship between statin therapy and IIM remains unknown.

Editorial comment

In his editor’s note, Curfman [6] writes that although statin exposure was not accurately captured in the study of Caughey et al. since in some patients it was self-reported and in others, the rheumatologists reported medications captured in medical records, these are probably the best existing data on this topic. He concludes: ‘Statin-associated myopathy as well as muscular aches and pains will continue to be a concern to patients and a diagnosis elusive to physicians. This debilitating adverse effect underscores the importance of prescribing statins only to patients who will clearly have a net benefit.’

Find this article online at JAMA Intern Med