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Lipid screening and statins alongside disease-modifying anti-rheumatic drugs for patients with rheumatoid arthritis.

Over the last 4 decades, a growing body of work has demonstrated the high burden of cardiovascular disease (CVD) among patients with RA. However, CVD risk assessment in RA patients can be confusing. On the one hand, longitudinal studies suggest that there is a decreased CVD risk associated with tight RA control [1]. On the other hand, an increase in high-density lipoprotein (HDL) function and an elevation in lipid levels, including low-density lipoprotein (LDL) cholesterol, after treatment with biologics and non-biologic DMARDs has been observed, despite the fact that the total cholesterol:HDL ratio does not change with these medications [2]. Consequently, there has been confusion related to the role of lipid panels and the value of screening for (and treating) hyperlipidaemia in this population. Herein we address the central question regarding the importance of screening for hyperlipidaemia among patients with RA and propose a simple approach for improved screening for hyperlipidaemia in this at-risk population. Lipid levels do fluctuate with RA disease activity and as a result of treatment. Patients with RA often have low total cholesterol levels during active inflammation, yet they experience higher rates of myocardial infarction than would be expected (the so-called lipid paradox) [3]. At the same time, total cholesterol, HDL cholesterol and LDL cholesterol levels increase in patients with early RA following treatment with DMARDs (either biologic or non-biologic). This suggests that DMARDs may normalize depressed levels of cholesterol as inflammation is reduced. Given the observation in clinical trials that tocilizumab, an IL-6 receptor blocker, and tofacitinib, a Janus kinase inhibitor, increase LDL cholesterol by an average of 20 mg/dl, the US Food and Drug Administration currently recommends surveillance of lipid profiles during the use of these agents in patients with RA. Notably, research has shown that such changes in the lipid profile are not limited to these two medications. Indeed, this was demonstrated in a subanalysis from the Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial, which revealed an average increase of 30 mg/dl in LDL cholesterol after 6 months across all treatment arms of DMARDs therapy [MTX monotherapy, triple therapy (MTX, SSZ, HCQ) or MTX plus etanercept] [2]. This evidence supports the need for close monitoring of cholesterol levels not only because of the increased CVD risk that exists among patients with RA, but also because of the changes in lipids that occur with the medications used to treat RA. Despite these findings, current recommendations for lipid screening in the USA remain restricted to only two specific RA medications (tocilizumab and tofacitinib). In contrast, the EULAR CVD treatment guidelines recommend screening and managing hyperlipidaemia in all patients with RA once they have achieved either low disease activity or remission [4]. This is because the lipid profile at that point is believed to be more accurate in terms of CVD risk prediction than during times of active inflammation when cholesterol levels may be deceivingly low [4]. The European guidelines recognize that treatment of any kind for RA may change the CVD risk profiles of patients with RA and that treatment should trigger an assessment (or reassessment) of their CVD risk once disease activity has been suppressed. Addressing modifiable risk factors such as hyperlipidaemia alongside tight control of RA is important to reduce overall CVD risk as much as possible. Indeed, statins are remarkably effective in reducing CVD risk in this population, as supported by a number of studies [5, 6]. The European Society of Cardiology (ESC) and the American College of Cardiology/American Heart Association (ACC/AHA) cholesterol treatment guidelines recommend lifestyle modifications and the addition of a statin medication based on a high 10-year risk for a CVD event (fatal or non-fatal coronary heart disease or stroke) and LDL cholesterol level [7, 8]. These guidelines apply to RA patients as much as any other patient [7, 8]. Unfortunately the ACC/AHA and ESC guidelines cannot be applied without assessing lipid levels, and lipid screening is woefully underperformed in patients with RA: 444% of RA patients are screened compared with 79% of patients with diabetes, another high-risk group [9]. This observation likely has multifactorial antecedents. First, lipid screening is not frequently considered by rheumatologists, whose specialty has not traditionally focused on CVD risk reduction. Second, although primary care providers screen patients with RA for hyperlipidaemia more frequently than rheumatologists, patients with RA are still screened less frequently by primary care providers compared with their patients with diabetes. This observation may relate to deficits in knowledge or lack of clarity about who should take responsibility for CVD screening [10]. Third, as many as one in four RA patients reports not having a primary care provider. The end result is underscreening in this high-risk population. To address these issues, we advocate for a simpler approach to screening of RA patients by more broadly