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Munro et al have demonstrated a salubrious effect of hydroxychloroquine (HCQ) on lipid profiles in patients with rheumatic arthritis (RA).1 In an accompanying editorial, Situnayake and Kitas highlight the potential importance of dyslipidaemia in RA.2 We concur with the relevance of this problem, and would like to call attention to some additional data that supports the authors’ points.
In an earlier study, we reported on the serum lipoprotein profiles of 60 men with RA.3 According to National Cholesterol Education Program guidelines,4 18% of the patients had dyslipidaemia to such an extent that they would be considered at “high risk” of developing atherosclerotic cardiovascular disease (ASCVD) (that is, total cholesterol (TC) ⩾ 6.21 mmol/l or LDL-cholesterol ⩾ 4.14 mmol/l). An additional 13% had “borderline” increases in lipids (TC ⩾ 5.17 mmol/l or LDL ⩾ 3.36 mmol/l), which would be significant and merit treatment in the setting of other risk factors for ASCVD. Also, 50% of patients had depressed concentrations of HDL-cholesterol, another risk factor for ASCVD. In all, 68% of this particular group of RA patients had significant dyslipidaemia. While this was a skewed subset of RA patients (that is, older men), the results are notable.
In agreement with the findings of Munro et al, we demonstrated cholesterol lowering effects of HCQ in systemic lupus erythematosus (SLE) patients.5 Although the numbers of patients in this pilot study were comparatively small, significant and dose dependent decreases in TC, TC/HDL ratio, and LDL/HDL ratio were noted in this double blind, placebo controlled study. As is the case for RA, accelerated ASCVD is an important contributor to morbidity and mortality among SLE patients.
Recently, another factor has been described that underlines the relevance of dyslipidaemia among patients with rheumatic diseases. Studies detailing the frequency of atherosclerotic complications among patients with homocystinuria have helped establish that increased concentrations of homocysteine are an important, independent risk factor for ASCVD.6 It has been estimated that increments in total plasma homocysteine as small as 5 μmol/l confer as much additional risk for ASCVD as increases in cholesterol of 0.5 mmol/l.7 Other than genetic background, one of the most important factors causing an increase in homocysteine is folate deficiency. This is of particular relevance to patients with rheumatic diseases, many of whom are older, and a number of whom have suboptimal dietary intake.8 Moreover, many patients are treated with agents that directly oppose the activity of folate, particularly methotrexate.9 Increased concentrations of homocysteine may thus represent a common risk factor for ASCVD among rheumatology patients, which at present is largely unrecognised. Because the presence of multiple ASCVD risk factors leads to a synergistic increase in disease,10 control of dyslipidaemia may be all the more important in the care of patients with rheumatic diseases.
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