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High iron stores and cardiovascular disease in systemic lupus erythematosus – reply

Dear Sir, Risk factors and underlying mechanisms that account for the high risk of cardiovascular disease (CVD) in systemic lupus erythematosus (SLE) are only partly known and the suggestion that iron overload may contribute is of interest. Indeed, the role of anaemia has been discussed for a long time in a historical perspective. In our nested case–control study where SLE patients with CVD were compared with ageand sex-matched SLE patients without CVD and population controls, both traditional risk factors including dyslipidaemia and non-traditional ones including lipid peroxidation, antiphospholipid antibodies and inflammatory factors like tumour necrosis factor (TNF) contributed [1–5]. Three mechanisms were proposed. First, increased activity in the TNF system promotes dyslipidaemia [2]. Secondly, aPL contributes to CVD by decreasing binding of Annexin V to activated and/or damaged endothelium, causing a procoagulant state and increased risk of plaque rupture, which may be inhibited by Annexin V [4]. A third possibility is that raised lipid peroxidation could promote inflammation and atherogenesis [5]. The role of ferritin in SLE is likely to be complex, and may reflect also disease activity and manifestations as serositis [6], but the possibility that ferritin in an inflammatory disease like SLE could also be related to underlying disturbances in iron metabolism cannot be excluded. Epidemiological studies have suggested that iron overload may be atherogenic, at least in early atherosclerosis development [7]. However, in patients referred for coronary angiography, higher ferritin concentrations and transferrin saturation levels were not associated with increased atherosclerosis [8]. Another possibility is that iron overload may play different roles depending on disease stage. The role of iron and iron overload was investigated in a rabbit model of atherosclerosis, and the results do not support the hypothesis proposed. Instead, iron deficiency was atherogenic, while iron overload decreased lesion formation [9]. The role of iron overload in SLE and SLE-related CVD (and in general) and its relation to lipid oxidation and inflammatory factors deserves further study, even though too little is known, in my opinion, to draw conclusions now.