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Lipids and inflammation: serial measurements of the lipid profile of blood donors who later developed rheumatoid arthritis

V P van Halm^1,2, M M J Nielen², M T Nurmohamed^1,2, D van Schaardenburg^1,2, H W Reesink³, A E Voskuyl¹, J W R Twisk⁴, R J van de Stadt², M H M T de Koning², M R Habibuw³, I E van der Horst–Bruinsma¹, B A C Dijkmans^1,2

¹ Department of Rheumatology, VU University Medical Centre, Amsterdam, The Netherlands
² Department of Rheumatology, Jan van Breemen Institute, Amsterdam
³ Sanquin Bloodblank Northwest Region, Amsterdam
⁴ Department of Clinical Epidemiology and Biostatistics, VU University Medical Centre

Correspondence to:
M T Nurmohamed
Departments of Internal Medicine and Rheumatology, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands; mt.nurmohamed{at}vumc.nl

Background: Rheumatoid arthritis is characterised by inflammation and an increased cardiovascular risk. It was recently shown that active early rheumatoid arthritis is associated with dyslipidaemia, which may partially explain the enhanced cardiovascular risk. However, it is unknown when this dyslipidaemia starts.

Objective: To investigate the progression of the lipid profile over time and the influence of inflammatory parameters on this lipid profile, in people who later developed rheumatoid arthritis.

Methods: Levels of total cholesterol, high-density lipoprotein cholesterol (HDLc), triglycerides, apolipoprotein AI (apo AI), apolipoprotein B (apo B) and lipoprotein(a) (Lp(a)) were determined in 1078 stored, deep-frozen, serial blood bank samples, collected between 1984 and 1999, of 79 blood donors who later developed rheumatoid arthritis. These samples were compared with 1071 control samples of unselected blood donors, matched for age, sex and storage time.

Results: Samples of patients who later developed rheumatoid arthritis showed, on average, 4% higher total cholesterol, 9% lower HDLc, 17% higher triglyceride and 6% higher apo B levels than matched controls (p0.05).

The magnitude of the differences in lipid levels between groups, explained by C reactive protein (CRP), was limited. For example, only 3.6% of the difference in HDLc levels between the groups was explained by the CRP concentrations.

Conclusion: Patients who later develop rheumatoid arthritis have a considerably more atherogenic lipid profile than matched blood donors at least 10 years before onset of symptoms. As inflammation only marginally explains the differences between the two groups, a modulating effect of lipids on inflammatory processes is hypothesised.

Abbreviations: anti-CCP, anti-cyclic citrullinated peptides; apo AI, apolipoprotein AI; apo B, apolipoprotein B; CRP, C reactive protein; HDLc, high-density lipoprotein cholesterol; IgM-RF, immunoglobulin M rheumatoid factor; Lp(a), lipoprotein(a); sPL-A2, secretory phospholipase A2

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