Effects of tumour necrosis factor alpha blockade on lipid profile in active rheumatoid arthritis

Abstract

SIR, We would like to thank Dr Armstrong for his helpful comment regarding lipid profile behaviour during anti-tumour necrosis factor (TNF)- treatment. Such a topic is of increasing interest in the literature, despite lack of long-term definitive supporting evidence [1–4]. Actually, in patients with rheumatoid arthritis (RA) under anti-TNF- treatment, early and transient high-density lipoprotein (HDL) level increase [1, 2], but even late atherogenic index (total/HDL cholesterol ratio) worsening has been reported [3]. In our study, significant reduction of common carotid artery intima-media thickness (cIMT) values has been observed in patients with active RA steadily responsive to anti-TNF- agents [5]. Despite the fact that data regarding lipid profile have not been shown, total-, HDL-, low-density lipoprotein (LDL)- cholesterol and triglyceride levels were actually measured before, 3, 6 and 12 months after therapy. we did not observe any significant change of lipoprotein pattern both in patients treated with disease modifying anti-rheumatic drugs (DMARDs) plus TNF- blockers (group A) and in those treated with only DMARDs (group B) at any time (Table 1). Moreover, no significant differences have been observed in the above-reported parameters between the two groups at any time (Table 1), nor any significant correlation between lipid profile and cIMT (Spearman’s correlation test). In agreement with the literature data [3], we suggest that lipid level modification should not be included among the main effects by which anti-TNFagents may influence atherosclerotic risk profile in active RA. In our study, only five patients (three in Group A and two in Group B) were also treated with statins (sinvastatin 20 mg/daily); all of them had started such therapy at least one year before the enrolment. Despite the fact that statin anti-inflammatory effects have been largely demonstrated in atherosclerosis (ATS) [6] and suggested also in RA patients treated with only DMARDs [7], we did not find any significant difference, at any time, in inflammatory marker levels or lipid plasma concentrations between statintreated and not-treated patients. Our results suggest that in high-grade systemic inflammatory diseases, such as active RA responsive to anti-TNF- agents, statin anti-inflammatory effect may hardly be considered playing a crucial role. In conclusion, although the Armstrong’s remark appears very intriguing, plasma lipid profile do not seem to be significantly influenced by anti-TNF- agents; the described statin anti-inflammatory effect also seems to be unapparent in this particular context, as overcome by the potent anti-inflammatory effect of TNF- inhibitory treatment. All the patients gave their written informed consent before being included in the study, which was performed according to the principles reported in the Declaration of Helsinki. This study has been ethically approved by the Faculty of Medicine Committee.