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Rheumatology Advance Access originally published online on September 1, 2007
Rheumatology 2007 46(10):1626-1627; doi:10.1093/rheumatology/kem195
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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

F. Del Porto, B. Laganà, I. Nofroni1, F. Tinti2, A. P. Mitterhofer2,* and R. D’Amelio*

"Sapienza" Università di Roma, II Facoltà di Medicina e Chirurgia, Azienda Ospedaliera S.Andrea, Dipartimento di Scienze Mediche; I Facoltà di Medicina e Chirurgia, 1Dipartimento di Medicina Sperimentale and 2Dipartimento di Medicina Clinica.

Correspondence to: Flavia Del Porto, MD, Università ‘La Sapienza’, II Facoltà di Medicina e Chirurgia, Azienda Ospedaliera Sant’Andrea, Dipartimento di Scienze Mediche, Via di Grottarossa 1039, 00189 Roma, Italia. E-mail: flavia.delporto{at}uniroma1.it

SIR, We would like to thank Dr Armstrong for his helpful comment regarding lipid profile behaviour during anti-tumour necrosis factor (TNF)-{alpha} 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-{alpha} 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-{alpha} 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-{alpha} 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-TNF-{alpha} agents may influence atherosclerotic risk profile in active RA.


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TABLE 1. Prospective analysis of mean values recorded at months 12 vs 0 within A and B groupsa and statistical analysis between A and B group delta values at 0 and 12 monthsb

 
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 statin-treated and not-treated patients. Our results suggest that in high-grade systemic inflammatory diseases, such as active RA responsive to anti-TNF-{alpha} 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-{alpha} 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-{alpha} 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.

The authors have declared no conflicts of interest.


    Notes
 
*The authors wish it to be known that, in their opinion, the last two authors contributed equally to this work. Back


    References
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 References
 

  1. Popa C, Netea MG, Radstake T, et al. Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis. Ann Rheum Dis (2005) 64:303–5.[Abstract/Free Full Text]
  2. Spanakis E, Sidiropoulos P, Papadakis J, et al. Modest but sustained increase of serum high density lipoprotein cholesterol levels in patients with inflammatory arthritides treated with infliximab. J Rheumatol (2006) 33:2440–6.[Abstract/Free Full Text]
  3. Popa C, van den Hoogen FH, Radstake TR, et al. Modulation of lipoprotein pattern plasma concentration during long term anti-TNF therapy in patients with active rheumatoid arthritis. Ann Rheum Dis (2007) May 1. [E-pub ahead of print] doi:10.1136/ard.2006.066191.
  4. Sattar N, Crompton P, Cherry L, et al. Effect of Tumor necrosis factor blockade on cardiovascular risk factors in psoriatic arthritis. A double-blind, placebo-controlled study. Arthritis Rheum (2007) 56:831–9.[CrossRef][Web of Science][Medline]
  5. Del Porto F, Laganà B, Lai S, et al. Response to anti-tumour necrosis factor alpha blockade is associated with reduction of carotid intima-media thickness in patients with active rheumatoid arthritis. Rheumatology (Oxford) (2007) 46:111–15.
  6. Palinski W, Napoli C. Unrevealing pleiotropic effects of statins on plaque rupture. Arterioscler Thromb Vasc Biol (2002) 22:1745–50.[Free Full Text]
  7. McCarey DW, McInnes IB, Madhok R. Trial of Atorvastatin in Rheumatoid Arthritis (TARA): double-blind, randomised placebo-controlled trial. Lancet (2004) 363:2015–21.[CrossRef][Web of Science][Medline]
Accepted 26 June 2007


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This Article
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