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• Long-term effects of etanercept treatment on lipid profile in patients with rheumatoid arthritis
  Bruno Seriolo
  Published on: 22 October 2007

• Published on: 22 October 2007

  Long-term effects of etanercept treatment on lipid profile in patients with rheumatoid arthritis

  • Bruno Seriolo, Academic Unit of Clinical Rheumatology
  • Other Contributors:
    • Sabrina Paolino, Carmela Ferrone, Maurizio Cutolo

  Dear Editor, We have read with great interest the article by Peters et al. concerning the changes on lipid profile during infliximab and corticosteroid treatment in patients with rheumatoid arthritis (RA) (1). Recently, we performed a similar longitudinal study over time using a different TNF blocker – namely etanercept. In this prospective study 22 RA female patients were analyzed. Patients received during the study etan...

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  Dear Editor, We have read with great interest the article by Peters et al. concerning the changes on lipid profile during infliximab and corticosteroid treatment in patients with rheumatoid arthritis (RA) (1). Recently, we performed a similar longitudinal study over time using a different TNF blocker – namely etanercept. In this prospective study 22 RA female patients were analyzed. Patients received during the study etanercept ( 25 mg twice weekly), stable doses of non-steroidal anti-inflammatory drugs, prednisolone (<7.5 mg/die) and methotrexate (MTX: 10 mg/week). A control group included 20 RA patients with baseline stable therapy (prednisone: <7.5 mg/die and MTX: 10 mg/week).

  The concentrations of total cholesterol, high density lipoprotein (HDL)-cholesterol, triglyceride (TG), lipoprotein (a) [Lp(a)] were determined by ELISA before the administration of etanercept treatment and after 12, 24, 36 and 48 weeks from the starting dosage. Low density lipoprotein (LDL)-cholesterol value was calculated with the Friedewald formula. Concerning the results, the study showed that DAS-28 score decreased significantly from baseline to week 12 (5.5±1.6 vs 3.2±1.5), week 24 (2.9±1.8,), week 36 (2.3±1.1) and week 48 (2.1±0.8, p<0.01 for all), in etanercept treated patients. Similar DAS-28 score significant decrease was observed in RA controls from baseline to week 12, 24, 36 and 48 (from 5.5±2.1 to 3.9±2.1, 3.3±1.8, 2.9±1.8 and 2.6±1.1, p<0.01). Since etanercept dramatically improved the outcome of RA, the prednisone dose was gradually decreased from a baseline median dose of 7.5 to 3.4 mg/day. In etanercept treated patients, total cholesterol and HDL-cholesterol levels were found in concentrations of 4.76±0.26 mmol/ L and 0.88±0.06 mmol/L at baseline; interestingly total cholesterol and HDL-cholesterol levels were found significantly increased at 12 and 24 weeks when compared to baseline values (4.84±0.32 mmol/ L, p<0.01 and 4.91±0.36 mmol/ L, p<0.001) and (0.96±0.09 mmol/ L, p<0.05 and 1.08±0.11 mmol/ L, p<0.01). However, at 48 weeks, total cholesterol and HDL-cholesterol levels approached again baseline levels (4.81±0.32 mmol/ L and 0.94±0.05 mmol/ L, respectively). In contrast, TG, Lp(a) concentrations and atherogenic index (calculated using the following formula: total / HDL cholesterol) were not significantly changed during anti-TNFá treatment at every time.

  Interestingly, no significant changes were observed in the RA untreated etanercept group in lipid profile when compared with baseline. During the treatment with etanercept, lipid levels were compared with changes in prednisone dose at different points after adjustment for age. The effects of etanercept treatment on the changes in prednisone dose were observed as changes in total cholesterol and HDL-cholesterol levels. Recent studies have found increased levels of total cholesterol and LDL- cholesterol levels, but also increased HDL-cholesterol concentrations and no modification of triglycerides and atherogenic index after six month of anti-TNF therapy (4-6). Therefore, our observations, in agreement with those of Peters et al., show that etanercept treatment increases total cholesterol and HDL-cholesterol levels after 24 weeks; these parameters returned to baseline levels under low dose prednisone reduction (1). In conclusion, these results seem to support a possible interference of TNFá blockers (i.e. infliximab or etanercept) with some of the mechanisms implicated in the development of atherosclerosis at least in patients with RA, through anti- inflammatory and anti-atherogenic effects exerted on lipid profile.

  References

  1. Peters MJL, Vis M, van Halm VP, Wolbink GJ, Voskuyl AE, Lems WF, et al. Changes in lipid profile during infliximab and corticosteroid treatment in rheumatoid arthritis. Ann Rheum Dis 2007;66:958-961.

  2. Gonzalez-Gay MA,De Matias M, Gonzalez-Juanatey C, et al. Anti-tumor necrosis factor-alpha blockade improves insulin resistance in patients with rheumatoid arthritis. Clin Exp Rheumatol 2006;24:83-86.

  3. Kiortis DN, Mavridis AK, Vasakos S, Nikas SN, Drosos AA. Effects of infliximab treatment on insulin resistance in patients with rheumatoid arthritis and ankylosing spondylitis. Ann Rheum Dis 2005;64:765-6.

  4. Seriolo B, Paolino S, Ferrone C, Cutolo M. Effects of etanercept or infliximab treatment on lipid profile and insulin resistance in patients with refractory rheumatoid arthritis Clin Rheumatol 2007 Jul 24; [Epub ahead of print]

  5. Allanore Y, Kahan A, Sellam J, Ekindjian OG, Borderie D. Effects of repeated infliximab therapy on serum lipid profile in patients with refractory rheumatoid arthritis. Clin Chim Acta 2006;365:143-8.

  6. Seriolo B, Paolino S, Sulli A, Fasciolo D, Cutolo M. Effects of anti-TNF-á treatmenton lipid profile in patients with active rheumatoid arthritis. Ann N Y Acad Sci 2006;1069:414-9.

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  Conflict of Interest:
  None declared.

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