Rheumatology International

, Volume 33, Issue 6, pp 1415–1418 | Cite as

Monoclonal anti-TNF antibodies can elevate hemoglobin level in patients with ankylosing spondylitis

Original Article


Anemia is one of the extra-articular findings of ankylosing spondylitis (AS), and anti-TNF therapy has been shown benefit in patients with anemia associated AS. In this study, we aimed to evaluate and compare the effects of biological and non-biological agents on hemoglobin levels in AS patients. One hundred consecutive patients who fulfilled ASAS criteria for AS were included in the study. Fifty-four of the patients treated with anti-TNF agents (20 patients treated with infliximab, 20 patients with adalimumab, and 14 patients with etanercept), and 46 patients treated with non-steroidal anti-inflammatory drugs and/or other disease modifying anti-rheumatic drugs. The C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), hemoglobin (HGB), hematocrit (HCT) counts, and BASDAI scores were compared before starting therapy and at 52 weeks. There was no statistically significant difference between patients about demographical data (age, sex) and disease age (p > 0.05 for all). Significant difference was determined between HGB, HCT, CRP, ESR, and BASDAI values before and after therapy (for infliximab p: 0.001; 0.000; 0.000; 0.000; 0.000, respectively, and for adalimumab p: 0.017; 0.03; 0.001; 0.002; 0.000, respectively). In etanercept group, there was no significant difference in HGB values, when compared with before starting therapy and at 52 weeks (p > 0.05). In the group of treated with non-biological agents, ESR values and BASDAİ scores showed distinctive improvement after 52 weeks of therapy, but was not a significant difference in hemoglobin and hematocrit values. Conclusion: Anti-TNF-alpha therapy with monoclonal antibodies (adalimumab and infliximab) did not only suppress disease activity but also provided a significant improvement in HGB levels. In the groups of treated with a TNF-alpha receptor antagonist (ETA) and non-biological agents, disease activity was suppressed, but there was not founded significant improvement in HGB levels after 52 weeks. Different outcomes of anti-TNF agents may be associated with their different effect mechanisms.


Ankylosing spondylitis Anti-tumor necrosis factor-alpha Hemoglobin 


  1. 1.
    Haywood KL, Garratt AM, Dawes PT (2005) Patient-assessed health in ankylosing spondylitis: a structured review. Rheumatology (Oxford) 44(5):577–586CrossRefGoogle Scholar
  2. 2.
    Maksymowcyh WP (2003) Spondyloarthropathies: ankylosing spondylitis. In: Hochberg H, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH (eds) Rheumatology, vol 3. Elsevier Lmt, Phildelphia, pp 1183–1192Google Scholar
  3. 3.
    Rosenbaum JT (1989) Characterization of uveitis associated with spondyloarthritis. J Rheumatol 16(6):792–796PubMedGoogle Scholar
  4. 4.
    Crowley JJ, Donnelly SM, Tobin M, FitzGerald O, Bresnihan B, Maurer BJ, Quigley PJ (1993) Doppler echocardiographic evidence of left ventricular diastolic dysfunction in ankylosing spondylitis. Am J Cardiol 71(15):1337–1340CrossRefPubMedGoogle Scholar
  5. 5.
    Reveille J (2008) Clinical features of ankylosing spondylitis. In: Hochberg M, Silman A, Smolen JS (eds) Rheumatology, vol 4. St. Louis, Mosby, pp 1109–1114Google Scholar
  6. 6.
    Levine DS, Forbat SM, Saifuddin A (2004) MRI of the axial skeletal manifestations of ankylosing spondylitis. Clin Radiol 59(5):400–413CrossRefPubMedGoogle Scholar
  7. 7.
    Braun J, van der Heijde D, Doyle MK, Han C, Deodhar A, Inman R et al (2009) Improvement in hemoglobin levels in patients with ankylosing spondylitis treated with infliximab. Arthritis Rheum 61(8):1032–1036CrossRefPubMedGoogle Scholar
  8. 8.
    Paulus HE (1988) FDA arthritis advisory committee: serious gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs, etc. Arthritis Rheum 31:1450–1451CrossRefGoogle Scholar
  9. 9.
    Roy CN, Andrews NC (2005) Anemia of inflammation: the hepcidin link. Curr Opin Hematol 12:107–111CrossRefPubMedGoogle Scholar
  10. 10.
    Braun J, Baraliakos X (2009) Treatment of ankylosing spondylitis and other spondyloarthritidies. Current Opinion Rheumatol 21(4):324–334CrossRefGoogle Scholar
  11. 11.
    van den Berg R, van der Heijde DM. How should we diagnose spondyloarthritis according to the ASAS classification criteria: a guide for practicing physiciansGoogle Scholar
  12. 12.
    Guignard S, Gossec L, Salliot C, Ruyssen A, Luc M, Duclos M et al (2006) Efficacy of tumour necrosis factor blockers in reducing uveitis flares in patients with spondylarthropathy: a retrospective study. Ann Rheum Dis 65(12):1631–1634CrossRefPubMedPubMedCentralGoogle Scholar
  13. 13.
    Sandborn WJ, Hanauer SB, Katz S, Safdi M, Wolf DG, Baerg RD et al (2001) Etanercept for active Crohn’s disease: a randomized, double-blind, placebo-controlled trial. Gastroenterology 121(5):1088–1094CrossRefPubMedGoogle Scholar
  14. 14.
    Grigorakaki C, Morceau F, Chateauvieux S, Dicato M (2011) Tumor necrosis factor alpha- mediated inhibition of erythropoiesis involves GATA-1/GATA-2 balance impairment and PU.1 over-expression. Chem Pharmacol 82(2):156–166CrossRefGoogle Scholar
  15. 15.
    Silva LC, Ortigosa LC, Benard G (2010) Anti-TNF-α agents in the treatment of immune- mediated inflammatory diseases: mechanisms of action and pitfalls. Immunotherapy 2(6):817–833CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  1. 1.Department of RheumatologyBakirköy Dr. Sadi Konuk Education and Research HospitalIstanbulTurkey
  2. 2.Department of RheumatologySakarya Education and Research HospitalSakaryaTurkey
  3. 3.Department of RheumatologyHisar Intercontinental HospitalIstanbulTurkey

Personalised recommendations