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• Response to Hjardem Elisabeth, et al article Ann Rheum Dis 2007; 66: 1184-1189
  Paul Emery
  Published on: 13 April 2016

• Published on: 13 April 2016

  Response to Hjardem Elisabeth, et al article Ann Rheum Dis 2007; 66: 1184-1189

  • Paul Emery, Professor
  • Other Contributors:
    • Maya H. Buch, Sarah J. Bingham and Paul Emery

  To the editor,

  We read with interest the article by Hjardem E et al which reported the experiences of switching between TNF-antagonists from the Danish patient registry, DANIBO. We would like to draw the authors’ attention to data published from our group 2 years ago which both highlights some aspects relevant to the current report and which provides some insights into the mechanisms involved. Non-response is seen...

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  To the editor,

  We read with interest the article by Hjardem E et al which reported the experiences of switching between TNF-antagonists from the Danish patient registry, DANIBO. We would like to draw the authors’ attention to data published from our group 2 years ago which both highlights some aspects relevant to the current report and which provides some insights into the mechanisms involved. Non-response is seen either as a primary phenomenon i.e. no response at the first point of assessment (usually 12 weeks using standard response criteria) or secondary non-response - loss of an initial demonstrable response. We described primary non-response in detail in a cohort of over 200 patients on infliximab (Buch MH, et al, A&R 05). Furthermore, distinctsub-groups of primary non-response were identified based on the presence or lack of CRP suppression, with the latter group demonstrating significantly high response rates upon switching to etanercept (68% ACR20, 51% ACR50). These observations have been confirmed in a larger cohort (Buch MH et al, Arth Rheum 07). The basis for such contrasting responses has been discussed and explored previously with a representative case suggesting a role for lymphotoxin-alpha, targeted by etanercept but not infliximab (Buch MH et al, ARD 04). We have also recently illustrated that secondary non-response occurs to a significant extent in a cohort of initial infliximab responders (Buch MH et al, Rheum 07). We suggested the kinetics of secondary non-response implies a pharmacokinetic basis for failure and showed that such patients demonstrate a higher response rate to adalimumab (Buch MH et al Arth Rheum abstract 05); probably by overcoming potential HACA issues. Thus the observations by Hjardem E et al have been well-described previously in a more homogeneous cohort and with the benefit of more stringent classification. Furthermore, tailored therapeutic intervention has revealed possible underlying basis for such non-response.

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  Conflict of Interest:
  None declared.

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