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DGI-037 Fingolimod in Relapsing Remitting Multiple Sclerosis: A Case Report
  1. M Merchante1,
  2. A Izquierdo1,
  3. S Martinez1,
  4. AP Zorzano1,
  5. L Sanchez-Rubio1,
  6. A Serrano1,
  7. MF Hurtado1,
  8. MA Alfaro1,
  9. I Cañamares2
  1. 1Hospital San Pedro, Hospital Pharmacy, Logroño, Spain
  2. 2Hospital Laprincesa, Hospital Pharmacy, Madrid, Spain


Background Fingolimod has recently been authorised in our country (April 2011). It is the first orally administered disease-modifying drug that has been approved for highly active relapsing remitting multiple sclerosis. So far, only one patient has been treated with it in our hospital, so we have limited experience in its use.

Purpose The case report relates to relapsing remitting multiple sclerosis (RRMS) patient with high disease activity under treatment with Fingolimod. We aim to describe the evolution of this patient during the treatment period.

Materials and Methods It was an observational, six-month prospective study.

The patient, a 32-year-old female, was diagnosed with RRMS in February 2004 after an episode of sensory deficits.

Results At first, she was treated with interferon b-1a, which was stopped in February 2006 and switched to mitoxantrone IV. The patient continued to have several relapses during the treatment with this immunosuppressant; one of these relapses required plasma exchange therapy. Her Expanded Disability Status Scale (EDSS) worsened to 6 points. Assuming a lack of efficacy, the patient started treatment with natalizumab in April 2007. During four years of treatment with natalizumab she showed remarkable clinical improvement and did not experience any new relapses. Her EDSS improved to 2.5. After this time and due to the high risk of developing progressive multifocal leukoencephalopathy (PML), she switched to fingolimod (December 2011).

Ten days after initiation, she developed a severe relapse that required hospital admission, high dose IV steroids and 3 cycles of plasma exchange therapy. Doctors concluded this relapse was in fact a rebound effect due to stopping natalizumab.

In February 2012 she restarted fingolimod; one month later she developed a new relapse, treated with high dose steroids.

In April and May 2012 she had two more relapses, with severe EDSS worsening and again managed with high dose steroids.

In May 2012, it was decided to stop treatment with fingolimod, and despite the risk of PML (JC virus +), natalizumab was restarted.

Conclusions During six months of fingolimod treatment, the patient’s condition further deteriorated (four relapses in six months), her EDSS worsened and showed a high disease activity. We conclude that the treatment was not effective in this patient.

No conflict of interest.

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