Contributions
Abstract: EP1729
Type: Poster Sessions
Abstract Category: Therapy - Others
Introduction: To present a case of idiopathic thrombocytopenic purpura (ITP) following treatment with Fingolimod.
Case History: A 26-years old woman diagnosed with relapsing-remitting multiple sclerosis(RRMS) in 2010, was initially treated with IFN beta-1a (Avonex) for 2 years and then Betaferon for 3 years respectively. Due to a new attack on Betaferon, the treatment switched to Fingolimod. She was then free of clinical and MRI activity for 2.5 years. At this time, we noticed a sudden drop in patient´s platelet count to 23000, whereas she had no symptoms of spontaneous bleeding, ecchymosis, petechia or purpura. Fingolimod was stopped and she was admitted to the hospital. The results of next day platelet count were 16000 and 9000 respectively and other blood tests, ultrasound investigations and bone marrow biopsy revealed normal findings. Consequently, with the diagnosis of ITP, IV immunoglobulin and dexamethasone started for her on the basis of hematologist advice. Daily blood tests revealed an increase in platelet count to 44000 in the second day of therapy. After 6 days admission in the hospital, she was discharged home with a platelet count of 116000, with prescription of Prednisolone, 50 mg once daily .The patient remained without treatment until 2 months, that she had a severe relapse, so she underwent pulse therapy for one day. Owing to ITP induced by Fingolimod and re-occurrence of relapses, it was decided to start Rituximab and she received the first dose during hospitalization. She has had a stable course of disease with no relapses and no changes in blood test results after 4 months of Rituximab initiation.
Conclusions: Co-existence or induction of other immune mediated disorders in MS patients has been reported previously. To the best of our knowledge, this is the first reported case of ITP in a Fingolimod-treated individual. This case highlights the potential risk associated with long-term immunosuppression which could lead to induction of a new autoimmune disorder. Further studies are required to determine if this is a co-incidence, an induction, or a random finding.
Disclosure: Negar Molazadeh: nothing to disclose
Samira Navardi: nothing to disclose
Mohammad Ali Sahraian: nothing to disclose
Abstract: EP1729
Type: Poster Sessions
Abstract Category: Therapy - Others
Introduction: To present a case of idiopathic thrombocytopenic purpura (ITP) following treatment with Fingolimod.
Case History: A 26-years old woman diagnosed with relapsing-remitting multiple sclerosis(RRMS) in 2010, was initially treated with IFN beta-1a (Avonex) for 2 years and then Betaferon for 3 years respectively. Due to a new attack on Betaferon, the treatment switched to Fingolimod. She was then free of clinical and MRI activity for 2.5 years. At this time, we noticed a sudden drop in patient´s platelet count to 23000, whereas she had no symptoms of spontaneous bleeding, ecchymosis, petechia or purpura. Fingolimod was stopped and she was admitted to the hospital. The results of next day platelet count were 16000 and 9000 respectively and other blood tests, ultrasound investigations and bone marrow biopsy revealed normal findings. Consequently, with the diagnosis of ITP, IV immunoglobulin and dexamethasone started for her on the basis of hematologist advice. Daily blood tests revealed an increase in platelet count to 44000 in the second day of therapy. After 6 days admission in the hospital, she was discharged home with a platelet count of 116000, with prescription of Prednisolone, 50 mg once daily .The patient remained without treatment until 2 months, that she had a severe relapse, so she underwent pulse therapy for one day. Owing to ITP induced by Fingolimod and re-occurrence of relapses, it was decided to start Rituximab and she received the first dose during hospitalization. She has had a stable course of disease with no relapses and no changes in blood test results after 4 months of Rituximab initiation.
Conclusions: Co-existence or induction of other immune mediated disorders in MS patients has been reported previously. To the best of our knowledge, this is the first reported case of ITP in a Fingolimod-treated individual. This case highlights the potential risk associated with long-term immunosuppression which could lead to induction of a new autoimmune disorder. Further studies are required to determine if this is a co-incidence, an induction, or a random finding.
Disclosure: Negar Molazadeh: nothing to disclose
Samira Navardi: nothing to disclose
Mohammad Ali Sahraian: nothing to disclose