Contributions
Abstract: EP1625
Type: ePoster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Background and aims: Fingolimod induces a fast reduction of lymphocyte counts in the blood, however, less is known about the recovery of immune cells after treatment discontinuation in real life clinical practice, especially in patients who begin with a new immunomodulatory treatment shortly after cessation of fingolimod. Therefore, we aimed to analyze the course of lymphocyte recovery and its potential influencing factors in the first year after fingolimod discontinuation in patients with multiple sclerosis.
Methods: We examined leukocyte, lymphocyte and neutrophil counts of 58 patients with multiple sclerosis, 3 (mean 79.1 ± 31.6 days), 6 (mean 193.3 ± 35.7 days) and 12 (mean 368.6 ± 48 days) months after cessation of fingolimod. Blood tests were available in 55 patients for the baseline (prior fingolimod), in 47 patients for the 3 months, in 46 for the 6 months and in 48 for the 12 months timepoint. Leukopenia was defined as ≤3500, lymphopenia as ≤900, neutropenia as ≤1300 cells per microliter. We included age, sex, EDSS and disease duration at fingolimod start, fingolimod treatment duration, transition time before therapy switch, lymphocyte baseline prior fingolimod and at start with a following medication, and previous immunomodulatory regimens into our analysis.
Results: All patients showed a drop of lymphocyte count under fingolimod with no relevant leukopenia or neutropenia. Three months after fingolimod discontinuation 11 patients showed decreased lymphocyte levels (23.4%), while six and twelve months later still 10 patients were lymphopenic (21.7%). 8 out of these 10 patients received rituximab as a follow-up treatment. 47% (8 out of 17) patients that switched to rituximab and 3 out of 4 patients pretreated with mitoxantrone showed delayed lymphocyte recovery. Patients with prolonged lymphopenia had a longer treatment duration of fingolimod and tended to have lower lymphocyte counts at baseline and at therapy switch.
Conclusion: Only 42% of patients reached their baseline lymphocyte levels, while 21.7% stayed lymphopenic after one year of cessation of fingolimod. Longer treatment duration of fingolimod, low lymphocyte counts at baseline and at therapy switch, successive treatment with rituximab, and pretreatment with mitoxantrone might contribute to a prolonged immune cell recovery and should be considered when changing treatment regimens.
Disclosure: The institution (University Hospital Basel) received in the last 3 years and used exclusively for research support: steering committee, consulting and speaker fees from Actelion, Addex, Bayer HealthCare, Biogen, Biotica, Genzyme, Lilly, Merck, Mitsubishi, Novartis, Ono, Pfizer, Receptos, Sanofi-Aventis, Santhera, Siemens, Teva, UCB and Xenoport; support of educational activities from Bayer HealthCare, Biogen, CSL Behring, Genzyme, Merck, Novartis, Sanofi-Aventis and Teva; royalties from Neurostatus Systems GmbH; grants from Bayer HealthCare, Biogen, the European Union, Merck, Novartis, Roche, the Swiss Multiple Sclerosis Society and the Swiss National Research Foundation.
Abstract: EP1625
Type: ePoster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Background and aims: Fingolimod induces a fast reduction of lymphocyte counts in the blood, however, less is known about the recovery of immune cells after treatment discontinuation in real life clinical practice, especially in patients who begin with a new immunomodulatory treatment shortly after cessation of fingolimod. Therefore, we aimed to analyze the course of lymphocyte recovery and its potential influencing factors in the first year after fingolimod discontinuation in patients with multiple sclerosis.
Methods: We examined leukocyte, lymphocyte and neutrophil counts of 58 patients with multiple sclerosis, 3 (mean 79.1 ± 31.6 days), 6 (mean 193.3 ± 35.7 days) and 12 (mean 368.6 ± 48 days) months after cessation of fingolimod. Blood tests were available in 55 patients for the baseline (prior fingolimod), in 47 patients for the 3 months, in 46 for the 6 months and in 48 for the 12 months timepoint. Leukopenia was defined as ≤3500, lymphopenia as ≤900, neutropenia as ≤1300 cells per microliter. We included age, sex, EDSS and disease duration at fingolimod start, fingolimod treatment duration, transition time before therapy switch, lymphocyte baseline prior fingolimod and at start with a following medication, and previous immunomodulatory regimens into our analysis.
Results: All patients showed a drop of lymphocyte count under fingolimod with no relevant leukopenia or neutropenia. Three months after fingolimod discontinuation 11 patients showed decreased lymphocyte levels (23.4%), while six and twelve months later still 10 patients were lymphopenic (21.7%). 8 out of these 10 patients received rituximab as a follow-up treatment. 47% (8 out of 17) patients that switched to rituximab and 3 out of 4 patients pretreated with mitoxantrone showed delayed lymphocyte recovery. Patients with prolonged lymphopenia had a longer treatment duration of fingolimod and tended to have lower lymphocyte counts at baseline and at therapy switch.
Conclusion: Only 42% of patients reached their baseline lymphocyte levels, while 21.7% stayed lymphopenic after one year of cessation of fingolimod. Longer treatment duration of fingolimod, low lymphocyte counts at baseline and at therapy switch, successive treatment with rituximab, and pretreatment with mitoxantrone might contribute to a prolonged immune cell recovery and should be considered when changing treatment regimens.
Disclosure: The institution (University Hospital Basel) received in the last 3 years and used exclusively for research support: steering committee, consulting and speaker fees from Actelion, Addex, Bayer HealthCare, Biogen, Biotica, Genzyme, Lilly, Merck, Mitsubishi, Novartis, Ono, Pfizer, Receptos, Sanofi-Aventis, Santhera, Siemens, Teva, UCB and Xenoport; support of educational activities from Bayer HealthCare, Biogen, CSL Behring, Genzyme, Merck, Novartis, Sanofi-Aventis and Teva; royalties from Neurostatus Systems GmbH; grants from Bayer HealthCare, Biogen, the European Union, Merck, Novartis, Roche, the Swiss Multiple Sclerosis Society and the Swiss National Research Foundation.