Contributions
Abstract: EP1705
Type: ePoster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Background: As a disease modifying therapy fingolimod (FTY) prevents lymphocytes egress into peripheral blood which results in peripheral lymphopenia. So accurate monitoring of lab data is necessary. In this real world study we analysed laboratory data of 128 FTY treated patients up to 36 months follow up.
Methods: 128 patients diagnosed with relapsing-remitting multiple sclerosis and highly active disease course were included. Real world monitoring of lab testing was performed before and every third months up to 36 months' follow-up. Generalized linear mixed models were used to assess the significance of the results.
Results: We analyzed peripheral immune cell populations including T, B, NK cells and granulocytes. Leukocyte presented at a significantly lower level compared to baseline in each analysis (p< 0,001) and remained stable after the 1st application. After FTY start, leukocytes decreased by approximately 40% during the entire observation period and decreased below 3.8 GPt/L in one-third of the treated patients. Within first month of therapy, lymphocytes declined by about 70%. Within treated patients, 98% presented lymphocyte count < 1,5 GPt/L, 93.7% < 1,0 GPt/L, 55.8% < 0.5 GPt/L and 2.1% < 0,2 GPt/L. During period of observation, levels of leukocyte respective lymphocyte counts fluctuated about 0.8 respectively 0.14 in FTY treated patients. Compared with the intra-individual variability of patients treated with natalizumab (fluctuation leukocytes 1.5 and lymphocytes 0.6), FTY treated patients demonstrated a narrow deviation range and more stable values. No significant changes were detectable in triglycerides, cholesterol, high and low-density lipoprotein. After first application aspartate-aminotransferase (ASAT) levels increased in 25%, alanine-aminotransferase (ALAT) in 22% and γ-glutamyl transferase (γGT) in 26% of patients higher than upper limit.
Conclusions: Although it is widely known that FTY induces lymphopenia, we have shown that as well in the real world the lymphocyte counts decreased in only a small number of patients under a critical limit of 0,2 GPt/L in a real-world cohort. Additionally we present stable levels in lymphocyte count and only small intra- and inter-individual fluctuations in treated patients during long-term follow up evaluation.
Disclosure:
K. Thomas received personal compensation for from Novartis, Biogen Idec and Roche for consulting service. Ziemssen received personal compensation from Biogen Idec, Bayer, Novartis, Sanofi, Teva, and Synthon for consulting services. Ziemssen received additional financial support for research activities from Bayer, Biogen Idec, Novartis, Teva, and Sanofi Aventis.
M. Kaufmann und R. Haas have nothing to disclose.
Abstract: EP1705
Type: ePoster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Background: As a disease modifying therapy fingolimod (FTY) prevents lymphocytes egress into peripheral blood which results in peripheral lymphopenia. So accurate monitoring of lab data is necessary. In this real world study we analysed laboratory data of 128 FTY treated patients up to 36 months follow up.
Methods: 128 patients diagnosed with relapsing-remitting multiple sclerosis and highly active disease course were included. Real world monitoring of lab testing was performed before and every third months up to 36 months' follow-up. Generalized linear mixed models were used to assess the significance of the results.
Results: We analyzed peripheral immune cell populations including T, B, NK cells and granulocytes. Leukocyte presented at a significantly lower level compared to baseline in each analysis (p< 0,001) and remained stable after the 1st application. After FTY start, leukocytes decreased by approximately 40% during the entire observation period and decreased below 3.8 GPt/L in one-third of the treated patients. Within first month of therapy, lymphocytes declined by about 70%. Within treated patients, 98% presented lymphocyte count < 1,5 GPt/L, 93.7% < 1,0 GPt/L, 55.8% < 0.5 GPt/L and 2.1% < 0,2 GPt/L. During period of observation, levels of leukocyte respective lymphocyte counts fluctuated about 0.8 respectively 0.14 in FTY treated patients. Compared with the intra-individual variability of patients treated with natalizumab (fluctuation leukocytes 1.5 and lymphocytes 0.6), FTY treated patients demonstrated a narrow deviation range and more stable values. No significant changes were detectable in triglycerides, cholesterol, high and low-density lipoprotein. After first application aspartate-aminotransferase (ASAT) levels increased in 25%, alanine-aminotransferase (ALAT) in 22% and γ-glutamyl transferase (γGT) in 26% of patients higher than upper limit.
Conclusions: Although it is widely known that FTY induces lymphopenia, we have shown that as well in the real world the lymphocyte counts decreased in only a small number of patients under a critical limit of 0,2 GPt/L in a real-world cohort. Additionally we present stable levels in lymphocyte count and only small intra- and inter-individual fluctuations in treated patients during long-term follow up evaluation.
Disclosure:
K. Thomas received personal compensation for from Novartis, Biogen Idec and Roche for consulting service. Ziemssen received personal compensation from Biogen Idec, Bayer, Novartis, Sanofi, Teva, and Synthon for consulting services. Ziemssen received additional financial support for research activities from Bayer, Biogen Idec, Novartis, Teva, and Sanofi Aventis.
M. Kaufmann und R. Haas have nothing to disclose.