Contributions
Abstract: P1915
Type: Poster
Abstract Category: Late breaking news
Introduction: Fingolimod is a sphingosine 1-phosphate receptor modulator which sequesters lymphocytes in lymph nodes and prevents them from entering the central nervous system. There have been increasing reports of severe rebounds with tumefactive demyelinating lesions (TDLs) in patients with Multiple Sclerosis (MS) under fingolimod treatment, as well as following therapy discontinuation.
Objective: To review de clinico-radiological characteristics of patients with TDLs associated with fingolimod.
Materials and methods: Retrospective review of medical records of MS patients from our center.
Results: We found 5 cases: 4 developed TDLs as rebounds after treatment cessation and 1 under treatment. The 4 rebound cases were women, with a mean age of 34.7 years (SD=3.59), a disease duration of 10.2 years (SD=3.92) and a mean EDSS of 3.62 (SD=2.01). The mean duration of fingolimod treatment before discontinuation was 35.61months (SD=23.08) and the mean time lapse between treatment withdrawal and rebound was 10.71 weeks (SD=8.97). The total pre-rebound lymphocyte count (cells/mm3) was 505 (SD=298.94) and 1017.5 (SD=364.81) during rebound. The TDL patient under fingolimod was a 36-year-old man who had been on fingolimod for 31.4 months, after switching from glatiramer acetate.
Tumefactive lesions were multiple in 2 cases and solitary in 3. Acute treatment for rebound included high dose steroids (5/5), plasma exchange (3/5) and rituximab (2/5). Disease modifying treatment elections after fingolimod included rituximab (2/5), alemtuzumab (2/5) and glatiramer acetate (1/5).
Conclusions: Our study, along with similar reports in literature, highlights the need for close monitoring in patients who plan to switch from fingolimod to other treatments because of the risk of severe rebound. The etiopathogenic association between fingolimod and TDLs is not clear, but given the increasing reports of cases it should be taken into account for treatment selection in patients with this type of lesions.
Disclosure:
Pedro Sánchez: nothing to disclose
Virginia Meca-Lallana: nothing to disclose
Clara Aguirre: nothing to disclose
Julio Dotor: nothing to disclose
Jose Vivancos: nothing to disclose
Abstract: P1915
Type: Poster
Abstract Category: Late breaking news
Introduction: Fingolimod is a sphingosine 1-phosphate receptor modulator which sequesters lymphocytes in lymph nodes and prevents them from entering the central nervous system. There have been increasing reports of severe rebounds with tumefactive demyelinating lesions (TDLs) in patients with Multiple Sclerosis (MS) under fingolimod treatment, as well as following therapy discontinuation.
Objective: To review de clinico-radiological characteristics of patients with TDLs associated with fingolimod.
Materials and methods: Retrospective review of medical records of MS patients from our center.
Results: We found 5 cases: 4 developed TDLs as rebounds after treatment cessation and 1 under treatment. The 4 rebound cases were women, with a mean age of 34.7 years (SD=3.59), a disease duration of 10.2 years (SD=3.92) and a mean EDSS of 3.62 (SD=2.01). The mean duration of fingolimod treatment before discontinuation was 35.61months (SD=23.08) and the mean time lapse between treatment withdrawal and rebound was 10.71 weeks (SD=8.97). The total pre-rebound lymphocyte count (cells/mm3) was 505 (SD=298.94) and 1017.5 (SD=364.81) during rebound. The TDL patient under fingolimod was a 36-year-old man who had been on fingolimod for 31.4 months, after switching from glatiramer acetate.
Tumefactive lesions were multiple in 2 cases and solitary in 3. Acute treatment for rebound included high dose steroids (5/5), plasma exchange (3/5) and rituximab (2/5). Disease modifying treatment elections after fingolimod included rituximab (2/5), alemtuzumab (2/5) and glatiramer acetate (1/5).
Conclusions: Our study, along with similar reports in literature, highlights the need for close monitoring in patients who plan to switch from fingolimod to other treatments because of the risk of severe rebound. The etiopathogenic association between fingolimod and TDLs is not clear, but given the increasing reports of cases it should be taken into account for treatment selection in patients with this type of lesions.
Disclosure:
Pedro Sánchez: nothing to disclose
Virginia Meca-Lallana: nothing to disclose
Clara Aguirre: nothing to disclose
Julio Dotor: nothing to disclose
Jose Vivancos: nothing to disclose