Author Of 2 Presentations
P0405 - The consequences of switching from Gilenya to generics for Fingolimod (ID 1129)
Abstract
Background
On May 2017, two generic drugs for fingolimod were introduced into the market in Israel, and many MS patients treated with Gilenya (Novartis) were switched to Fingolimod (Teva), or to Finolim (Rafa).
Objectives
To analyze the consequences of switching from original Gilenya to generic fingolimod preparations in a single MS center.
Methods
Inclusion criteria included relapsing MS patients who were treated with Gilenya (G) for at least one year before May 2017, switched to and remained on generic fingolimod (F) for at least one year thereafter. Retrospective data within one year before and after the switch were compared.
Results
Twenty seven patients fulfilled the inclusion criteria (F=20, RRMS=20, SPMS=7, average age 49±11.4, average disease duration=16.6±7.6 years). Ten patients had to be switched back to the original Gilenya by the request of their neurologist due to intolerable new or worsening adverse events (n=9), clinical relapse (n=1), or elevation of liver enzymes > X3 ULN (n=1). Liver enzyme abnormalities were detected in 2/27 patients during G treatment and in 4/27 during F treatment (p=NS). There was a trend towards reduced lymphocyte count after G-F switch (644±221 vs. 593±182, p=0.149). Median EDSS increased from 2.75 (1.0-6.0) to 3.0 (1.5-6.5) (p=NS). Age, disease duration and disease type (RRMS or SPMS) did not predict the need for switching back to G.
Conclusions
The tolerability of generics for fingolimod seems to be lower than the original Gilenya. Despite the small number of patients, short follow-up period and the minor or no differences between F and G treated patients detected in most parameters which do not allow for drawing definite conclusions regarding the comparative efficacy and safety of G and F, these results raise concerns about the use of generics, even for simple chemical drugs such as fingolimod, in a complex and heterogenous disease such as MS that spans over many domains. This may suggest that pharmacodynamic and clinical evaluations, not merely the demonstration of bioequivalence, are needed before approving generic drugs for MS.
P0554 - Cervical disc disease is not associated with demyelanting lesions in multiple sclerosis (ID 1009)
Abstract
Background
Multiple sclerosis (MS) is characterizes by demyelinating lesions in the brain and spinal cord. Some studies suggest that disc herniation may contribute to the development of cord lesions in MS
Objectives
To investigate whether cervical spinal disc disease is associated with demyelinating lesions in the spinal cord in patients with MS.
Methods
Cervical MRI scans of 47 MS patients were reviewed for the presence of demyelinating lesion and cervical disc disease. Compressive-myelopathic lesions were excluded. The severity of the disc disease was further classified as grade I (no pressure), grade II (pressure on the dural sac) and grade III (pressure on the spinal cord). The spinal cord in each scan was divided into 6 segments corresponding to the intervertebral space of the cervical cord (C1-7). Each segment was defined as containing a demyelinating lesion and disc pathology (group 1), demyelinating lesion without disc pathology (group 2), disc pathology without demyelinating lesion (group 3) and no demyelinating lesion or disc pathology (group 4). Fisher exact test was used to test the association between demyelinating lesions and disc herniation.
Results
Two hundred and eighty two cervical spinal segments of 47 MS patients (M-16, average age 47.8±12.5, average disease duration 8.2±5.6 years) were evaluated. Twenty four segments fulfilled the criteria for group1, 55 segments for group 2, 52 segments for group 3 and 151 segments for group 4. There was no association between demyelinating lesions and the grade of disc disease (p=0.45 for grade I, p=0.85 for grade II, p=0.33 for grade III disc disease).
Conclusions
Our study did not find any association between cervical disc disease and demyelinating spinal cord lesion. These results do not suggest herniated disc as a trigger for developing demyelinating lesions in the spinal cord in MS.