Alvarez-Gonzalez C, Adams
A, Mathews J, Turner BP, Giovannoni G, Baker D, Schmierer K.
Ann Clin Transl Neurol 17 May 2017
PLEASE READ IT IS OPEN ACCESS (CLICK ON THE TITLE)
Abstract
Rebound disease
following cessation of disease modifying treatment (DMT) has been reported in
people with both relapsing and progressive multiple sclerosis (pwRMS, pwPMS)
questioning strict separation between these two phenotypes. While licensed DMT
is available for pwRMS to counter rebound disease, no such option exists for
pwPMS. We report on a pwPMS who developed rebound disease, with 45
Gadolinium-enhancing lesions on T1 weighted MRI brain, within 6 months after
fingolimod 0.5 mg/day was stopped. Treatment with a short course of
subcutaneous cladribine 60 mg led to effective suppression of inflammatory
activity and partial recovery with no short-term safety issues or adverse
events.
We have been accused of
beating the drum for cladribine a little too often. However, please read this
case of one of my patients, consider the alternatives, and you may agree there
aren't many with a comparable risk:benefit profile. The arguments are detailed in
the discussion.
There are a few lessons
beyond the effect of the drug used such as:
(i) Even in somebody
with the clinical phenotype "primary progressive" MS, the principal
mode of disability accrual may be through inflammatory lesions that look no
different on MRI from relapsing MS.
(ii) Based on this and
previous reports one should be very careful stopping a DMT known to be
effective in relapsing MS, even when efficacy in the trial (INFORMS) was not
significant *on the cohort level*. In our case, my impression would certainly be
that fingolimod did work.
Unfortunately, our acknowledgement appears
to have been lost in the course of proof editing the paper: We would like to
thank Novartis for letting us use the clinical data of this participant, and for providing the lymphocyte counts, acquired during INFORMS.
CoI: multiple