I have a 56yo patient who was diagnosed CML-CP in 2010.
Conventional Ph chr and bcr-abl p210
Commenced Imatinib (IM)
Achieved >4 log reduction in bcr-abl…but then late r lost this response and converted to nilotinib (NIL) by early 2014
The interesting part is that the patient has multiple sclerosis (MS).
From neurologist – he has high clinical suspicion that her MS has been exacerbated, both in terms of frequency and severity since starting NIL
There is no doubt conceptually, MOA via TK-dep pathways - particularly PDGFR, c-kit, SRC – this is certainly feasible
Interesting there are mouse models looking at IM in MS and other autoimmune diseases
It has also been a particular cold winter in Melbourne!
It terms response to NIL.
Commenced late 2013/early 2014 – has achieved >4-log reduction (pretty quickly) and sustained since
So our questions
1. What is the likelihood of this association with nilotinib and exacerbation of MS?
2. Safety of considering trial cessation NIL
3. Alternative TKI…lesser of evils given her comorbidity 9Das and PON are also potent inhibitor PDGFR, c-Kit, SRC)