Rebound post-natalizumab: is it such a problem? #MSBlog #MSResearch
“The study below reports MS rebound post-natalizumab. They make a general statement that ‘no treatment is unable to abolish disease activity reactivation after natalizumab discontinuation’. There are two problems with this statement. Firstly, there is a double negative in the statement that should cancel each other out; i.e. ‘no’ and ‘unable’. Secondly, they fail to mention the washout period. All MSers who were switched from natalizumab to fingolimod has a 3 month washout. This has now been shown to be too long. No washout, i.e. switching from natalizumab to fingolimod within 4 weeks of the last infusion, has been shown to prevent relapses and rebound. Interesting that they used cyclophosphamide post-natalizumab in one MSer; the same issues hold for cyclophosphamide, as does for alemtuzumab, post-natalizumab; as cyclophosphamide is an induction agent and is irreversible the real danger is carry-over PML. This is why I have proposed using a bridging strategy for alemtuzumab, and by inference other induction agents, to limit the danger of carry-over PML.”
“Another worrying bit of information in this paper is that this centre has had two cases of natalizumab-associated PML. It just shows you that it is a numbers game; you treat a sufficient number of JCV+ve MSers for long enough and you will get cases of PML. More reason for us to continue to de-risk our natalizumab population at the Royal London Hospital.”
Epub: Capobianco et al. No impact of current therapeutic strategies on disease reactivation after natalizumab discontinuation: a comparative analysis of different approaches during the first year of natalizumab discontinuation. Eur J Neurol. 2014 Jul . doi: 10.1111/ene.12487.
BACKGROUND AND PURPOSE: Natalizumab discontinuation induces the recurrence of multiple sclerosis disease activity: currently no therapeutic approach has been found able to abolish disease reactivation.
METHODS: The recurrence of disease activity after natalizumab discontinuation was retrospectively evaluated in 79 MSers who had been treated with immunomodulating agents, other first-line therapies, fingolimod or not treated.
RESULTS: No differences have been found in clinical or magnetic resonance imaging recurrence of disease activity amongst the groups. Interestingly, no disease reactivation was observed only in one patient treated for 6 months with monthly pulses of cyclophosphamide.
CONCLUSION: Disease modifying treatment or ‘no treatment’ is unable to abolish disease activity reactivation after natalizumab discontinuation.