Leucopaenia (low white blood cell) has become a hot topic of the past week, with the realisation that people who get leucopaenia (low white blood cell counts) are more at risk from infection and the dreaded PML.
So now there is a rush to stop the level of lymphopaenia from occurring, but one question is. Do we want our cake and eat it?Because we have to ask how do the MS-drugs stop MS?
In many cases it is because of leucopaenia. This may be physical depletion of cells out of the body and the blood, in particular, such as with alemtuzumab or rituximab or it may be a functional leucopaenia, such as with Tysabri, where the cells are in the blood but because they cant get out of the blood they are powerless to deal with the infection within the brain.
I have heard it said that the efficacy of alemtuzumab or cladribine does not relate to the level of leucopaenia, which may be in part the case, but if you did not get leucopaenia would these drugs work…I really doubt it.
To deplete or not to deplete that is the question?
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