ClinicSpeak: do you understand what an induction therapy is?

To be induced or maintained that is the question? #ClinicSpeak #MSBlog #MSResearch

“I am at a MS-related meeting and discovered that many people in the field don’t distinguish between maintenance and induction therapies. The following are some of my slides to try and illustrate the differences. Are they understandable to you (yes/no)? If no then we have a lot of work to do. Thanks.”

CoI: multiple

18 thoughts on “ClinicSpeak: do you understand what an induction therapy is?”

  1. Thanks for the slides… why is NEDA an effective measure of efficacy in maintenance treatments but not in induction treatments? Bojana

    1. Can you explain this a little more MD? I'm still not sure why NEDA is not a bench mark for induction therapies? I thought it was the same aim for all DMT's? I'm not sure what HSCT has to do with it.

    2. NEDA is the desirable outcome for all therapies. However if you are not NEDA and you are taking maintainence therapy it is a signal to change drug but if you are not NEDA on induction therapy this is not a signal to change drug or treatment it is a signal to have another dose of the induction treatment. However if you apply the maintainence logic then you escalate the induction treatment to a more aggressive treatment and this would be hsct. However this does not happen

    3. Thank you. I understand there is no where else to go, I'm just still not sure why NEDA is not a reliable indicator of efficacy for induction therapies?

    4. It is a good indicator but some of the outcomes have issues e.g. atropht by MRI=NEDA-4 because it is a balance of water removing water makes the brain look likeit is shrinking when you are getting rid of inflammation

  2. Shouldn't this be obvious from the vocabulary? My fairly dim opinion of doctors only grows…

  3. I think the vocabulary is the problem. Why are the cures not called cures? Why are they called induction therapies?

  4. Isn't brain shrinkage the cause of disability in SP and so ifinduction stops this in years 1-5 or 1-10..isn't it obviousthat SP will not occur..?Also since DMT does not stop SP why are they even used.Someonewith mild disease on DMT may just be mild disease case totallyunrelated to the DMT.

    1. Even if SP is inevitable, you want to minimise the damage during the RR phase so that you enter SP with less damage & fewer areas for neurodegeneration to occur (assuming it acts exclusively on sites of existing damage acquired during the RR phase).

    2. Don't think there is any connection between mild RR and mild SP. They are separate processes.SP is age dependent onset..tends to occur mid 40's probably when testosterone and estrogen levels decline.

  5. My understanding of the early alemtuzimab group (involved in early trials) is that only 5% or so had transition to SPMS despite the fact that it's been over 10 years since they received treatment. If the median time to SPMS transition is around 10 years, then this would indicate (to a layment like me anyway) that brain atrophy is indeed what triggers SPMS and alemtuzimab (and HSCT) should prevent the transition, as otherwise you'd expect roughly 50% to have transitioned by now.

    1. EFFECTIVE is the key word. So far it seems only HSTC and Lemtrada offer the only hope for a potential long term disability free future life.

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