[ Englisch] Why Does a Reduced Dose of a JAK Inhibitor Improve Anemia?

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Topics include: Treatments

Dr. Naval Daver from MD Anderson Cancer Center responds to Patient Power community member Jean’s question, “Why does a reduced dosage of ruxolitinib (Jakafi) allow red blood cells to improve the level of anemia?” Dr. Daver shares an in-depth response, including ad explanation of the JAK-STAT pathway and results of a clinical trial for a reduced dosage of ruxolitinib (Jakafi) designed to reverse anemia.

The Ask the Expert series is sponsored through an educational grant to the Patient Empowerment Network from Incyte Corporation.

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Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.            

Andrew Schorr:    

Here’s a question we got from Jean.  Jean writes in, “Why does a reduced dosage of Jakafi allow red blood cells to improve the level of anemia?  My hematologist wants to put me on 5 milligrams of ruxolitinib (Jakafi) instead of 10.  It seems logical that less Jakafi would yield more anemia.  Do you have an explanation?” 

Dr. Daver:             

Yes, actually that one that we do have a very clear explanation.  So the JAK inhibitors are—so the JAK-STAT pathway actually plays a role in three major functions in the body: inflammation, immunity, and actually development and growth of red cells and platelets.  So when the JAK pathway is overactivated, you get too much inflammation and immunity and then red cell production, like with PV, and those result in the symptoms. 

So when you shut down the JAK pathway, it’s good because you’re using inflammation immunity.  But the negative side of that is you slow down red cell and platelet growth.  So this is not truly—I don’t even call it an adverse effect.  This is actually an extension of the physiological effect of a JAK inhibitor, that you get anemia.  Now, what is very interesting—and we knew this for many years when we started using the ruxolitinib.  But what now is being seen as interesting is that we also know in the last three years that the JAK inhibitor has reduced bone marrow fibrosis.                 

 

And we know that it’s the fibrous tissue in the bone marrow that kind of has slowed down the production of red cells.  So when we started seeing that the fibrosis is reduced, Dr. Talpaz actually did a study with low-dose Jakafi, 5 milligrams twice a day, with the idea that in the long term, over two, three years, we will reduce the fibrosis but not suppress the JAK pathway so much. And that will then allow the non-fibrous red cell precursors to grow and produce hemoglobin. 

And he was actually showing that.  And that a low dose, you don’t suppress a JAK pathway so much that you block red cell development. But at the same time, over time in at least 40 percent of patients, you can reduce fibrosis. And that reduction in fibrosis allows your red cells to grow in the bone marrow, and your hemoglobin improves.  So this is a good strategy and is valid.  Now, one caveat is if the main reason to start the Jakafi is big spleen and high symptoms, then you have to go up on the dose, because you’re starting it for symptom and spleen control. And you cannot think about the anemia component.

But if the main reason to start it is to slowly improve hemoglobin, then this is a good idea.

Andrew Schorr:                   

Well, okay. 

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

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Page last updated on July 19, 2017