So first of all, I think we shouldn’t give up on JAK inhibitors when we see that the hemoglobin starts to drop because despite patients becoming anemic, you know, quite often they still benefit from ruxolitinib exposure or any JAK inhibition in terms of constitutional symptoms, etc. However, there are some possible tweaks and improvements that we can put in place. Some of that is about dose...
So first of all, I think we shouldn’t give up on JAK inhibitors when we see that the hemoglobin starts to drop because despite patients becoming anemic, you know, quite often they still benefit from ruxolitinib exposure or any JAK inhibition in terms of constitutional symptoms, etc. However, there are some possible tweaks and improvements that we can put in place. Some of that is about dose. Dose reduction might not be necessarily the answer at the very start of the treatment. So my advice would be to probably continue with full dose for a little bit longer because sometimes what we see is that there is a drop in the hemoglobin level and then eventually an improvement in the hemoglobin level and that could be as a response to the spleen size reduction which can help the hemoglobin level. However, in longer-term exposure to ruxolitinib, if the hemoglobin keeps going down, so I would suggest reducing the dose. And then consider the addition of another drug. Obviously, outside clinical trials, erythropoietin is probably the drug of choice. And my advice is to start sooner rather than later, because if the transfusion burden starts to build up, then the problem we see is that there is resistance to erythropoietin-stimulating agents. Sometimes a small dose of steroids can help in combination with erythropoietin. Sometimes the addition of a different growth factor, such as G-CSF, can be helpful as well. But clearly, anemia is still an unmet need, which is why drugs such as elritercept seem to be extremely promising.
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