A roundtable discussion on anemia management in myelodysplastic syndromes. Featuring moderator Guillermo Garcia-Manero, MD, of the University of Texas MD Anderson Cancer Center; Amy DeZern, MD, MHS, Johns Hopkins Medicine; Tiffany Tanaka, MD, of the University of California San Diego; and Uma Borate, MBBS, of Ohio State University.
The following is an unedited transcript:
I’m going to go back to something that you started to mention that I think is where the field is going. You were talking about transfusion dependent versus transfusion independent, and then Uma is the world expert on CHIP CCUS. So now we’re going into this kind of, so can you tell us a little bit of what does this mean and how we’re going to be approaching this.
Well I think where a lot of medicine is going is the question of do we intervene earlier before whatever disease entity is becoming more extreme? In the case of this, do we intervene when someone is not transfusion dependent but is becoming anemic? And one thing I’m always humbled by is the difference in global approaches. I think our European colleagues treat when someone’s hemoglobin is much higher than I personally start treatment, sometimes ten and a half.
I’ll find them starting, and they really think that helps people live longer and better. And I think uma can certainly comment on treating other sort of precursor entities. It’s just when do we intervene to make sure we can change the natural history and help a patient feel better?
What do you think about CCUS as an entity?
Well, I think there was a great abstract at ASH. That Zoe Xi presented where she really described that high risk CCUS and low risk MDS are essentially the same clinically. So I don’t necessarily think clinically there’s that much of a difference. I think the question is, do we think we significantly impact people’s lives if we treat them early with ESA like agents, whether it’s an ESA or luspatercept. And I think we, you know, are asking this question in the element MDS trial, right, where you’re treating non transfusion dependent or very minimally transfusion dependent patients. But luspatercept versus ESAs.
And what we are finding is when you try to find that perfect balance where the patient is not transfusion dependent but almost ready to get a transfusion.
Well, by then they’ve had a fall. They’re already in the hospital. They’ve been something has happened. They had have had an MI. Now they’re they’re at that borderline. They’re getting blood. And so I question a little bit where we wait for that transfusion dependency. Is there a subset of patients we’re not serving. Well because we’re waiting for them to get sicker and manifest.
Whereas if you intervened a little earlier, like Amy mentioned, the Europeans are doing, could you prevent some of those outcomes? I don’t we don’t have information, right? We don’t have patient reported outcomes. We don’t have good OS data. So I think there’s a lot to learn. But I am biased in that. I think for some patients early intervention is probably beneficial.
Yeah. This is something actually that I reflect because sometimes I make mainly most of the times I make kind of wrong ideas. And then like years later, I was really wrong about this because when we were when I was thinking early on about anemia and improving the survival, I couldn’t understand this because my mind was, oh, we need to fix the disease,
The anemia is kind of secondary, and this is actually not that obvious. So it may be that you control anemia and maybe through some other effect, you are really helping the well-being of that patient, not just the quality of life. So there’s a lot of data now coming out in terms of cardiac remodeling with some of this agent. And so we don’t know, you know, we’re giving these drugs, we think that we are enhancing Myelopoiesis and maybe we’re doing something that we are really not measuring.
