Steroid-Refractory Chronic GVHD Background

EP: 1.Graft versus Host Disease Background

EP: 2.Overview of GVHD Risk Factors

EP: 3.Current GVHD Prophylaxis Strategies

EP: 4.Signs and Symptoms of Acute and Chronic GVHD

EP: 5.Statistics on the Incidence of Chronic GVHD

EP: 6.Identification of Patients at High Risk for GVHD

EP: 7.Assessment of Chronic GVHD Symptoms

EP: 8.The NIH Clinical Scoring of Organ Systems

EP: 9.The Chronic GVHD Treatment Paradigm

EP: 10.Patient Case: A 48-Year-Old Man with Chronic GVHD

EP: 11.Treatment Goals for a Patient With Chronic GVHD

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EP: 12.Steroid-Refractory Chronic GVHD Background

EP: 13.Therapy Options for Steroid-Refractory Chronic GVHD

EP: 14.Ibrutinib as Second-Line Therapy for Steroid-Refractory Chronic GVHD

EP: 15.The iNTEGRATE Trial: Ibrutinib With Prednisone as First-Line Therapy for cGVHD

EP: 16.The REACH3 Clinical Trial of Ruxolitinib in Chronic GVHD

EP: 17.Clinical Experience with Ruxolitinib for cGVHD

EP: 18.The ROCKstar Study of Belumosudil in cGVHD

EP: 19.Real-World Experience with Belumosudil

EP: 20.Summary of Axatilimab for cGVHD

EP: 21.Therapy Selection for Patients with Chronic GVHD

EP: 22.Discussion of Long-Term Effects of GVHD Therapy

EP: 23.Future Directions in Graft Versus Host Disease

Transcript:

Yi-Bin Chen, MD: To continue with the case, prednisone was initiated at the dose that Catherine talked about, 0.5 mg per kg per day. And after 7 days of prednisone, there was initial improvement in the extent of involvement, I assume as well as sort of the subjective feeling of scleroderma. And so, a 4-week taper was begun. During that taper, however—and that might be a little bit faster taper than many of us would think about—but during that taper, the patient noticed sort of an increase in the body surface area. So that generally means an increase in scleroderma somewhere else on their body, either in the same place or somewhere else. And the prednisone was increased and then a subsequent taper was attempted, which was unsuccessful. And so, right now, we find our patient is at stable disease, on 0.5 mg per kg every other day. Some providers like the every other day steroid regimen thinking it better protects the adrenal axis rather than daily dosing. But regardless, our patient is stuck here at this dose of steroids, a stable disease with attempts to taper resulting in either flares of disease or progression. I think we’d all feel this patient requires another line of therapy, but it gets to how do we define steroid refractory or steroid dependent chronic graft-versus-host disease in this case? Corey, what’s your best definition? You know, I think we know if we see it, right? And so, is there a way you can articulate it?

Corey S. Cutler, MD, MPH, FRCPC: Sure. I think this case does represent nicely what we would all think about as steroid dependence. This is someone who you are unable to wean off of a pretty good dose of corticosteroids, assuming, you know, this is an average size man. This is 40-ish mg of prednisone every other day, and that is not an insignificant amount of prednisone. So, typically, failure to be able to wean below this dose on a couple of attempts would meet the definition of steroid-dependent chronic graft-versus-host disease. And like you suggest, this would be an indication to add in a second drug, both to help with the response rate, but also as a steroid sparing agent.

Yi-Bin Chen, MD: I mean, I think we see this a good amount. Wouldn’t you guys say? Colleen, when we add a second-line therapy to our patients, you want to just estimate, I mean as to what percentage is it do we add for actual steroid refractoriness or what percentage are we adding for steroid dependence or what percentage are we doing it because, you know, steroids are causing just awful side effects.

Colleen Danielson, NP: It’s a lot of our patients that fall into one of those 3 categories. I’d say upwards of, I don’t know, maybe 60% to 70% of our patients were adding a secondary agent.

Yi-Bin Chen, MD: But how many fall into each group? Do you have any guess there?

Colleen Danielson, NP: It seems to be kind of equal between each group. I think there’s a smaller portion that we use for true steroid sparing reasons. Steroids are just not a great option for them. It would lead to other issues, whether that’s blood sugar issues, blood pressure issues. They’re already weak and frail. We worry about myositis and things like that. I feel like that’s probably a little bit of a smaller group, and the other 2 are the bigger categories.

Yi-Bin Chen, MD: I’d agree. You know, I think there are patients that all of us know that we can’t bear to either start or increase steroids on for those medical reasons or those comorbidities you bring up. But it’s mostly steroid … and steroid dependence that drives a need for a second agent. You know, I think the other indication, I think is that people achieve some sort of response, a partial response, but yet- to steroids, but that response just isn’t good enough. And even if they don’t flare or do anything, it’s just not acceptable for their quality of life. I think improving that partial response would be the other indication that’s oftentimes not quoted in clinical trials, but that we use in common practice for a second-line agent.

Transcript edited for clarity.