Frontline Management of GVHD

EP: 1.Overview of Graft vs Host Disease (GVHD)

EP: 2.Role of Early Intervention in GVHD Treatment

EP: 3.Risk Factors for GVHD

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EP: 4.Frontline Management of GVHD

EP: 5.Approaching Initial Treatment of Chronic GVHD

EP: 6.Third-Line Treatment Approaches for Acute GVHD

EP: 7.Management of Chronic GvHD

EP: 8.Challenges in Managing Chronic GvHD

EP: 9.JAK Inhibitors: Managing Cytopenias in Chronic GVHD

EP: 10.Practical Considerations for the Treatment of GVHD

EP: 11.Role of Ruxolitinib in GVHD Treatment

John DiPersio, MD, PhD: Let’s talk about how we’d manage patients who get transplanted. The first issue we’re presented with after a transplant, when they develop symptoms and signs of acute GVHD [graft-vs-host disease]. I’m wondering, Mike, how you initially manage your patients with acute GVHD.

Michael Bishop, MD: With acute or a chronic?

John DiPersio, MD, PhD: Acute.

Michael Bishop, MD: It’s the same thing I learned when I was a fellow. The first 3 treatments for graft-vs-host disease are steroids, steroids, and steroids. I still think corticosteroids form the foundation. For acute graft-vs-host disease, most of the time they’re going to be on a calcineurin inhibitor. We’ll add corticosteroids, and we’ll do 1 to 2 mg/kg. I might make that even 0.5 mg/kg, and it will have to do with the organ involvement and the severity.

If I have somebody with grade 2 cutaneous graft-vs-host disease, I may use 0.5 mg/kg. If I have somebody with rip-roaring GI [gastrointestinal] and hepatic graft-vs-host disease, I’ll definitely use over 1 mg/kg, and I’ll usually use 2 mg/kg to try to begin the process. I’ll be thinking very quickly. One thing that’s underappreciated and comes back is early intervention. I’ll be looking for the steroid-refractory patients. At that point, I’ll be looking to add an additional agent. Most commonly it will be ruxolitinib. Ruxolitinib has changed our management of acute graft-vs-host disease. We have to make sure we identify those steroid-refractory patients as soon as possible.

John DiPersio, MD, PhD: I agree. As I was referring to initially, early intervention—there’s a prophylactic treatment, there are preventive therapies, and there are treatment-related approaches. To intervene too late is a problem because once you get a lot of tissue damage, then you get the circular circuits of inflammation that are hard to stop after awhile.

Michael Bishop, MD: In that context, John, do you use biomarkers? For early intervention do you do biomarker studies on your patients for early identification of patients at risk for acute graft-vs-host disease?

John DiPersio, MD, PhD: We haven’t generally. Obviously in select clinical trials, we do. We’ve come a long way with biomarkers, but they’re still not mainstream. What is the best day to get these biomarkers, which is the most predictive? James Ferrara and John Levine would provide some better insights than either you or I could. But there’s still debate about whether it’s at 7 days or at 21 days. The timing for these biomarkers as the most predictive for severe GVHD is a little debatable at this point.

Transcript Edited for Clarity