Vibeke Strand, MD, MACR, FACP, shares the advantages and limitations of the AIMS and comparative cohort studies in the treatment of RA.
Vibeke Strand, MD, MACR, FACP: If you find you’ve got a patient who’s a nonresponder to a TNF [tumor necrosis factor inhibitor], it can be difficult to prescribe another therapy. A good example of this is the JAK inhibitors. where our US FDA has required that a patient fail a TNF before they receive a JAK inhibitor. That’s not a great idea. If you know the patient is unlikely to respond to a TNF inhibitor, you’re then, shall we say, forcing them to spend 3 or 6 months with an incomplete clinical response before they can move to some other therapy. As I said to you before, there are certain situations where JAK inhibitors are much preferable. But we also have abatacept, which works well in early disease, especially if they’re CCP [cyclic citrullinated peptide] positive. And we have IL-6 [interleukin-6] inhibitors, and we also have rituximab. So we have these other alternatives, and unfortunately, none of them we are able to use early in the course of RA [rheumatoid arthritis] after, say, methotrexate failure, or even with methotrexate as moving on, unless there’s some way to negotiate through the insurance companies and the formularies.
When you’re talking about treating a patient with moderate vs high disease activity, we’re going to use the same choices of therapy that we have. All classes of these therapies are effective, and we know that. And unfortunately, we don’t know why to argue for one therapy vs another. Again, I might think for a patient with early disease who is CCP positive, whether they’re moderate or high, I might choose abatacept. But I have every other reason to think about an IL-6 inhibitor, rituximab, or a TNF inhibitor, or a JAK inhibitor. The only reason you would treat a patient with moderate disease activity differently from one with high disease activity is whether you use concomitant therapy. With high disease activity, you may continue the background methotrexate if the patient can tolerate it. You may also add a short course of prednisone to try to encourage onset of response. You may add a combination therapy, although in general, other than using methotrexate with a biologic or a targeted synthetic, we don’t use others. Although sometimes physicians will use hydroxychloroquine. The biggest difference is simply being able to treat the patient, and treat them efficiently and see them more frequently, if they have high disease activity in hopes of being able to control their therapy.
We should be optimistic that other classes of therapies will be developed because we’re treating 40, 50, 60 years of disease. It’s simply a matter of time until patients have need of another therapy. That’s an important point.
We have many effective therapies now, which is nice, because I remember when we only had methotrexate. There are many still in development, even if I haven’t told you that I’m particularly excited about some of them because they’re not in late development. And the fact that we already have choices for oral as well as self-injected therapies. That’s a big advantage. Patient selection is crucial, and following patients closely and monitoring them is obviously crucial if you can get them into low disease activity or remission in a shorter period of time, such as 3 or 6 months. But selection of the agent for the patient, as crucial as it is, we have so little to guide us on that, other than essentially clinical practice and long-term acumen from lessons learned. But I can’t tell you now, even after 40 years, what patient should receive what therapy, which is unfortunate.
Transcript edited for clarity