Management of Rheumatic Diseases with Biologic Agents: Key Takeaways



Schwartzman, MD: I tried to kind of give you 3 examples in 3 diseases, not limited by who is promoting the talk, because here, we had a complete clean slate, and we used 3 different drugs in 3 different patients. I think my kind of take-home message from all of these 3 examples is that we have a plethora of therapies that are available to us. I would argue that they are not all the same, that they all have a unique feature that, in a certain circumstance, would make one therapy more attractive than another therapy. I would argue that’s the case even within the anti-TNF (tumor necrosis factor) class. Technically, we have 5 anti-TNF agents, and they’re not all the same.

I’ll give you 2 examples where one is potentially preferable over the other. If I have a patient who has uveitis and axial spondyloarthritis, I’m going to use a monoclonal antibody, probably adalimumab, because it’s been studied in certain types of uveitis. I think any of the monoclonal antibodies would be helpful there, but I would not use etanercept.

I’ll give you the opposite example. I have a patient who travels to Vietnam, or used to travel to Vietnam once a month for business, where TB (tuberculosis) is endemic, so I know he’s going to be exposed. He’s responded to anti-TNF therapy and wants to stay on that. The TNF with the least TB risk is etanercept. I think we could argue that for every single drug that we have, each one of them may have a unique feature.

That’s not always the case with patients, though. Your garden-variety rheumatoid is going to be your garden-variety rheumatoid. I would probably say my most important take-home message is that we have a number of drug therapies. Take a careful history, and do a careful physical exam. Look for a unique feature in that patient that would lead you in the direction of one therapy over another. I think the 3 examples that I gave you kind of reflect that.

The first one was a patient with a possible history of a neurological illness. I would not use an anti-TNF. I would use an anti-IL-17. The second patient was a typical RA (rheumatoid arthritis) patient but had high disease markers, high CRP (C-reactive protein), sedimentation rate, maybe IL-6. The IL-6 pathway would make the most sense. The third patient was in the setting of contemplating pregnancy, where I needed a biologic. Although I could use many therapies, the one that I know doesn’t cross the placenta is certolizumab.

Transcript Edited for Clarity

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