Practice Perspectives on Optimal Patient Care in the Management of Psoriatic Arthritis - Episode 11

When and How to Change Therapies for Psoriatic Arthritis

A panel of experts and colleagues recall the indicators and steps that need to be taken when changing PsA therapies.

John Tesser, MD: Jen, when patients aren’t doing well, what things do you do to try to help them? Do you manipulate the dose? Do you change the frequency? Do you add other things? Of course, this gets to the question of when do you switch. How do you think about this?

Jennifer Simpson, DNP: It depends on what’s preceded their current issue. Have they called you the week before, the month before saying they’re flaring and you acted on that already and then they come in and they’re flaring again or they’re still flaring? That definitely will affect the aggressiveness of whatever decision you need to make. That would be a reason. If the patient tells you, “I’ve been flaring with my joints and with my skin, maybe once a month, once every other month,” that’s not ideal. If they’re on a biologic that’s every 4 weeks and they tell you it takes about a week for it to kick in, and it’s a week or 10 days before it’s due, and they start flaring up again, then we’re not fully capturing it with what they’re on.

That’s definitely a situation where I may add a DMARD [disease-modifying anti-rheumatic drug], as Dr Soloman alluded to—methotrexate, sulfasalazine, or leflunomide—to what they’re doing. If it’s something where I have dose variability, maybe they’re on infliximab or a biosimilar and I’m able to change their dosing or their frequency depending on what they’re on, that’s something to consider. Is it something where I need to have lifestyle conversations with them, or do I know that they’re still smoking? Do I know that they’ve had a lot of stress, whatever it may be? Maybe someone is getting ready to retire, so this may be changing what options they have or the daily stress they’re dealing with. I definitely like to have a conversation.

More times than not, I have a patient where I’m identifying that they’re flaring and that we need to make a change, and they’re thinking they’re doing OK. Maybe they’re remembering, “When I started, I came into you.” They were having more body surface area, and they were having more tender swollen joints. Maybe they’ve gotten that ACR50 [American College of Rheumatology 50% improvement]response—they’re feeling 50% better, but I want to treat to target. I want to get that disease activity under better control to limit their complications and their comorbidities as their disease progresses through their lifetime.

Often, having that frank conversation with a patient, our goal is to get you as close to remission as possible, if not in remission, by looking at different measures. And these are our goals to get there: adding something, changing their biologic, adjusting the dose, sometimes adding an anti-inflammatory if that’s appropriate for the patient, ideally avoiding steroids if possible. Of course, that’s a case-by-case basis depending on the patient and what their other comorbidities are. Sometimes it’s necessary, but we try to avoid especially in a psoriatic patient.

John Tesser, MD: Absolutely. Nehad, are you quick on the trigger to switch treatments? At what point do you decide there’s been enough time on that specific treatment and it’s not working?

Nehad Soloman, MD: Psoriatic arthritis and psoriatic disease is a bit different from rheumatoid. It’s a bit more resistant to treatment, so I tend to be more gracious allowing it for beyond 3 months, maybe even 4 to 6 months with various therapies. It’s outcomes and measures, looking specifically at a CDAI [Clinical Disease Activity Index] but some other aspects as well—body surface area, tender entheseal points—and then deciding are they really improving and by how much. If I see some improvement at the 3-month mark, we’ll stick to it and keep it around. At 6 months, if they’re not maximally improved, at least 80% to 90% improved, that’s when I start to think, “Should I add another agent, or do we need to change mechanisms of action?” I’m grateful that we have options.

I remember a time where switching would be from 1 TNF [tumor necrosis factor] to another TNF to another TNF. Then there was ustekinumab, which we used to use a lot, no pun intended, because of that very reason, right? We didn’t have other options, so we wanted to use a different MOA [mechanism of action]. But now we’ve got tons to choose from. It’s almost become a bit frustrating because it’s like, “Which 1 do you use first, and how do you know?” There’s really no Holy Grail to help us navigate through this.

John Tesser, MD: Absolutely. Those are all very good points. That’s a lead-in to mentioning all the therapies we have—interestingly enough, if you think about it, it’s only in the last 5 or 6 years that we’ve have so many new therapies. Before 2016, we didn’t have any IL-17s. We certainly didn’t have any IL-23s. The JAK inhibitor tofacitinib was not approved yet for psoriatic disease. Now we have [plenty of] agents. We have the 2 IL-17s. We have 1 IL-23 already approved and 2 others that are begging for approval. And we have a second JAK inhibitor that was just approved for psoriatic arthritis. I’m aware of the development, and we’ve been involved in our practice, of agents that inhibit both IL-17, forms of IL-17A and F. There’s an agent that inhibits the receptor for IL-17A, and there are other small molecules in development. Are either of you aware of some other things as well?

Nehad Soloman, MD: There are TYK2 inhibitors in development and, I believe, IL-17/23 inhibitors are in the pipeline as well. But as you mentioned, IL-17A and IL-17F inhibitors are emerging, as well as a bunch of other IL-23s that are champing at the bit to get approved.

John Tesser, MD: That’s right. Thank you for that. We’ve had a robust discussion about all this. It’s reasonable to mention that we have the option and the luxury of performing clinical trials in our office, so I can brag about our practice. We’ve investigated every single molecule that’s been approved by the FDA over the last 25 to 30 years. That’s true for osteoporosis as well, for RA [rheumatoid arthritis], for psoriatic arthritis, lupus, and many diseases. Because of this, we have another option for our patients, which is clinical research. Some of our patients have participated in some of the trials that wound up winning the award and getting FDA approval.

This transcript has been edited for clarity.