Switching Therapies in RA

Nehad Soloman, MD: As far as objective data and making changes, how often do you follow your patients? How often do you follow the data? How often are you assessing CDAI’s [Clinical Disease Activity Index] or Rapid3’s? What prompts you to change or escalate therapy? How do you know what’s next?

Joy Schechtman, DO: Bob alluded to this, as well. What is next? When we start with a certain treatment and a mode of action, and a patient is not doing well with that treatment, we may either go to the same type of mode of action or, if we feel that the patient never really got a response to that type of treatment, we may want to change it. The science is not always there as to which treatment we go to next. I think that is a very personal decision between that physician and that patient. That personal decision is because we’re considering all the different things I’m measuring in the office. I see my patients frequently. If they’re on methotrexate, I’m going to see them every 6 to 8 weeks, especially if they’re out of control. I’m going to take those measurements every time. I get a feel for how that patient is doing this way. It’s not just the first time, maybe there was something that came up in their life. Maybe they were stressed. Maybe they weren’t taking their medication. Sometimes, I’ll also check drug levels of methotrexate just to make sure they’re getting a good response there. Maybe I need to move up my disease-modifying drugs. There are all these different steps in the way that I look at. Then if we’re going to change the mechanism of action, then I discuss that new medication with them. They must be ready to change, too, which is sometimes a little bit of a barrier between the physician and the patient, as well. We need to know patients don’t like change. There are rheumatologists who don’t like to change, as well. The thing is, we have to recognize when a medication is not doing well for a patient. We have to bring this up early, rather than late. We can’t wait a year to make a change. I think it needs to be done within a few months.

Nehad Soloman, MD: You have a limit as far as expectation. Three months, 6 months, 12 months, whatever you decide.

Joy Schechtman, DO: I would do 3 months, myself.

Robert Levine, MD: I think, to answer your previous question, I would say that when I initiate a new therapy, whether it’s a traditional DMARD therapy or an advanced therapy, I’m seeing that patient back relatively soon. I want to assess how they’re doing on it. I want to assess compliance with it. I want to make sure that their questions are answered. A lot of times, they’re not comfortable because of the unknown of the medication. I see them back within a month, initially. Then I’m making assessments on these patients every 3 months. That’s when they’re getting, that’s the minimum to do their CDAI and to do their composite index, to do all those assessments. I think we’re doing it on a regular basis. That gives us the opportunity and the flexibility to change therapy relatively quickly. As we’ve mentioned already, and I won’t beat a dead horse, so to speak, I think we need to get the patients to low disease activity and remission as quickly as possible, but being cognizant of the length of time it takes to actually get that response out of that individual treatment.

Nehad Soloman, MD: You mentioned in a minority of patients, maybe 10% to 20% may respond to methotrexate. We give them 3 months, maybe 6 months to get to it. We may measure methotrexate levels, make sure that they’re therapeutic. What percentage of your patients when we escalate therapy may then, maybe you find, aren’t working for biologics or targeted synthetics? Do you feel like it’s more than 50%, or is it a greater number or proportion than those who fail methotrexate?

Robert Levine, MD: I think that the percentage of patients who don’t respond to your advanced targeted therapy, whether it’s a target synthetic or a biologic, I think is a lot lower in general than the number that we get as failures of traditional DMARD therapy. I think it’s been very well proven that those drugs work in our clinical trials, also in our collection of real-world data, which has been really, I think, more apropos to what we do in practice. The clinical trial populations are curated to have no comorbidities or minimal comorbidities. That’s not the group we see. Also, a certain level of disease activity. For example, if you have 1 or 2 risks as your joints that you—that are bad and it’s affecting their daily living. They may not have a joint count that meets the entry criteria to get into a clinical trial. You look at all the composites and all the rest of them and it says, this patient needs more advanced therapy, an intensification. I think that the numbers are a lot higher with our biologic therapies and with our targeted synthetics. It gives us the opportunity to get our patients better, faster. I’m not sure if I completely answered your question.

Nehad Soloman, MD: Absolutely. I think part of the challenge here is we’ve got so many choices: We have JAK [Janus kinase] inhibitors, we have TNF, different mechanisms of action. Clearly there’s a difference in their mechanisms of action. Do you perceive a difference when deciding to choose one over the other? Or are you mandated by insurance companies and feel like those liberties are taken from you?

Robert Levine, MD: For the most part, those liberties are taken away. The group of patients where we have the option is in our Medicare population who have a supplemental insurance. Therefore, a formulary, for the most part, is not dictated to us. We don’t have to start with a TNF, we could choose trying to stay cognizant of what the package insert says and which drugs should be not used before a TNF. I think we have much more freedom. Then we can individualize therapy according to the patients’ comorbidities, and also preferences, and it gives us much more opportunity. I think that’s the way it really should be.

Transcript edited for clarity