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Assessing Treatment Effectiveness in RA

Drs Nehad Soloman, Joy Schechtman, and Robert Levine share insights on how to measure treatment efficacy in the management of RA.

Nehad Soloman, MD: Joy, what clinical parameters do you use to access escalation of therapy? Have you found that sometimes patients are floundering on these synthetic DMARDs [disease-modifying antirheumatic drugs] and haven’t had effectiveness or even escalated to a biologic but find a partial response? How do you gauge that? When do you decide?

Joy Schechtman, DO: First, many patients get started on their first biologic and get a very good response—80% will say they felt pretty good on this medication. As time goes on, you’re starting to see more activity disease. We usually do the hack in our office. We do joint count. We do the RAPID3 [Routine Assessment of Patient Index Data 3]. We do the CDAI [Clinical Disease Activity Index]. We look at all these parameters, and I look at the clinical exam and listen to what the patient is saying. What’s their quality of life? How are they doing with their pain and fatigue? I try to look at all those factors on a patient and account for those areas.

If I’m seeing, and if the patient is saying, that they don’t feel like they’re getting that response that they got, then we have to say, “You’ve already been on this mode of action.” Perhaps we need to switch it because you’re losing effectiveness right now. I also use a Vectra disease activity score and look at that because sometimes I can’t see the active inflammation that the patients complain of. I try to look at all these parameters, weigh them, and keep looking at the patient and listening to what they’re saying.

I switch to a different mode of action if the patient isn’t doing well in that respect. Sometimes we have to go back to the formulary. That’s the frustrating process between the clinician, the rheumatologist, and the patient: we have a third party coming in and intervening with my decision. When I’m sitting in front of that patient, I’m looking at all these complex areas and trying to think about and negotiate the best drug for them to go onto next. I’d prefer going to a different mode of action, especially if they tried a TNF [tumor necrosis factor] drug in the beginning, and then move into a different direction.

Then we have to look at adverse effects in medications. Some of the different medications we use have different adverse effects and a box warning. I have to look at those. For example, if a patient is going on to a synthetic targeted treatment, we have to look at whether they’ve had previous cardiovascular disease, whether they’re a smoker, whether they have hypertension, whether they’re high risk. The other area I look at is their infection risk. Then we look at the mode of action and the way they’re going to be taking it. Are they going to be taking by IV? Are they going to be getting it by shot? Is that patient going to be able to come to the office? Do they travel? Are they out of state a lot? All those have to come into play when we’re thinking about which medication to go to next. These are very complex decisions. It takes a lot of time to think through all these areas.

Transcript edited for clarity

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