QD 69 - Part 5, EULAR RA Treatment Guidelines Save

This is QD Video, and I'm doctor Jack Cush. QD Video is brought to you by rheumnow.live. This is our fifth installment, final installment on our discussion regarding the 2,020 EULAR management guidelines for rheumatoid arthritis. We previously discovered the five overarching principles, discussed the first nine items or 10 items actually in a 12 item and recommendation, and today we're gonna finish up with two more. Number 11 says, if a patient is in persistent remission after having tapered glucocorticoids, one can consider tapering biologic DMARDs or targeted synthetic DMARDs, especially if the patient if the treatment is combined with a conventional DMARD, meaning the patient's on a background DMARD in addition to the.

So the patient's on a conventional DMARD and a biologic or a targeted synthetic JAK inhibitor, which one would you target if someone is in persistent remission? I think it's important here to note a few things. They're saying first that you have to be in persistent remission. Right? And it's remission, not LDA.

Second, they talk about tapering, not discontinuing. These guidelines are kind of against discontinuing because if you discontinue drug, even in patients who are doing great, the chance of long term success is probably around ten to fifteen percent based on prior studies. So they're talking about tapering. That means dose reduction or interval increase, and that's an important distinction. This particular item, item 11, says that if you're on a conventional DMARD and then an expensive drug in addition in combination and you achieve remission off of glucocorticoids, then you would stop the expensive therapy, the biologic or the targeted synthetic or JAK inhibitor.

And the question is, is that the right choice or should it be the cheaper drug, the conventional DMARD? Again, that's dealt with it actually actually in item 12. So what does it mean to achieve a target? Here they are largely talking about persistent remission and there is no firm definition of persistent remission. It could be six months in or twelve months of achieving remission via DAS or CDI or rapid three score.

But again, the longer the better. Many of the studies that have been that have done that have researched this issue with different regimens have looked at patients in remission for six or twelve months and showed that it does work sometimes with some stipulations which I guess we'll go over. So it can't be just low disease activity and doing well or well enough. They really talk to remission. What I say in my clinic is and a patient asks, doc, when can I go off these medicines?

I say, RA is a lifelong disease and it's not likely you're gonna get off therapy. Chance of going into drug free remission are only ten percent. Let's try to get to remission and then we'll have that discussion. Let's you show me one year of remission and then we'll lessen your therapies. You show me two years, well, maybe even less less than more.

So I think twelve months is probably the right number. Again, the I wanna remind you of the ACR guidelines on this, the 2015, I think, guidelines, which basically said if you're an LDA, low dose activity, you don't change therapy. But if you're in remission, you could stop one or less than one, but not both. So what we do know is that if you try to go off therapy completely, there's a high flare rate. The good news that they the the authors say here is that the consequences of flares are minimized if you're stopping the targeted synthetic or the biologic because you can recapture disease control in over eighty percent of patients with those drugs.

However, if you stop the conventional DMARD, you don't recapture control as well, less than fifty about fifty percent can will revert back to where they once were. So I think that, again, it makes great sense to be in in persistent remission, and then there's this argument about deep remission. There are research studies showing that patients who have a DAS score of like 2.1 or less are more likely to stay in remission and not have flares. So, again, there are consequences to stopping or therapy, there are consequences to lessening therapy. We do know that, again, the main consequence is flares.

The question is, will there be, with flares, a consequence as far as radiographic progression or long term disability? That's really unknown and not been studied. Item number 12, what does that say? Well, it says, if a patient is in persistent remission, tapering the conventional biologic conventional DMARD should be considered. They want to consider that separately because, again, you have to weigh which is the more prudent choice.

Is it going to be the drug the patient likes the most that they stay on or the drug that they hate the most that they go off of? Is it going to be the most expensive drug that you stop? Is it going to be the drug that gave the most persistent or most impressive response when it was added to the regimen? These all have to go in, and it is not unreasonable to taper the conventional DMARD in patients who are on a combination and in remission. Persistent remission, even better, deep remission, if you can find that and if you know what that is.

So what are the downsides to these European EULAR guidelines? There are but a few. And first off, how do they differ from the ACR guidelines? Note that the ACR is actually in the process of updating its guidelines, which I think came out in 2015. The ACR guidelines do not make use of poor prognostic indicators in choosing the level of therapy, whereas the UR guidelines do.

The ACR guidelines are all about how severe the disease activity is when it comes to choosing therapy. Neither of them talk about what to do in preclinical patients who may be at risk because of a first degree relative, and they are seropositive and now they have arthralgias. A lot is not known about that. There are recent papers out there including one by Paul Emory and others that are looking and commenting on this. Again, I don't start DMARR therapy on these patients unless I have synovitis.

There's no real depth here on switching within a class. If you fail a JAK inhibitor, can you go to another JAK inhibitor? If you fail an IL-six inhibitor, can you go to another IL-six inhibitor? They did address the issue of failing a TNF inhibitor and whether you go to a second one or another MOA. They came around just blanketly a priori saying it's probably better to go to another MOA than to go to a second TNF inhibitor, but we talked about that, I think, in part four of this series.

They really don't give you a lot on when monotherapy is prudent. They sort of talked about it in terms of, well, if you can't use combinations of drugs or whatever, then maybe a JAK inhibitor or an IL-six inhibitor may be the better choice. But I think a better definition of who should be getting monotherapy. Drug companies want to tout their monotherapy data because it distinguishes them from all other drugs. We know patients do best when they're given a combination of drugs because we really can't predict who's going to do great on one drug.

Let time tell that. There's no indication or no study that actually says that really well. They don't have much in the way about how safety factors into this. I call that defensive prescribing. It's sort of a secondary, tertiary, quaternary decision making tool when because the patient has this, then you do that.

So I think we need better guidelines on if this, then that management of RA. So what do you do in the in someone who's had a deep tissue fungal infection in the past? I had a patient with coccidioidomycosis that I saw today, that's coloring the treatments that she can take. Again, think it's a much larger discussion, that's probably why it's not in these guidelines. And lastly, maybe the biggest challenge we have in managing our patients is that of adherence to therapy and non compliance with therapy, not even filling the prescription that you prescribe for the disease that you know is going to maim them if not kill them.

So, again, we need to have better strategies and a better understanding on how we can better address the needs of our patients by sort of safeguarding against the temptation to look at wacky internet sites and natural therapies or something sold by cousin Alfie out of the back of his car, which seems so much more appealing than that biologic that has a one in thirty thousand risk of PML. Again, there's a lot of reasons why patients don't follow through on your instructions. We need to have strategies to better deal with that. I hope you found this review interesting and helpful. I found it interesting to review.

Tune in next week for more QD clinic. And by the way, RheumNow live. You know, let me close with something about that. I think it's kind of a cool thing to be involved in someone else's great project or a great dream or incredible vision. Artie Cavanaugh and I, when we sat down and dreamed up RheumNow Live, we wanted a meeting where people are gonna be connected, where they're gonna be highly engaged, not only with the other audience members, but also mainly with the faculty when there was gonna be a high degree of interactivity, and that we're gonna be Internet based, and that we could not only just do it within the room, which was gonna be fabulous, but outside of the room.

We have these TED talks, we call them step talks, that are intermingled throughout the the the program that are just tremendous. Short, wham bam, you know you know, sort of groundbreaking kind of new thinking on things that you've heard about or you'd like to know more about. Anyway, a lot's happening. Go to rheumnow.live to check out the program and to register. Next week.