ACR2019 Panels Group A Save
ACR2019 Panels Group A by Dr. Cush
Transcription
Hi. I'm doctor Jack Cush, and this is the ACR two thousand nineteen podcast. We're coming to you from the annual meeting in Atlanta, Georgia. This episode is a collection of our faculty reports, interviews, and panel discussions recorded live from the RheumNow booth. I hope you enjoy and learn.
Hi. I'm Jack Cush.
I'm here
in the RheumNow booth at ACR two thousand nineteen in Atlanta. We've convened a panel of experts on gout. I'd like them to introduce themselves.
I'm Nicola Delbeth from Auckland, New Zealand.
Hi, Jack Canseagg, University of Alabama at Birmingham.
And Rob Keenan, Duke University.
Alright. So there's been a lot of presentations here. Why don't we hear from each of you what you think was a highlight presentation that either struck you or that you were involved with?
Yeah. So, well, I think for me the clinical trial that has been really interesting is Lisa Stemp's trial about tart cherries. So we know that patients often take different dietary factors or you know different supplements and there's been a lot of interest in tart cherry. It may well reduce flares, but we really haven't understood why. And Lisa's study has shown in patients with gout, tart cherry does not change serum urate levels.
So if it's if it works, it's gonna work through a different mechanism, maybe through reducing flares, I think that's really the next step. But, really interesting to see some RCT data of these, specific dietary factors.
It's been anecdotalism up to now. Yeah. That's true.
It's about time.
Yeah. We need
a study. We really do.
We need some data. Patients like the idea, you know? Yeah. And they'll buy the juice and the the extract and all that kind of stuff.
So what
is it though? Is it vitamin c or is
it just I don't think it's vitamin c.
Well, it's mechanism would be Well a weak antioxidant effect, has nothing to do with the type. It's possible. It's it's I'm sorry?
The polyphenol effect, the weak antioxidants that are potentially anti inflammatory.
I think
it must be an anti inflammatory.
It does
have a
weak COTS two effect. That's been shown in in in multiple studies. Weekly uric reserve too. But yeah.
Well, wouldn't we expect to see a a urate lowering effect in that context?
Yeah. I just don't think the studies are large or long enough to fully appreciate the relatively small effect that you might see.
And there really aren't good studies like Lisa's that are out there, to be honest. So Ken, what struck you?
Yeah. Well, I presented some data on what's called the ANIGO study. This was an active comparator looking at anakinra versus triamcinolone. We all, many of us in the gout field and many rheumatologists in general have been using some anakinra in their patients who aren't good candidates for other acute therapies such as nonsteroidals, colchicine or even glucocorticoids. The impetus is to really generate some high quality data in a real study, real well designed clinical trial that speaks to the efficacy of Anakinra.
The study was designed as a superiority study and in fact was not shown to be superior for the primary endpoint of pain measured using a visual analog scale but it looks the same. Anakinra looks the same as triamcinolone in reducing pain and in terms of a number of important secondary endpoints it actually looked a little bit better. So we're not totally sure why pain is the same but other things are better. Regrettably from a regulatory standpoint, it appears unlikely that this drug is going to move forward to approval as an indication
for
gout. Our issue in The US at least is that we're going to continue to be using it off label when we feel we absolutely need it.
But I think it's again really great to have some RCT data on Anakinra and we've also seen very similar data from The Netherlands as well with their RCT that's just been published. So, you know, sense is that at least for patients who, you know, have contraindications or haven't had a good response to the kind of standard therapies, at least we now have some clinical trial data around safety, around efficacy.
The safety looked fine in this Yep, I
mean it
makes sense, pathophysiologically, given that the is so important in the acute pathogenesis of gout and we want to inhibit IL-one as a primary biologic mechanism.
Rob, what struck you at this meeting?
So, the immunogenicity studies with peglodecase have been interesting in general and it's kind of illuminated some moist sweat. To my surprise a little bit initially, didn't think methotrexate for example would actually look like it had response that it has with these patients and decreasing potential risk for antibody development with peglodecase as well as fusion reaction subsequently or loss of efficacy in general.
This is follow-up study to what was done through open label out in the community last year and this is how many patients were in the study here?
How many patients have enrolled?
I think
there were about
10. There
was a small report.
Were some
really well designed RCTs were
on our way.
One looking at methotrexate, one looking at azathiopin. We finished a study looking at mycophenolate that I hasn't been sorted out think we're not clear what's going to be the right strategy. Maybe that all these things work. The other population that's going to be studied are transplant patients who are already on these drugs and we're anecdotally we sense that they may be less likely to have immunogenicity as well. But this immunogenicity issue with pigleticase is really the treatment limiting problem with being able to continue it for more than a few doses, particularly in our younger patients where they're more likely to have a problem and a bump in serum urate that requires you to stop the therapy.
You can't go further and you don't want to have bad infusion reactions which is what we worry about when the serum urate bumps.
So Robin, your patients who use piclodecasin, will you use a background drug like azathioprine, mycophenolate or methotrexate?
I do and I have. So I've used azathioprine and I've used methotrexate. Interesting. And I also have patients who are transplant patients who are on methotrexate. Works out Works it works out well.
What about quality of care? What are each of you doing to address the issue of quality of care in gout?
Well, think there's been some really interesting data at this this meeting about some strategies for that. I mean, it's still really difficult. I have to say one of the really interesting posters yesterday was a study looking at serum urate reference ranges and within laboratories huge differences in reference ranges. So you know, even if we're trying to treat to target these, you know patients with hyperuricemia are not being flagged that that you know with gout and hyperuricemia that we need to increase the urate levels. But I think at this meeting and over the last year or so we've seen some really exciting strategies, new systems approaches, as well as, you know, nurse led care, pharmacist led care.
So I think that we really need to look at how our healthcare system works, what the barriers are for patients, and try and address that. I think we're really starting to see that.
I think that's spot on. It's the old adage with trying to improve quality and change behavior, one size fits none. Yeah. And unfortunately our health systems are also varied.
Yeah. But I agree with you
that system approaches, using nurses, pharmacists, other non physician health professionals to help in this problem is really a promising approach. We actually have a study that we're just starting where we're going to be working from the ED in identifying people with gout in the emergency department, where we know a lot of people don't get the necessary follow-up, they don't get on urate lowering therapy and trying to do a direct to patient approach to improve quality in that way. We'll see if that works.
The other thing that I think has been really interesting at this meeting is several abstracts which have shown that when patients get admitted to hospital, their allopurinol is stopped or reduced. And so again, you know, we need to be looking at what's going on in hospitals because that's that's a really lost opportunity. And in effect, you know, it's it's even worse when you get admitted to hospitals. So it's it's a real problem for hospitalists as well as, you know, primary care.
It's it's it speaks to the battle with education and
and Yeah.
And racing the current dogma around gout and what gout is and how it works actually even to the primary care physicians, the hospitalists and really the bulk of gout patients sit in these offices with these physicians and providers and we got to this. It's always a battle to try to get the word out and disseminate the disseminate the word and how to appropriately treat and proper treat properly treat gout. And I think that goes along with everything else we've said as far as trying to change, you know, our processes, the system itself, and that's just
it's it's
a it's a uphill battle, but, you know, we're ready for it
right now. Yeah.
So what is this goutspecialist.org?
So this is gout goutspecialist.org is a network of gout specialists. Can sign up for and to as long as you adhere to the ACR guidelines as far as how to treat gout, you can sign up and be a gout specialist and gout patients can actually find your name and your office location anywhere in the country. It's only US based right now anywhere in the country to seek their gout treatment. And it's basically and you can find that through gouteducation.org, which has both physician or provider references and and sources as well as patient sources. And they they get upper range of 22,000 hits from predominantly patients on a regular basis and it's just I think a it's good source for patients and patients seem to love it.
Of course, lots of gout cartoons which my patients like and I like as well. So it's a good opportunity for both patients and providers to get additional resources as well as have their name out there as a gout specialist.
Alright, we're on the elevator ride up with the viewer. We got eight seconds each. What's the one thing you want to tell them about gout from this meeting?
Oh, I saw this amazing new therapeutic agent which looks fantastic. So this is an enteric uricase Which is stable in the small intestine and looks like it's going to act on intestinal intestinal transport and Has a urate lowering effect with an agent that is not absorbed systemically. I think this is just new mechanism of action, really exciting. It's definitely the most exciting thing I've seen in gout at this meeting.
Cool. So I know this is a gout session, but the thing we haven't talked about is asymptomatic hyper uricemia and the effects of hyperuricemia on other systems in the body. There's been a lot of interest in cardiovascular disease and hypertension. At this meeting, my colleague Angela Gaffo presented the SURFER study, which showed that allopurinol in a crossover design may actually have effects on vascular endothelium although curiously that didn't translate into direct effects on blood pressure. So more to learn about that.
GATA is associated with multiple comorbidities and other disease states as well as it's a very disabling condition for a lot of patients and it's most importantly it's curable and I think we need to get that word out
that
we can actually fix it out.
I just left Jazz Singh's poster about opioid use and trends in The United States and it's actually look, gout's low on there and it's not much of a problem, not compared to RA, OA, low back pain, other things. So thankfully, gout is not getting wrapped up in the opioid epidemic. I want to thank each of you for being a part of the panel. Thanks for
Thank you, Jack.
Thank you. Hi.
My name is Eric Ruterman. We're here with RheumNow at the ACR meeting in Atlanta. And we have a group of us here together to talk about psoriatic arthritis. Before we begin, let's give you a little more background. As I said, I'm Eric Ruderman.
I'm from Northwestern University in Chicago.
Alexis Agde, Rheumatologist, University of Pennsylvania in Philadelphia.
Jesse Walsh, Salt Lake City.
Postache, NYU Langone Health, New York City, New York.
Okay. So, the big news in psoriatic arthritis at this meeting has got to be the two phase three trials with gazelkumab. I want to talk about this a little bit but I think it's really going to be helpful to talk about what's that going to say about that pathway for psoriatic disease. Alexis, start us off by what did these trials show?
Well, they're the first two phase three studies in the P19 inhibitors, so that's really exciting. There was one trial that was completely treatment naive. The other trial had some TNF non responders or biologic non responders in that trial. So in the trial that was combined with biologic responders and treatment naive, a lot of them there was two doses tested, a Q4 week and a Q8 week compared to placebo. And in that trial, the Q4 week looked numerically a little bit better than the Q8 week, but it wasn't that much different overall.
When they split it out by TNF versus not TNF experience, they saw actually that the TNF experience people did equally well between either dose, which was a little interesting. And then in the other trial, among all treatment naive patients, the two doses looked identical. But the one caveat there was that the radiographic progression was statistically significant at the q four week dose, but not at the q eight week dose. So some interesting things to kind of grapple with in terms of dosing and how we'll use that or what what the FDA will think when that's
submitted. And and both show the drug work.
Yes.
Very effective. And I want to get into where that is going to fit for us. But before we go there, Jesse, the dermatologists are all in on IL-twenty three inhibitors. What's that about?
Well, it makes sense. Their outcomes look great. They're achieving good skin clearance with IL-twenty three inhibitors. Dosing wise, they're somewhat easier to give. Patients like the less frequent dosing than with some of the TNF inhibitor alternatives.
I think there are some hints that there may be some safety advantages, particularly compared to the IL-17s inhibitors, where we don't have to think so much about Candida or inflammatory bowel disease. I think the jury's still out on serious infection rates, but it may be a little bit more favorable with IL-23s compared to IL-17s and TNFs.
Before we talk about where these drugs are going to fit, the last thing I want to touch on, and Jose, tell me, so the dermatologists have successfully upped the ante with each round of treatments from TNF to IL-seventeen, IL-twenty three and it doesn't look like that we've achieved the same thing for the arthritis. What's that about?
Biology. It's all about pathophysiology. We have nailed down the pathways for psoriasis. As you go upstream on the molecular pathway, you achieve better and better outcomes. We're jealous.
They get passy one hundred's. Since the year 2004, our metrics have not changed. It's ACR20. Not only they haven't changed, the efficacy of these drugs are about the same. You get a fifty five-sixty percent ACR20 on the drug versus placebo.
What do we do with that information? I think one of the progressive thought approaches or thought processes is that we may be late when we treat psoriatic arthritis patients. Later in disease process, not in the patient, in the disease process. Is there room to perhaps conceive preventive trials or very, very early psoriatic disease clinical trials?
All right, so now we've got the data, we know what the skin is. I want to open this up. So this is the first. Two phase three trials that are clearly going to get this drug approved for psoriatic arthritis and we have two more drugs waiting in the wings that are likely to follow. We have TNF inhibitors, we have IL-seventeen inhibitors, we have one and eventually more JAK inhibitors, have a premilast.
Where are these IL-twenty three inhibitors going to fit in our patients?
A great question. So, I mean, think some of the easy things are that in practice we're still going to use the drugs we have first most likely and then this will be the next drug. So, most of our patients we're going to prescribe gaseoximab for probably are going be TNF experienced already because that's where it's going to come into the line. I would probably use it in a patient with more severe skin disease.
Probably avoid it in anybody who were concerned about axial disease.
What's that about?
It didn't work. The IL-twenty three data are not showing efficacy with axial disease. We haven't really specifically been studied in psoriatic disease, but in AS populations it's just not working. That probably again comes back to the biology. Maybe there's something different about these Yeah.
A little bit more synovial involvement.
That's right.
Look, these are good drugs. The p nineteens, we're not talking about a lower effect class in terms of efficacy. We gotta be careful now. Now it's about the side effect profile. Now it's about dosing.
Now it's about having a conversation with our patients, which we used to not have to do. We had methotrexate and nothing else. And then we had methotrexate plus minus a DNF, which was an easy conversation. By now, we open it up and we include the patients in the decision making.
I think we also need more studies that are going help us differentiate this because right now we just have a bunch of trials in polyarticular patients. We don't actually know anything about how to target therapies. There's a huge opportunity for this now moving I
think you're specifically referring to patients who may have lower peripheral joint burdens and more diverse phenotypes.
Right? Yeah, exactly.
Jess, you made an interesting comment, you were like, Well, we use the drugs we're sort of used to using, and I think that's important. We're creatures of habit. We get used to doing certain things, and the dermatologists have a compelling reason to use the IL-twenty three inhibitors because they're so much better for skin disease. I don't think we have that compelling reason, at least yet, in joint disease. Is that right?
Right. I mean, there's nothing really in terms of joint outcomes that differentiates them well.
Alright, let me shift gears for a minute and let's talk about another trial that was presented here at the ACR meeting which I thought was really interesting. It's a question that's come up in rheumatoid before. We haven't looked at psoriatic arthritis and that is if you have a patient who's doing really, really well, can you back off their medication? The ixekizumab study which took all these patients, put them on ixekizumab, If they got into minimal disease activity, they were randomized to withdraw the ixekizumab and just stay on placebo or stay on the ixekizumab in a blinded fashion. What happened?
Almost all of them went back up onto therapy again. So once they withdrew, they they flared. A median, I think it was about six months or something like that, they looked at over forty weeks. There were significantly more flares than people who were pulled off the drug from compared to people that were stayed on the drug. But the interesting thing is that once they restarted them on drug, you could recapture most of them, which was also interesting.
I mean, the survival curves were fascinating. Basically, you said, if you went on placebo and you waited long enough
You were gonna flare.
Your disease was gonna come back.
Yeah. Okay.
Should we not have expected that?
I expected that. We expected
that based on rheumatoid experience with TNF blockers, right? We've this before, this behavior. What we haven't seen and it's new is this easy recapture, which may have to do with immunogenicity, where TNFs do create immunogenic responses, and the 17A class is not for that. So that may be an advantage.
Although seventy percent of them were on methotrexate in the study which is really interesting to me so maybe that led to some baseline treatment that you could then make it easier to recapture some of them. Don't know.
So one last question. And I look at that study. Wish they had had an arm where they gave placebo every other dose because in RA at least, we've seen you can decrease the biologic, just you're sort of nodding your head. Mean, that's the question. You know, stopping the drug doesn't make any sense.
Wouldn't it be nice if we were able to look and cut Patients
want to do it that way. They say, Can I decrease my dose rather than come off it all at once? I think it's logical and preferred by
To close the circle on that one, going back to P19s, this is a drug that is every two months. But if you leave people off of drug for six months, fifty percent of them will remain with good skin outcome. So you could argue that frequency is one thing we should look at in other targets.
So the message is anybody out there who is involved in trial design, we'd like to see not necessarily withdrawal trials, maybe spacing trials to give us some of those answers. Alright, I think we'll wrap there. Thank you everybody for doing this. Again, RheumNow coming from ACR in Atlanta in 2019. Thanks for watching.
Hi, I'm Jack Cush. I'm here in the RheumNow booth with a panel of experts on spondyloarthritis. I want them to introduce themselves.
I'm Jack Cush in Dallas. Christopher Richland, University of Rochester.
Sofia Romero from The Netherlands.
Leanne Gensler, UCSF in San Francisco.
Jessie Walsh, Salt Lake City.
Alright. So what I'd like you to do is, why don't we just introduce some of the interesting new trials and new data that's been presented in AS and Spinal Arthritis. Doctor. Walsh, why don't you start with one of your favorites?
One of the most interesting trials for me at this meeting is the MAXIMIZE trial in which secukinumab was evaluated in patients with axial psoriatic arthritis. Was diagnosed according to the clinician's opinion of whether they had axial disease. It appeared to have efficacy in this population of axial psoriatic disease patients. Maybe similar to what we're seeing with AS and non radiographic trials.
So is axial psoriatic arthritis going to be a new indication? Is that an unmet need? And there's a little bit more buzz about that.
Yeah, I think the axial to arthritis phenotypes are a little bit different than what we typically think of with ankylosing spondylitis and non radiographic disease. And we still don't really have any great consensus or definition of what it is, but we do know in a lot of patients it looks quite different. Maybe there's less sacroiliitis and more spinal, even when they've got spinal involvement, not contiguous lesions, spinal involvement bony production looks different. So I expect and they may or may not be a little bit less symptomatic.
Yep.
So I expect this population may have some differences in terms of of how they respond, and it's very appropriate to look at them separately.
Another trial.
I think we need a stronger definition of who these patients are.
I was going to say exactly the same because they may or not be different but I don't know what are talking about when we are talking about patients with psoriatic arthritis that have actual involvement. Why isn't it actual spondyloarthritis then with psoriatic with psoriasis with skin involvement? And and those trials, how have been they defined? Because you're saying maybe they have more inflammation in in the spine, but I don't think that has been measured. What has been they have been defined.
The population has been defined based on the presence of back pain. So that is a bit ambiguous and I think non specific definition. And I think if we want to study it, we need a better definition and I doubt there is a difference between actual SPA and PSA with axial involvement.
Yeah, I agree with that statement. If you look at the paper from Deepak Jaden, he serially looked at patients with axSpA SpA and also patients with psoriatic arthritis who had axial involvement. They were remarkably similar in terms of their level of pain, in terms of other findings. The only thing that was really different was the extent of radiographic bilaterality in the ankylosing spondylitis group. But I think one of the interesting aspects of this trial is that it was a peripheral psoriatic arthritis group and they had to have a bad score of greater than four and a pain score of four.
We don't know about the imaging yet, apparently they've done it, right? So this is going to be really exciting to sort of layer that over, these results, we see it. We're all waiting with bated breath, so I agree.
Do you that this is representative of all of the psoriatic axial patients? My suspicion is the ones who we are recognizing are the ones who look most like AS and they more traditionally non radiographic disease and that when we get into the phenotypes that may be less recognized, for example, the patients with spinal involvement without sacroiliitis, I think there's where we may find bigger differences.
And we might. The imaging will help us sort that out, I hope.
Yeah. But I I think it's better to first work on the definition and then look at the trials because at this moment, did any of us expect different results from this trial than the ones we got? I think not. Because if patients have actual involvement, if we know that the drug works Yeah. In actual SPA, why would it not work in patients with PSA in which it works with actual involvement?
I think it's an unmet need. Think there needs to be more research, more
Yeah. Exactly. We need a more data first.
Leanne, what do you wanna talk about?
Yeah. I'll I'll switch, pods just a little bit. The first study in non radiographic axial spondyloarthritis using an IL seventeen a inhibitor, ixekizumab, presented at this meeting showing efficacy in this population. It was a fifty two week double blind randomized controlled trial. So that's an incredibly long period potentially for placebo with the option to crossover to treatment.
But clearly showing efficacy in this group of patients with non radiographic disease. I think that's been a question. Do these patients really need to be treated with biologics or is their natural history more mild? Showing that the drug works and that these patients don't
remain in
a placebo group for the duration.
And we're talking about non radiographic action SPA with objective signs of inflammation?
Thank you for the clarification. Right, absolutely. So these patients going into that trial were required to have some amount of objective information either on MRI or by CRP, or both. And so that is typically the way we treat these patients though I think in daily clinical practice. We expect to see if there's no damage that they have some amount of inflammation.
So we have a drug now that's approved for non radiographic axial SpA and cerdulizumab, right? Yes. And now we're seeing more trials than this. Are each of you using the term and treating patients as such as non radiographic? Forget the fact we don't have an ICD DENC code for it, but do you actually do this in your clinic?
Yes. Absolutely not. We see a difference overseas, but in Europe we do that.
Chris, you? We do it, yes.
But actually to be more correct, what I do is use the term
actual SPA. I do not.
Yes. Because it doesn't really matter whether it matters for some indications for the indication of some drugs but for the patient it doesn't really matter whether it's non radiographic or radiographic but I call it actual SPA.
I want to let the panel know last year we had another panel of our austere great RheumAt ologists here in the spondyloarthritis space and, four out of five were like, no, it's really not a useful term for us in clinic. And maybe what you said is more right. They just if they have axial disease, they have axial disease and you treat it
as such.
And I think as experts,
we we see them as one patient population warranting the same treatment. I think in The US, unlike the Europe, is we now only have one drug approved. So if I label someone as non radiographic, and the payer sees that there isn't a drug approved for that, then I will get And so for me, the more appropriate term is really how I diagnose someone, not how I classify them.
That's true.
And we also know how little reliable is the scoring or the reading of the x rays and the presence of radiographic sacroiliitis. So in the end matters is whether patients have actual SPA or not. And the classification is more for study purposes than for daily clinical practice. Alright,
next trial. What do you got?
Another trial, another molecule that we have seen is bimekizumab. So it's an EL17 inhibitor, but it inhibits IL17A and IL17F with a rationale that the double inhibition will lead to more suppression of inflammation. It's a phase IIb trial. It had previously shown positive results at the primary endpoint of twelve weeks and now we have seen extension until forty eight weeks. And what we see is that patients continue showing an increase in their response more or less up to week twenty four.
There we see a plateau and then the response continues stable until week forty eight. So it's a positive trial with promising results. The phase three trial will start, so we will have to wait until we have more data to see if this drug makes it to daily clinical practice, but it's promising so far.
So Chris, you did the trial with Bemekizumab in psoriatic arthritis, what do you think of the AS data?
I think the AS data is very impressive, extremely so, as was the psoriatic arthritis data. So the idea that blocking IL-17F is
going
to add a little zip above IL-17A looks to have some validity. Obviously, Phase II trials you have to be careful of getting too excited about the data and so the Phase III are going be very informative. Think they're both underway. Know PSA is
And radiographic and actually SPA also they're also underway.
And you know despite adding a blockade of IL-17F, the safety looks pretty similar to what
we see
with IL-17A blocking agents. That's really encouraging.
Chris, do have a trial that you're excited about?
Yeah, Jack, I do. I think that we're all looking forward to additional mechanisms and therapies for treating ankylosing spondylitis axial SpA, and of course the new entry into these therapies are the JAK STAT molecule, the agents that block the JAK STAT pathway. We've seen data so far from tofacitinib and filgotinib, but at this trial there is data on another JAK1 inhibitor which is affectionately called UPA. And in this, phase two trial, they showed a very, sizable effect size using the ASAS40 as the outcome measure, and I think this is another, piece of evidence that an oral medication that focuses on the JAK STAT pathway has some potential to be a therapy for this disease. Obviously, know that Tofa is in Phase III, I think filgotinib is as well, and we'll have look for phase three data but I'm very hopeful that we'll have additional, treatment, options for our patients with axial SpA ankylosing spondylitis.
And I think I so appreciate this as well because otherwise all we have are biologic, injectable biologics, and this is a young population of patients, so having an oral option for them will be really important.
And it's also very good to have an option for patients that have extra articular manifestations and that have failed to a TNF inhibitor. We know that with IL-seventeen inhibitors we have more difficulties in treating those patients, so this may open up possibilities to treat those patients.
I agree. I'll ask
an obscure bizarre question to end. Is there a trial that any of you are looking forward to or waiting on that you think is the next big thing or is important to you coming up, but not yet ready?
This phase three trials we were mentioning? Yeah. I mean, I
think that I think what's coming, not this meeting, but, I'm looking forward to head to head
trials. Yeah.
We're all
We're as well. If we start having more options, I think it would be good to also have strategy trials. Yes.
At the end of the day, it's it's easy to show compared to nothing, but we don't use nothing anymore. And And so really what's superior becomes important.
We could question ourselves to what extent it's relevant in twenty twenty to show superiority to nothing.
Right. Right.
I'm also interested in looking at more real world data and patients with less severe disease and seeing how some of the particularly the JAKs may
perform in
a broader population of spondyloarthritis patients.
The other I'm interested in is in the Jack stat category. How much of the improvement is related to pain and how much is related to suppression of inflammation and osteitis? I think that's a fascinating question and we're going to get some answers when we have additional imaging in the future.
I want to thank the panelists for their great insights and for coming here and sharing their perspectives from the meeting. That's it from RheumNow on spondyloarthritis.
Hi. I'm Jack Cush.
I'm here
in the RheumNow booth at ACR two thousand nineteen in Atlanta. We've convened a panel of experts on gout. I'd like them to introduce themselves.
I'm Nicola Delbeth from Auckland, New Zealand.
Hi, Jack Canseagg, University of Alabama at Birmingham.
And Rob Keenan, Duke University.
Alright. So there's been a lot of presentations here. Why don't we hear from each of you what you think was a highlight presentation that either struck you or that you were involved with?
Yeah. So, well, I think for me the clinical trial that has been really interesting is Lisa Stemp's trial about tart cherries. So we know that patients often take different dietary factors or you know different supplements and there's been a lot of interest in tart cherry. It may well reduce flares, but we really haven't understood why. And Lisa's study has shown in patients with gout, tart cherry does not change serum urate levels.
So if it's if it works, it's gonna work through a different mechanism, maybe through reducing flares, I think that's really the next step. But, really interesting to see some RCT data of these, specific dietary factors.
It's been anecdotalism up to now. Yeah. That's true.
It's about time.
Yeah. We need
a study. We really do.
We need some data. Patients like the idea, you know? Yeah. And they'll buy the juice and the the extract and all that kind of stuff.
So what
is it though? Is it vitamin c or is
it just I don't think it's vitamin c.
Well, it's mechanism would be Well a weak antioxidant effect, has nothing to do with the type. It's possible. It's it's I'm sorry?
The polyphenol effect, the weak antioxidants that are potentially anti inflammatory.
I think
it must be an anti inflammatory.
It does
have a
weak COTS two effect. That's been shown in in in multiple studies. Weekly uric reserve too. But yeah.
Well, wouldn't we expect to see a a urate lowering effect in that context?
Yeah. I just don't think the studies are large or long enough to fully appreciate the relatively small effect that you might see.
And there really aren't good studies like Lisa's that are out there, to be honest. So Ken, what struck you?
Yeah. Well, I presented some data on what's called the ANIGO study. This was an active comparator looking at anakinra versus triamcinolone. We all, many of us in the gout field and many rheumatologists in general have been using some anakinra in their patients who aren't good candidates for other acute therapies such as nonsteroidals, colchicine or even glucocorticoids. The impetus is to really generate some high quality data in a real study, real well designed clinical trial that speaks to the efficacy of Anakinra.
The study was designed as a superiority study and in fact was not shown to be superior for the primary endpoint of pain measured using a visual analog scale but it looks the same. Anakinra looks the same as triamcinolone in reducing pain and in terms of a number of important secondary endpoints it actually looked a little bit better. So we're not totally sure why pain is the same but other things are better. Regrettably from a regulatory standpoint, it appears unlikely that this drug is going to move forward to approval as an indication
for
gout. Our issue in The US at least is that we're going to continue to be using it off label when we feel we absolutely need it.
But I think it's again really great to have some RCT data on Anakinra and we've also seen very similar data from The Netherlands as well with their RCT that's just been published. So, you know, sense is that at least for patients who, you know, have contraindications or haven't had a good response to the kind of standard therapies, at least we now have some clinical trial data around safety, around efficacy.
The safety looked fine in this Yep, I
mean it
makes sense, pathophysiologically, given that the is so important in the acute pathogenesis of gout and we want to inhibit IL-one as a primary biologic mechanism.
Rob, what struck you at this meeting?
So, the immunogenicity studies with peglodecase have been interesting in general and it's kind of illuminated some moist sweat. To my surprise a little bit initially, didn't think methotrexate for example would actually look like it had response that it has with these patients and decreasing potential risk for antibody development with peglodecase as well as fusion reaction subsequently or loss of efficacy in general.
This is follow-up study to what was done through open label out in the community last year and this is how many patients were in the study here?
How many patients have enrolled?
I think
there were about
10. There
was a small report.
Were some
really well designed RCTs were
on our way.
One looking at methotrexate, one looking at azathiopin. We finished a study looking at mycophenolate that I hasn't been sorted out think we're not clear what's going to be the right strategy. Maybe that all these things work. The other population that's going to be studied are transplant patients who are already on these drugs and we're anecdotally we sense that they may be less likely to have immunogenicity as well. But this immunogenicity issue with pigleticase is really the treatment limiting problem with being able to continue it for more than a few doses, particularly in our younger patients where they're more likely to have a problem and a bump in serum urate that requires you to stop the therapy.
You can't go further and you don't want to have bad infusion reactions which is what we worry about when the serum urate bumps.
So Robin, your patients who use piclodecasin, will you use a background drug like azathioprine, mycophenolate or methotrexate?
I do and I have. So I've used azathioprine and I've used methotrexate. Interesting. And I also have patients who are transplant patients who are on methotrexate. Works out Works it works out well.
What about quality of care? What are each of you doing to address the issue of quality of care in gout?
Well, think there's been some really interesting data at this this meeting about some strategies for that. I mean, it's still really difficult. I have to say one of the really interesting posters yesterday was a study looking at serum urate reference ranges and within laboratories huge differences in reference ranges. So you know, even if we're trying to treat to target these, you know patients with hyperuricemia are not being flagged that that you know with gout and hyperuricemia that we need to increase the urate levels. But I think at this meeting and over the last year or so we've seen some really exciting strategies, new systems approaches, as well as, you know, nurse led care, pharmacist led care.
So I think that we really need to look at how our healthcare system works, what the barriers are for patients, and try and address that. I think we're really starting to see that.
I think that's spot on. It's the old adage with trying to improve quality and change behavior, one size fits none. Yeah. And unfortunately our health systems are also varied.
Yeah. But I agree with you
that system approaches, using nurses, pharmacists, other non physician health professionals to help in this problem is really a promising approach. We actually have a study that we're just starting where we're going to be working from the ED in identifying people with gout in the emergency department, where we know a lot of people don't get the necessary follow-up, they don't get on urate lowering therapy and trying to do a direct to patient approach to improve quality in that way. We'll see if that works.
The other thing that I think has been really interesting at this meeting is several abstracts which have shown that when patients get admitted to hospital, their allopurinol is stopped or reduced. And so again, you know, we need to be looking at what's going on in hospitals because that's that's a really lost opportunity. And in effect, you know, it's it's even worse when you get admitted to hospitals. So it's it's a real problem for hospitalists as well as, you know, primary care.
It's it's it speaks to the battle with education and
and Yeah.
And racing the current dogma around gout and what gout is and how it works actually even to the primary care physicians, the hospitalists and really the bulk of gout patients sit in these offices with these physicians and providers and we got to this. It's always a battle to try to get the word out and disseminate the disseminate the word and how to appropriately treat and proper treat properly treat gout. And I think that goes along with everything else we've said as far as trying to change, you know, our processes, the system itself, and that's just
it's it's
a it's a uphill battle, but, you know, we're ready for it
right now. Yeah.
So what is this goutspecialist.org?
So this is gout goutspecialist.org is a network of gout specialists. Can sign up for and to as long as you adhere to the ACR guidelines as far as how to treat gout, you can sign up and be a gout specialist and gout patients can actually find your name and your office location anywhere in the country. It's only US based right now anywhere in the country to seek their gout treatment. And it's basically and you can find that through gouteducation.org, which has both physician or provider references and and sources as well as patient sources. And they they get upper range of 22,000 hits from predominantly patients on a regular basis and it's just I think a it's good source for patients and patients seem to love it.
Of course, lots of gout cartoons which my patients like and I like as well. So it's a good opportunity for both patients and providers to get additional resources as well as have their name out there as a gout specialist.
Alright, we're on the elevator ride up with the viewer. We got eight seconds each. What's the one thing you want to tell them about gout from this meeting?
Oh, I saw this amazing new therapeutic agent which looks fantastic. So this is an enteric uricase Which is stable in the small intestine and looks like it's going to act on intestinal intestinal transport and Has a urate lowering effect with an agent that is not absorbed systemically. I think this is just new mechanism of action, really exciting. It's definitely the most exciting thing I've seen in gout at this meeting.
Cool. So I know this is a gout session, but the thing we haven't talked about is asymptomatic hyper uricemia and the effects of hyperuricemia on other systems in the body. There's been a lot of interest in cardiovascular disease and hypertension. At this meeting, my colleague Angela Gaffo presented the SURFER study, which showed that allopurinol in a crossover design may actually have effects on vascular endothelium although curiously that didn't translate into direct effects on blood pressure. So more to learn about that.
GATA is associated with multiple comorbidities and other disease states as well as it's a very disabling condition for a lot of patients and it's most importantly it's curable and I think we need to get that word out
that
we can actually fix it out.
I just left Jazz Singh's poster about opioid use and trends in The United States and it's actually look, gout's low on there and it's not much of a problem, not compared to RA, OA, low back pain, other things. So thankfully, gout is not getting wrapped up in the opioid epidemic. I want to thank each of you for being a part of the panel. Thanks for
Thank you, Jack.
Thank you. Hi.
My name is Eric Ruterman. We're here with RheumNow at the ACR meeting in Atlanta. And we have a group of us here together to talk about psoriatic arthritis. Before we begin, let's give you a little more background. As I said, I'm Eric Ruderman.
I'm from Northwestern University in Chicago.
Alexis Agde, Rheumatologist, University of Pennsylvania in Philadelphia.
Jesse Walsh, Salt Lake City.
Postache, NYU Langone Health, New York City, New York.
Okay. So, the big news in psoriatic arthritis at this meeting has got to be the two phase three trials with gazelkumab. I want to talk about this a little bit but I think it's really going to be helpful to talk about what's that going to say about that pathway for psoriatic disease. Alexis, start us off by what did these trials show?
Well, they're the first two phase three studies in the P19 inhibitors, so that's really exciting. There was one trial that was completely treatment naive. The other trial had some TNF non responders or biologic non responders in that trial. So in the trial that was combined with biologic responders and treatment naive, a lot of them there was two doses tested, a Q4 week and a Q8 week compared to placebo. And in that trial, the Q4 week looked numerically a little bit better than the Q8 week, but it wasn't that much different overall.
When they split it out by TNF versus not TNF experience, they saw actually that the TNF experience people did equally well between either dose, which was a little interesting. And then in the other trial, among all treatment naive patients, the two doses looked identical. But the one caveat there was that the radiographic progression was statistically significant at the q four week dose, but not at the q eight week dose. So some interesting things to kind of grapple with in terms of dosing and how we'll use that or what what the FDA will think when that's
submitted. And and both show the drug work.
Yes.
Very effective. And I want to get into where that is going to fit for us. But before we go there, Jesse, the dermatologists are all in on IL-twenty three inhibitors. What's that about?
Well, it makes sense. Their outcomes look great. They're achieving good skin clearance with IL-twenty three inhibitors. Dosing wise, they're somewhat easier to give. Patients like the less frequent dosing than with some of the TNF inhibitor alternatives.
I think there are some hints that there may be some safety advantages, particularly compared to the IL-17s inhibitors, where we don't have to think so much about Candida or inflammatory bowel disease. I think the jury's still out on serious infection rates, but it may be a little bit more favorable with IL-23s compared to IL-17s and TNFs.
Before we talk about where these drugs are going to fit, the last thing I want to touch on, and Jose, tell me, so the dermatologists have successfully upped the ante with each round of treatments from TNF to IL-seventeen, IL-twenty three and it doesn't look like that we've achieved the same thing for the arthritis. What's that about?
Biology. It's all about pathophysiology. We have nailed down the pathways for psoriasis. As you go upstream on the molecular pathway, you achieve better and better outcomes. We're jealous.
They get passy one hundred's. Since the year 2004, our metrics have not changed. It's ACR20. Not only they haven't changed, the efficacy of these drugs are about the same. You get a fifty five-sixty percent ACR20 on the drug versus placebo.
What do we do with that information? I think one of the progressive thought approaches or thought processes is that we may be late when we treat psoriatic arthritis patients. Later in disease process, not in the patient, in the disease process. Is there room to perhaps conceive preventive trials or very, very early psoriatic disease clinical trials?
All right, so now we've got the data, we know what the skin is. I want to open this up. So this is the first. Two phase three trials that are clearly going to get this drug approved for psoriatic arthritis and we have two more drugs waiting in the wings that are likely to follow. We have TNF inhibitors, we have IL-seventeen inhibitors, we have one and eventually more JAK inhibitors, have a premilast.
Where are these IL-twenty three inhibitors going to fit in our patients?
A great question. So, I mean, think some of the easy things are that in practice we're still going to use the drugs we have first most likely and then this will be the next drug. So, most of our patients we're going to prescribe gaseoximab for probably are going be TNF experienced already because that's where it's going to come into the line. I would probably use it in a patient with more severe skin disease.
Probably avoid it in anybody who were concerned about axial disease.
What's that about?
It didn't work. The IL-twenty three data are not showing efficacy with axial disease. We haven't really specifically been studied in psoriatic disease, but in AS populations it's just not working. That probably again comes back to the biology. Maybe there's something different about these Yeah.
A little bit more synovial involvement.
That's right.
Look, these are good drugs. The p nineteens, we're not talking about a lower effect class in terms of efficacy. We gotta be careful now. Now it's about the side effect profile. Now it's about dosing.
Now it's about having a conversation with our patients, which we used to not have to do. We had methotrexate and nothing else. And then we had methotrexate plus minus a DNF, which was an easy conversation. By now, we open it up and we include the patients in the decision making.
I think we also need more studies that are going help us differentiate this because right now we just have a bunch of trials in polyarticular patients. We don't actually know anything about how to target therapies. There's a huge opportunity for this now moving I
think you're specifically referring to patients who may have lower peripheral joint burdens and more diverse phenotypes.
Right? Yeah, exactly.
Jess, you made an interesting comment, you were like, Well, we use the drugs we're sort of used to using, and I think that's important. We're creatures of habit. We get used to doing certain things, and the dermatologists have a compelling reason to use the IL-twenty three inhibitors because they're so much better for skin disease. I don't think we have that compelling reason, at least yet, in joint disease. Is that right?
Right. I mean, there's nothing really in terms of joint outcomes that differentiates them well.
Alright, let me shift gears for a minute and let's talk about another trial that was presented here at the ACR meeting which I thought was really interesting. It's a question that's come up in rheumatoid before. We haven't looked at psoriatic arthritis and that is if you have a patient who's doing really, really well, can you back off their medication? The ixekizumab study which took all these patients, put them on ixekizumab, If they got into minimal disease activity, they were randomized to withdraw the ixekizumab and just stay on placebo or stay on the ixekizumab in a blinded fashion. What happened?
Almost all of them went back up onto therapy again. So once they withdrew, they they flared. A median, I think it was about six months or something like that, they looked at over forty weeks. There were significantly more flares than people who were pulled off the drug from compared to people that were stayed on the drug. But the interesting thing is that once they restarted them on drug, you could recapture most of them, which was also interesting.
I mean, the survival curves were fascinating. Basically, you said, if you went on placebo and you waited long enough
You were gonna flare.
Your disease was gonna come back.
Yeah. Okay.
Should we not have expected that?
I expected that. We expected
that based on rheumatoid experience with TNF blockers, right? We've this before, this behavior. What we haven't seen and it's new is this easy recapture, which may have to do with immunogenicity, where TNFs do create immunogenic responses, and the 17A class is not for that. So that may be an advantage.
Although seventy percent of them were on methotrexate in the study which is really interesting to me so maybe that led to some baseline treatment that you could then make it easier to recapture some of them. Don't know.
So one last question. And I look at that study. Wish they had had an arm where they gave placebo every other dose because in RA at least, we've seen you can decrease the biologic, just you're sort of nodding your head. Mean, that's the question. You know, stopping the drug doesn't make any sense.
Wouldn't it be nice if we were able to look and cut Patients
want to do it that way. They say, Can I decrease my dose rather than come off it all at once? I think it's logical and preferred by
To close the circle on that one, going back to P19s, this is a drug that is every two months. But if you leave people off of drug for six months, fifty percent of them will remain with good skin outcome. So you could argue that frequency is one thing we should look at in other targets.
So the message is anybody out there who is involved in trial design, we'd like to see not necessarily withdrawal trials, maybe spacing trials to give us some of those answers. Alright, I think we'll wrap there. Thank you everybody for doing this. Again, RheumNow coming from ACR in Atlanta in 2019. Thanks for watching.
Hi, I'm Jack Cush. I'm here in the RheumNow booth with a panel of experts on spondyloarthritis. I want them to introduce themselves.
I'm Jack Cush in Dallas. Christopher Richland, University of Rochester.
Sofia Romero from The Netherlands.
Leanne Gensler, UCSF in San Francisco.
Jessie Walsh, Salt Lake City.
Alright. So what I'd like you to do is, why don't we just introduce some of the interesting new trials and new data that's been presented in AS and Spinal Arthritis. Doctor. Walsh, why don't you start with one of your favorites?
One of the most interesting trials for me at this meeting is the MAXIMIZE trial in which secukinumab was evaluated in patients with axial psoriatic arthritis. Was diagnosed according to the clinician's opinion of whether they had axial disease. It appeared to have efficacy in this population of axial psoriatic disease patients. Maybe similar to what we're seeing with AS and non radiographic trials.
So is axial psoriatic arthritis going to be a new indication? Is that an unmet need? And there's a little bit more buzz about that.
Yeah, I think the axial to arthritis phenotypes are a little bit different than what we typically think of with ankylosing spondylitis and non radiographic disease. And we still don't really have any great consensus or definition of what it is, but we do know in a lot of patients it looks quite different. Maybe there's less sacroiliitis and more spinal, even when they've got spinal involvement, not contiguous lesions, spinal involvement bony production looks different. So I expect and they may or may not be a little bit less symptomatic.
Yep.
So I expect this population may have some differences in terms of of how they respond, and it's very appropriate to look at them separately.
Another trial.
I think we need a stronger definition of who these patients are.
I was going to say exactly the same because they may or not be different but I don't know what are talking about when we are talking about patients with psoriatic arthritis that have actual involvement. Why isn't it actual spondyloarthritis then with psoriatic with psoriasis with skin involvement? And and those trials, how have been they defined? Because you're saying maybe they have more inflammation in in the spine, but I don't think that has been measured. What has been they have been defined.
The population has been defined based on the presence of back pain. So that is a bit ambiguous and I think non specific definition. And I think if we want to study it, we need a better definition and I doubt there is a difference between actual SPA and PSA with axial involvement.
Yeah, I agree with that statement. If you look at the paper from Deepak Jaden, he serially looked at patients with axSpA SpA and also patients with psoriatic arthritis who had axial involvement. They were remarkably similar in terms of their level of pain, in terms of other findings. The only thing that was really different was the extent of radiographic bilaterality in the ankylosing spondylitis group. But I think one of the interesting aspects of this trial is that it was a peripheral psoriatic arthritis group and they had to have a bad score of greater than four and a pain score of four.
We don't know about the imaging yet, apparently they've done it, right? So this is going to be really exciting to sort of layer that over, these results, we see it. We're all waiting with bated breath, so I agree.
Do you that this is representative of all of the psoriatic axial patients? My suspicion is the ones who we are recognizing are the ones who look most like AS and they more traditionally non radiographic disease and that when we get into the phenotypes that may be less recognized, for example, the patients with spinal involvement without sacroiliitis, I think there's where we may find bigger differences.
And we might. The imaging will help us sort that out, I hope.
Yeah. But I I think it's better to first work on the definition and then look at the trials because at this moment, did any of us expect different results from this trial than the ones we got? I think not. Because if patients have actual involvement, if we know that the drug works Yeah. In actual SPA, why would it not work in patients with PSA in which it works with actual involvement?
I think it's an unmet need. Think there needs to be more research, more
Yeah. Exactly. We need a more data first.
Leanne, what do you wanna talk about?
Yeah. I'll I'll switch, pods just a little bit. The first study in non radiographic axial spondyloarthritis using an IL seventeen a inhibitor, ixekizumab, presented at this meeting showing efficacy in this population. It was a fifty two week double blind randomized controlled trial. So that's an incredibly long period potentially for placebo with the option to crossover to treatment.
But clearly showing efficacy in this group of patients with non radiographic disease. I think that's been a question. Do these patients really need to be treated with biologics or is their natural history more mild? Showing that the drug works and that these patients don't
remain in
a placebo group for the duration.
And we're talking about non radiographic action SPA with objective signs of inflammation?
Thank you for the clarification. Right, absolutely. So these patients going into that trial were required to have some amount of objective information either on MRI or by CRP, or both. And so that is typically the way we treat these patients though I think in daily clinical practice. We expect to see if there's no damage that they have some amount of inflammation.
So we have a drug now that's approved for non radiographic axial SpA and cerdulizumab, right? Yes. And now we're seeing more trials than this. Are each of you using the term and treating patients as such as non radiographic? Forget the fact we don't have an ICD DENC code for it, but do you actually do this in your clinic?
Yes. Absolutely not. We see a difference overseas, but in Europe we do that.
Chris, you? We do it, yes.
But actually to be more correct, what I do is use the term
actual SPA. I do not.
Yes. Because it doesn't really matter whether it matters for some indications for the indication of some drugs but for the patient it doesn't really matter whether it's non radiographic or radiographic but I call it actual SPA.
I want to let the panel know last year we had another panel of our austere great RheumAt ologists here in the spondyloarthritis space and, four out of five were like, no, it's really not a useful term for us in clinic. And maybe what you said is more right. They just if they have axial disease, they have axial disease and you treat it
as such.
And I think as experts,
we we see them as one patient population warranting the same treatment. I think in The US, unlike the Europe, is we now only have one drug approved. So if I label someone as non radiographic, and the payer sees that there isn't a drug approved for that, then I will get And so for me, the more appropriate term is really how I diagnose someone, not how I classify them.
That's true.
And we also know how little reliable is the scoring or the reading of the x rays and the presence of radiographic sacroiliitis. So in the end matters is whether patients have actual SPA or not. And the classification is more for study purposes than for daily clinical practice. Alright,
next trial. What do you got?
Another trial, another molecule that we have seen is bimekizumab. So it's an EL17 inhibitor, but it inhibits IL17A and IL17F with a rationale that the double inhibition will lead to more suppression of inflammation. It's a phase IIb trial. It had previously shown positive results at the primary endpoint of twelve weeks and now we have seen extension until forty eight weeks. And what we see is that patients continue showing an increase in their response more or less up to week twenty four.
There we see a plateau and then the response continues stable until week forty eight. So it's a positive trial with promising results. The phase three trial will start, so we will have to wait until we have more data to see if this drug makes it to daily clinical practice, but it's promising so far.
So Chris, you did the trial with Bemekizumab in psoriatic arthritis, what do you think of the AS data?
I think the AS data is very impressive, extremely so, as was the psoriatic arthritis data. So the idea that blocking IL-17F is
going
to add a little zip above IL-17A looks to have some validity. Obviously, Phase II trials you have to be careful of getting too excited about the data and so the Phase III are going be very informative. Think they're both underway. Know PSA is
And radiographic and actually SPA also they're also underway.
And you know despite adding a blockade of IL-17F, the safety looks pretty similar to what
we see
with IL-17A blocking agents. That's really encouraging.
Chris, do have a trial that you're excited about?
Yeah, Jack, I do. I think that we're all looking forward to additional mechanisms and therapies for treating ankylosing spondylitis axial SpA, and of course the new entry into these therapies are the JAK STAT molecule, the agents that block the JAK STAT pathway. We've seen data so far from tofacitinib and filgotinib, but at this trial there is data on another JAK1 inhibitor which is affectionately called UPA. And in this, phase two trial, they showed a very, sizable effect size using the ASAS40 as the outcome measure, and I think this is another, piece of evidence that an oral medication that focuses on the JAK STAT pathway has some potential to be a therapy for this disease. Obviously, know that Tofa is in Phase III, I think filgotinib is as well, and we'll have look for phase three data but I'm very hopeful that we'll have additional, treatment, options for our patients with axial SpA ankylosing spondylitis.
And I think I so appreciate this as well because otherwise all we have are biologic, injectable biologics, and this is a young population of patients, so having an oral option for them will be really important.
And it's also very good to have an option for patients that have extra articular manifestations and that have failed to a TNF inhibitor. We know that with IL-seventeen inhibitors we have more difficulties in treating those patients, so this may open up possibilities to treat those patients.
I agree. I'll ask
an obscure bizarre question to end. Is there a trial that any of you are looking forward to or waiting on that you think is the next big thing or is important to you coming up, but not yet ready?
This phase three trials we were mentioning? Yeah. I mean, I
think that I think what's coming, not this meeting, but, I'm looking forward to head to head
trials. Yeah.
We're all
We're as well. If we start having more options, I think it would be good to also have strategy trials. Yes.
At the end of the day, it's it's easy to show compared to nothing, but we don't use nothing anymore. And And so really what's superior becomes important.
We could question ourselves to what extent it's relevant in twenty twenty to show superiority to nothing.
Right. Right.
I'm also interested in looking at more real world data and patients with less severe disease and seeing how some of the particularly the JAKs may
perform in
a broader population of spondyloarthritis patients.
The other I'm interested in is in the Jack stat category. How much of the improvement is related to pain and how much is related to suppression of inflammation and osteitis? I think that's a fascinating question and we're going to get some answers when we have additional imaging in the future.
I want to thank the panelists for their great insights and for coming here and sharing their perspectives from the meeting. That's it from RheumNow on spondyloarthritis.
If you are a health practitioner, you may Login/Register to comment.
Due to the nature of these comment forums, only health practitioners are allowed to comment at this time.