ACR2018 Chicago Day1 Save

Hi. You are listening to ACR two thousand eighteen podcast. I'm Jack Cush, executive editor of RheumNow. This is a compilation of podcasts from the ACR two thousand eighteen meeting in Chicago wherein you'll hear daily reports from the experts, the KOLs, and people making the news. Hope you enjoy the recording.

Hi. I'm Jack Cush, executive editor of rheumnow.com. I'm coming to you from the Exhibit Floor here at ACR two thousand eighteen in Chicago. The meeting's just going to start. The poster session's just opened up.

The Exhibit floor opens up soon thereafter. I hope you enjoy this meeting. If you're at the meeting, make sure you go to the plenary sessions. Make sure you go to the meet the professor and the great debate. Find the sessions that you like.

If you'd like to learn about what we thought was important, what our faculty thought was important, go to the acr18.roomnow.com. A lot of interesting features you'll see on our site this year, including panel discussions by experts in select areas, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and gout. And then you can also when you're looking at our page, you can read the tiles of important reports, and you'll see little talking heads, little circles over these tiles that you click on them, you'll hear audio commentary from KOLs in the field. A lot of interesting stuff here at the meeting. Make sure you follow us on roomnow.com.

Enjoy.

Hi. This is Arti Kavanagh coming to you from the ACR meeting in cold Chicago and giving you a preview of the meeting for RheumNow. It looks like it's gonna be, another meeting chock full of some good information. Things I'm looking forward to include, of course, looking at predictors. We have a lot of therapies now for our various diseases.

We don't really have a good way to pick one over the other. So there looks like some promising abstracts and presentations at this meeting that will hopefully be able to tell us how to best pick therapies for rheumatoid arthritis, psoriatic arthritis, and or other diseases. Also looking forward to the issue of comorbidity. Our patients with rheumatic diseases, and we focus on that, we treat that, but they have other conditions, cardiovascular disease, metabolic syndrome. I think we're paying more attention to that, learning more about how the disease activity interacts with comorbidity and those issues, and how to manage them all in a way to best get the patient to be as good as they could possibly be.

So looking forward to an exciting meeting. We'll have more videos. This is Artie Kavanaugh from RheumNow.

Hi. I'm Bill Scherge. I'm at the ACR in Chicago 2018, and I'd just like to talk a little bit about a, gout abstract I saw that was quite thought provoking. It went and told us a great deal about what we already know about gout or at least thought we knew, And it's nice to have some data about it. It's from, the Auckland's in New Zealand, the University of Auckland, and it's abstract number two sixty eight.

The premise of the study and the title is that changing the name may make a difference. So what is in a name? They did a study of an indigenous population of people who had a high incidence of gout and had a great deal of anxiety and guilt about their disease. And so the effort was made to change the name to Crystal Arthropathy. And they studied roughly 50 patients in two groups.

They filled out questionnaires as they were both diagnosed, one group diagnosed with gout, one group diagnosed with crystal arthropathy. And they evaluated the patients on their feelings of the disease, what they thought affected the disease, was the disease their fault, was it diet, was it heredity, was it genes, was it exercise. And as it turned out, it seemed that people with the diagnosis of gout thought it was all diet, they thought it was their fault, and they were less likely to seek medical attention because they were afraid of these things. They're also less compliant with their medications. When we look at patients that were diagnosed with crystal arthritis, these patients thought more of heredity, they viewed it more as a long term and chronic disease, and had a much healthier outlook towards treatment of the disease.

Now, I don't know if I'm gonna start calling my gout patients crystal arthritis, but I think what it does do is it gives us a further reason to let the patients know this isn't their fault. It's not all diet. It's not that extra beer you had at the ACR. It's genes. It's genes, and it's a little bit of diet.

So with that, thank you, and come to the ACR.

I'm Cassie Calabrese here in Chicago at ACR twenty eighteen. I just left the poster hall where I'm so happy to see that at this year's meeting there are over 20 abstracts on IRAEs from checkpoint inhibitor therapy, which is double the number of abstracts there were last year and speaks to the really rapidly growing pace of the field of IRAEs. There were abstracts from Hopkins, from MGH, from Spain, and from our group at the Cleveland Clinic. We described a systematic review and our experience with a PMR like entity related to checkpoint inhibitor therapy and showed that there are some atypical features and that not all cases meet EULAR ACR criteria for a PMR diagnosis, with the main reasons being they have other joint involvement, they might have normal inflammatory markers, or positive rheumatoid factor. This shows that this is a new and unique entity, which is not surprising.

If you want to hear more, come to the study group tomorrow morning at 11AM and follow us on roomnow.com.

Hi. I'm David Lee. I'm from Melbourne Australia reporting here for RheumNow at ACI twenty eighteen in in sunny Chicago. I've had the pleasure of looking on the poster floor today at a couple of the IRAE posters and there's some fascinating concepts going on out there. The first post I'd like to talk about is one from Cleveland Clinic from Casket Sandra Calabrese.

Fascinating concepts regarding PMR like disease. We still don't really know what PMR IREs, these adverse events from checkpoint inhibitor immunotherapy really look like. We're still looking at the point where we were describing them. Some of them certainly do seem to look like polymyalodramatica, A lot of them seem to. But maybe the criteria that we're trying to apply them aren't the right ones.

She looked at classical ULA twenty twelve criteria for PMR and tried to have see how that applied to her PMR IREs, and unsurprisingly, it doesn't apply well. I think that really tells us we've really got to stop trying to put the boxes that we conventionally think about classical disease, trying to put those onto onto IREs, to rheumatic IREs. We need to think a little bit more broadly. Need to think of it outside the box. The second poster was another fascinating one from Laura Capelli's group at Johns Hopkins.

We've always been uncertain what's driving rheumatic IREs. We know there's a response with there's a relationship with oncological response, we but don't know what underpins that. A lot of people have postulated whether there might be a genetic basis to that. So she's had a a look at one of the obvious things to look at, HLA markers, and but no one's done it yet, looked at rheumatic RAs and and HLA markers, and she's found some associations with some shared epitope some some shared epitopes. So really, it gives us an idea that there might well be an immunogenetic basis worth exploring as far as rheumatic ARIA is concerned.

More work needed in that area. I'm sure she's gonna be doing more in the near future, and I'm looking forward to it. I'm Dave Liu. If you need some more information, go to rheumnow. Thanks for joining us.

Hi. I'm doctor Janet Pope. I'm here at RheumNow, ACR twenty eighteen here in lovely Chicago. I wanted to talk about a very interesting study that has a lot of questions. It has more questions actually than answers.

So abstract number two zero eight in the posters, basically looks at the MISA cohort, are community dwelling people. They don't have disease, and they're studying cardiovascular risk and what happens to these patients. In women, not men, in this cohort, what they found was that if you didn't have any rheumatoid arthritis, no rheumatic diseases, but if you were ACPA positive, in the women they had more coronary artery disease, more events such as angina and other CV events. I think the questions are really threefold. Is this something seen only in women and not in men or is it a sample size problem?

Is autoimmunity itself really bad for you and there's uncontrolled inflammation that's preclinical or maybe atherosclerosis itself and ACPA are related. I think more will come in this. Thank you. Hi. I'm doctor Janet Pope here at RheumNow, ACR twenty eighteen in Chicago.

I have an interesting study to tell you about. You're gonna hear a lot at ACR about checkpoint inhibitors. On abstract number 23, a poster, they had some tantalizing ideas that if you have melanoma and you're treated with one of the checkpoint inhibitor, classes of drugs, it looks like if you make more autoantibodies, you actually prolong survival. Now that wasn't statistically significant, but it's almost like if you get that immune regulation, you're gonna have autoantibodies as an off target, but it might really mean that the tumor's getting a lot better. Others have shown this, and I think as data are pooled over time, we'll know more about it.

Thanks, and I'll talk to you later. Hi there. I'm doctor Janet Pope. I'm one of the RheumNow reporters, and it's the ACR here in Chicago 2018. I'd like to talk to you today about a Canadian study.

It's, number six twenty two on the ACR abstract number, and I have a disclosure. I'm the primary author. This is a Canadian real world study in rheumatoid arthritis. Patients had active disease and were prescribed in the real world, cirtulizumab pegol. They were on background one or more DMARDs, and when they had a treatment response of a DAS of greater than or equal to 1.2 at three or even potentially six months, they were randomized to stop background DMARDs or continue.

And this is something patients want to know the results of because a lot of them when they feel a lot better would like to get off nuisance drugs or get off drugs that they thought didn't work. The bottom line is one year later, so a total of eighteen months being followed, six months everyone on drug, background DMARDs and then randomize to stop or not. The proportion in low disease activity, a sixty some percent in both groups. The proportion in dose remission, less than two point six, forty some percent in both groups. And so there was no statistical difference.

One small word of caution is that the DAS of greater than or equal to 1.2 by eighteen months was numerically a little bit better, seventy two percent in the group that were, continuing combo therapy and sixty percent or so on the group that were randomized to monotherapy. P was only 0.3, but in general it looks like you can have the same proportion in low dose and remission, but you might not want to lose benefits so you're going to follow those patients over time. Nice talking to you again. Hi. It's doctor Janet Pope.

I'm a room reporter here at ACR two zero one eight in Chicago. I'd like to talk about a session on Sunday that was a scleroderma session, and I think there's some lesson learned. So, professor Dinesh Khanna and also Oliver Dissler had presentations in this session. And the bottom line was we looked at abatacept and found in a phase two study that there was a trend towards improvement in skin and other outcomes, but the p value was negative. There was a phase three study of tocilizumab, a big trend on improvement on skin and improvement or stabilization of force vital capacity, but the primary outcome was negative.

There was also a study with, professor Distler and Cona and others on it that looked at rheocquat and had some interesting data on skin score and also on prevention or treatment of, digital ulcers, but again didn't quite meet the endpoint. I think what this says to us is that there's a lot going on in scleroderma that's reassuring and that maybe we have to look at clinical trial design because we don't wanna damn drugs that might be positive and I think this is time to relook at our endpoints in scleroderma. Thank you.

I'm doctor Jonathan Kaye, topic editor for rheumatoid arthritis here at ACR twenty eighteen in Chicago, Illinois. Today in the plenary session, there were two very interesting presentations, one by Nick DeVries from Amsterdam who talked about dominant b cell receptor clones predicting rheumatoid arthritis development in patients with arthralgia. The presence of at least nine of these dominant clones predicted the development of rheumatoid arthritis with a ninety one percent predictive value, whereas the presence of fewer, pretty much, said that patients with arthralgia would not go on to develop rheumatoid arthritis and could be followed up three years later with another test. This is an exciting potential biomarker to predict rheumatoid arthritis development. There was another presentation by Doctor.

Iris Colmena from Montreal, Quebec, who looked at the use of a high, concentration trivalent, influenza vaccination in patients with rheumatoid arthritis compared to the standard quadrivalent vaccination and found greater immunogenicity of the high concentration vaccine, which was not affected by methotrexate or tofacitinib, hydroxychloroquine, sulfasalazine, or anti TNF agents. The use of rituximab did reduce the immunogenicity of this vaccination. So potentially for patients with rheumatoid arthritis younger than age 55, we might wanna use this high concentration vaccination. Those were two really interesting presentations in the plenary session today, both relevant to rheumatoid arthritis. For more information, go to roomnow.com.

I'm Jonathan Kaye. See you again soon.