ACR2018 Chicago Day1 Part2 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.

This is Artie Kavanaugh. I'm at the ACR meeting in Chicago right now, and I'm on RheumNow. A lot of good information here. And one way that we all get to benefit from this is sharing information. And with that in mind, I'd like to invite you to come and join us at RWCS this year coming up in Maui.

We'd love to have you here. You get a chance to digest some of the incredible amount of information that we have at meetings like this and other meetings throughout the year and share it with their colleagues and discuss. In that way, we all get to be better at taking care of our patients. So come join us, RWCS twenty nineteen. Mahalo.

So my name is Atul Devdar. I'm a rheumatologist in Portland, Oregon, Oregon Health and Science University. And I'm here at the ACR meeting in 2018 in Chicago, and this is RheumNow. And I saw today two abstracts, both presented by fellows, and both are related to the non steroidal anti inflammatory use and their effect in ankylosing spondylitis patients. And, I like them mainly because both are presented by fellows and, both actually have, potential of finding newer ideas about what non steroidal anti inflammatory drugs do in patients with Ankylosing spondylitis.

So the first one was by Jean Liu. Jean Liu actually trained with us in Portland. Now she's a fellow at University of Washington. And she was looking at the hypertension in patients with ankylosing spondylitis. And the reason why she was looking at that is because patients with ankylosing spondylitis have increased risk of cardiovascular disease.

And the question is, is it related to the non steroidal anti inflammatory drugs or something else? And she looked at it by taking the, looking at the data from SOAS database. This is a 18 hundred-nineteen 100 patient database longitudinally followed in North America. These are patients with ankylosing spondylitis. And she was looking at the use of nonsteroidals low dose versus high dose and the relationship of that with the hypertension.

And she found out that patients who have high dose use of nonsteroidals with ankylosing spondylitis have a odds ratio of two point one compared to those who use low dose of nonsteroidor. Was she's going to take this. This is of course association. So her next project is going to be looking at incident hypertension, whether taking nonsteroidors will cause new onset hypertension. The second abstract was presented by Sarah Alehashemi, who is a fellow in the National Institutes of Health.

And she was looking at the cancer risk in ankylosing spondylitis in The US and Medicare beneficiaries detection of a chronic non steroidal anti inflammatory use signature. So the question was non steroidal anti inflammatory drugs. Do they have any effect on the cancer in patients with ankylosing spondylitis? And to find that out, they use the Medicare database and they found patients above the age of 65, of course, the Medicare database, thirteen thousand of them, and compared them with about eleven million patients who don't have ankylosing spondylitis. And they compared their age and sex matched.

They were matched for age and sex, and they figured out that, patients on non steroidal anti inflammatory drug have reduced risk of esophageal, stomach, liver, pancreas, and colon cancer, whereas they had increased risk of thyroid, kidneys, and hematological malignancies. Now we know that non steroidal anti inflammatory drugs do have reduced risk of gastrointestinal malignancy in general population, but this was also found in ankylosing spondylitis patient. What was surprising was this increased risk of hematological malignancies and also increased risk of thyroid malignancies and melanoma. And that actually the answer we don't know the causality of this. She wasn't able to tease out the effect of biologics and nonsteroidal anti inflammatory drugs in this population.

I thought these both the abstracts taught us new things about the use of nonsteroidal in ankylosing spondylitis patients, and both are represented by fellows. Thank you.

Hello. This is Jonathan K from Chicago at ACR twenty eighteen for RheumNow. I just heard the great debate on hydroxychloroquine eye monitoring where Jim Rosenbaum of Oregon Health Sciences University talked about the new American Academy of Ophthalmology guidelines to use doses of hydroxychloroquine less than five milligrams per kilogram with appropriate monitoring. Visual fields and optical computed tomography to look at the retina with regular monitoring and these dosing guidelines, patients should do well, on hydroxychloroquine without developing ophthalmologic toxicity for twenty or twenty five years. Michelle Petrie from Johns Hopkins University presented the con argument where she agreed that hydroxychloroquine should be monitored, but doses of less than five milligrams per kilogram may be inadequate to control their systemic lupus erythematosus or other diseases.

She argued that with appropriate monitoring and appropriate doses of hydroxychloroquine, disease can be controlled, and ophthalmologic toxicity ought not to occur with great frequency. There are other toxicities of hydroxychloroquine, but the toxicities of the underlying disease left untreated exceed those potential risks. For more information, go to roomnow.com. I'm Jonathan Kaye. See you soon.

This is Catherine Dow reporting for RheumNow. I just got out of the great debate between Michelle Petrie and doctor James Rosenbaum. Incredible session. There were insults flung, there were great scientific data that were being presented. Doctor Rosenbaum says that you know, Rheumatologists were using such high doses of hydroxychloroquine and at what cost?

Because the twenty sixteen guidelines from the American Academy of Ophthalmology says that Rheumatologists should not prescribe more than five milligrams per kilogram per day because the risk for retinopathy after ten years of use can be as high as forty percent. So at this point Doctor. Michele Petrie was furrowing her eyebrows kind of giving him this intense like ugly look and also Doctor. Rosenbaum was mentioning you know hydroxychloroquine may not be all that safe of a drug. There's been several abstracts at this ACR meeting where he mentioned hydroxychloroquine in rheumatoid arthritis may increase the risk of atrial fibrillation, congestive heart failure, so he really cautions us that we should have more data about this medication and its toxicity.

Then Doctor. Petrie, here she is sauntering up onto the stage, very confident, confident woman knows what she's talking about in fact she says that the H for hydroxychloroquine stands for health insurance especially in this time and age when health insurance is so expensive. Anyways so she goes over all the data that's been published and in her John Hopkins lupus cohort she mentioned the risk for retinopathy after sixteen to twenty years of use in her patient population is only about ten percent. And not only that, the benefits so far outweigh the low risk of retinopathy. And in fact, we're probably under dosing.

And the reason why is because patients aren't that compliant. In young patients with lupus, only about maybe sixty to seventy percent of them actually take their medicine. So that means a non compliance rate of thirty percent. And in other studies, compliance rates can be as high as fifty percent. And she suggests maybe we should measure blood levels of hydroxychloroquine because that's the only way of knowing whether or not our patients are taking it and if the levels are She also expounds on the benefits of hydroxychloroquine including decrease in thrombosis, improved survival, decreased cardiovascular mortality, benefits in pregnancy.

So there's just so many great benefits related to hydroxychloroquine. She also mentioned that what and this is the point that I really love she says you know, in the guidelines of the American Academy of Ophthalmology, it says that one of the risks for retinopathy is combination Tamoxifen plus Hydroxychloroquine. But heaven forbid, if we ever tell the ophthalmologist to lower the dose of tamoxifen or to stop tamoxifen, right? And why? Because we're worried about the risk for cancer recurrence but yet you know we say nothing to the opposition, quote quote the opposition, particularly when they say lower your dose of because of risk of retinopathy.

Well why would we do that? Because you know, that's like if we lowered the dose of hydroxychloroquine the risk for death, thrombosis is high. I mean cancer recurrence, death, thrombosis, come on. So clearly in my mind Michelle Petrie had won the debate. Take home point actually is actually very interesting.

She also mentioned that there's a new that is an anti malarial that has the benefits of hydroxychloroquine without the ocular toxicity or the retinal toxicity and that's desethyl hydroxychloroquine. So that's a drug to be looked for. Towards the end of the debate, Doctor. Rosenbaum tried to do his best to rebuke her claims by saying, well can you explain about the cardiovascular risk such in RA? Well I got to remind you, number one, this debate is on lupus and use of low dose hydroxychloroquine and number two is these are abstracts, we need more data and what's interesting when I was tweeting the debate was that somebody from Denmark tweeted me back with regards to his claims about cardiovascular risk, hydroxychloroquine and rheumatoid arthritis saying that actually in their study they found that the risk, the cardiovascular death risk for RA patient actually is lowered if they're on hydroxychloroquine.

So food for thought, I still believe hydroxychloroquine is a very important medicine in the management of lupus and I still will use doses that may be a little bit higher than five milligrams per kilogram. This is Catherine Dow reporting.

I'm Kelly Cron, RheumNow, and Jack Cush have asked me to talk about what things I've learned about bone. Although I'm a rheumatologist, I do about ninety five percent metabolic bone disease. I work in a very large academic orthopedic practice. So the rheumatology meeting has always been a little slim on metabolic bone and osteoporosis. One of our colleagues, Oscar Gluck, many years ago became a strong advocate to get us more bone content at the ACR meeting.

We lost Oscar about fourteen years ago, but through his family, his friends, and the ACR, we now have an Oscar Gluck memorial lecture every year. So I attended today's Oscar Gluck memorial lecture. It was done by, doctor Rosen from Maine. Doctor Rosen is an endocrinology bone expert, a basic scientist, and what he understands better than anybody else I know is the role of fat cells, adipocytes. And what I've learned from Doctor.

Rosen over the days and today I learned even more that fat cells, adipocytes, have the potential to become osteoblasts or mature fat cells. And there are things that can change their trajectory, and there are some drugs that change their trajectory. For instance, pulsatile PTH pushes them to become osteoblasts. On the flip side, they make a lot of rank ligands, so fat cells in the bone marrow are actually significantly impacted when we give the antibody to rank ligand known as denosomat. So what we learned from doctor Rosen today was fat cells are really important.

They're important in the genesis of osteoblast cells, and they're probably also very important to the response to our pharmacological treatment for people with osteoporosis. I would urge you to get online and and and review doctor Rosen's lectures, doctor Clifford Rosen. It was the Oscar Gluck Memorial Lecture, and I think we can you can learn a lot. I wanna prompt a little bit about tomorrow. Tomorrow, there's actually a couple of good sessions, and I'm gonna cheat and use my phone.

At 02:30 tomorrow afternoon, Ken Segg is talking on complications of osteoporosis therapy. I think this is really important so that we have a better understanding of up to date insights into how do we continue or stop treatment, etc. And then at 03:15 in the same session, Susan Ott from Seattle, is just an expert bone biologist, she's talking about bone issues in complicated patients, which would describe about eighty percent of patients in a rheumatology office. So, yes, there's lots of bone here. We'll do our best as a bone editorial team to post about it and give you daily updates.

Thanks very much,

and enjoy your meeting at the ACR.

I'm Nicole and we're here at the ACR National Conference in Chicago in 2018. And I'm here with, Dana Dempsey and, Alex Hernandez and I'll let them we're going to talk today a little bit about, camps for children with, rheumatic diseases and so I'll let them, introduce themselves and tell us a little bit about themselves first.

So hi, my name is Alex Hernandez. I am one of the nurses at Texas Scottish Rite Hospital and I serve as the nursing director for Camp Joint Adventure.

Hi, my name is Dana Dempsey and I'm the director of therapeutic recreation at Scottish Rite.

So we are very excited to come to you to talk to you about camps for kids with rheumatic disease. We are here at the twenty eighteen ACR ARHP meeting, where we get to really share ideas with physicians, with nurses, with different subspecialties that come to visit with us. We are concentrating on just sharing the wealth of information that we've collected regarding how to take care of our kids in a very holistic manner. So we definitely want to make sure that they're physically able to do camp, we also want to make sure that they're that we're meeting their psychosocial needs, that they may not be able to have met close to home either because parents are really busy or they just don't have an outlet for activity.

Tell us a little bit about just what camp is and what you see as the benefits of camp for children with rheumatic illness. Sure.

Well at Scottish Rite we've been running a camp called Camp Joint Adventure for over twenty five years and it services patients of the hospital seen through their rheumatology department. We generally take around 80 children each year to camp for a week at a place called Camp John Mark. Oh, and the benefits, they're endless. They're amazing.

They're very very awesome. Actually have a group that we work with that whose main motto is challenge by choice so where parents may be a little hyper vigilant the kids can actually go out to these camps and say, I want to try that. And they don't have someone in the background saying, you probably can't do that because of your your JIA. Or maybe we'll try that next time knowing full well that they probably won't let them do that.

So children get to have a chance to run and play, ride horses, do archery, play with a ropes course, swim, just all kinds of arts and crafts. And there are not only physical benefits, but they get to be a part of something larger than themselves. They also get a chance to meet other children and make friends. In fact, that's probably one of the largest things that we hear from the children, and that is, I got to just have fun, or I got to meet other people who were like me so I didn't feel so strange.

To share. Yeah. Camps that have rheumatic disease and how to go about, sticking to guidelines, but then ensure that the kids have what they need when it comes to activities and and, just coordination. Yes.

So you may be out there asking yourself, how do I start a camp? And there are a lot of resources through the American Camp Association or the Camp Nurse Association that provide a wealth of information on their websites, not only about how to start a camp, but then also if I already have an existing camp, how can I make good even better? So you have the opportunity to polish and be able to address some of the trends, make sure that the programming is right, check-in to the standards, also that the children have a wonderful experience.

Well that sounds like a wonderful opportunity for kids and I'm here with the room now and if you guys have any more questions you can check us out online. Thank you.

Thank you.

Good morning, everyone. I'm Olga reporting from the annual ACR meeting here in Chicago. I wanted to share findings of the abstract presented by research group from Hong Kong. The abstract number is two one two, where the researchers evaluated mortality of patients with inflammatory arthritis over time. They took three groups of patients, ankylosing spondylitis, psoriatic arthritis, and rheumatoid arthritis patients, and evaluated their mortality rates in the last twenty years, and also mortality by cause.

In this study, they showed that overall mortality decreased significantly in the last twenty years in patients with the bowel conditions, and the most significant decrease was in cardiovascular mortality. Unfortunately, in all three study groups, mortality from infection increased over time and still remained high. It is unknown if infection related mortality is linked to the more aggressive treatment with biologic therapies. I guess future study will be needed in this regard, but at least we know that overall mortality trend is improving with new treatments. Thank you for your time.

And if you want to learn more, please follow us on RheumNow.

Hi. This is Paul Supka coming to you from ACR twenty eighteen in Chicago. Just earlier this morning, I came out of the urine review presentation. And one of my favorite studies, from 2017 was described there, is the CANTOS study, where they looked at the use of canakinumab, which is an interleukin-one blocker receptor blocker for the prevention of recurrent cardiovascular disease. These were non rheumatologic disease patients, so they selected patients that had an elevated, C reactive protein, and the result was that using canakinumab over the course of, I believe, two years reduced cardiovascular events and all cause mortality.

So this is super exciting because it's a new target for cardiovascular disease. One thing to stay tuned for will be that there is a trial that should be presented fairly soon, probably from a cardiology conference perspective, where they looked at methotrexate with a very similar patient group. It was actually a trial that was ended early, we don't know the results of that, but inflammation looking like a really, really big target in rheumatology and in patients with cardiovascular disease. For more information, stay tuned on roomnow.com and we'll what we find out. Thanks.

Okay, hi I'm Doctor. Rachel Tate and I'm coming to you live from ACR 2018 in Chicago, Illinois And I just attended an amazing plenary session, and I'm going to tell you a little bit about Abstract eight thirty six. So we all know that the time from disease onset until diagnosis for AS is about eight-eleven years. And we also know that early intervention helps with disease outcomes for our patients. So this study actually looked at early intervention, using genetic risk scores, or GRS, using genome wide SNPs.

So what I want you to know is there were 700 or pardon me, seven 7,500 patients of European descent with known AS and six thousand patients who had AS of East Asian descent. And what the what they actually looked at, they compared the genetic risk scores, GRS, compared to normal healthy controls with these patients. And they actually found that the genetic risk scores were more sensitive and more specific than HLA B27, and they were at least as good as MRI results. So, and that was using area under the curve calculations. So, it seems that genetic risk scores may actually be useful clinically.

And since a microarray for SNPs is actually under $50 it's less expensive than an HLA B27 as well as an MRI. So hopefully there'll be a few more studies on this determining if genetic risk scores are actually effective for us to use clinically. But at this point, this is promising information. So check us out on RheumNow and follow us on Twitter at RheumNow and ACR2018. So more coming to you soon.

Thanks. Hi, I'm Doctor. Rachel Tate coming to you live from day one of ACR twenty eighteen in beautiful yet a little bit chilly Chicago, Illinois. So I wanna tell you something that's really, really exciting today that I learned in the MACRA and MIPS update. So number one, and this is just a little bit of information.

There's a lot more coming. So check us out on at roomnow.com. But because of you and your advocacy, the, payment adjustments will not apply to Part B, drug costs in 2019. This was a huge effort on part of the ACR and by individuals as well as a team effort in general. So why that's important is there are lot of proposed changes from CMS coming down the pipeline and we need to be aware of them.

So there are three things that I really want you to focus on for 2019. Number one, make sure that you are eligible. Go to cms.gov to make sure that you enter all of your information and make sure you have to actually go through the MIPS process this year. Number two, consider using the RISE registry. If you are an ACR member, you do not have to pay the fee for RISE this year, so make sure you're looking into that.

And also, you may get a potential bonus for your patients. So that's huge for us. Another bonus potential is that if you are using a twenty fifteen EHR that meets the twenty fifteen criteria instead of 2,014, you may actually get a 10% bonus. So these are just three things that I want you to remember for the macro and MIPS changes coming up in 2019, which affects all of us from solo practice to academics. So if you have any further questions, please see the ACR, especially if you're here.

Come by the booth at RheumNow. We are at C 12 location this this particular at ACR in Chicago. And also check out roomnow.com for further live updates, and check out ACR eighteen. We'll see you soon.

Hi. I'm Sam Whittle from Adelaide, South Australia, I'm here at ACR twenty eighteen in Chicago. I've been in the poster hall today checking out some of the posters looking at imaging in spondyloarthritis. There were a series of really interesting posters and I want to bring you three take home messages that I got from these. Most of this work is by Walt Maximovich and his colleagues and it's looking specifically at the role of MRI in the diagnosis of axial spondyloarthritis.

The first take home message is in regard to the role of active lesions on MRI such as bone marrow edema versus structural lesions such as erosions or fatty lesions. What we learned from one of the posters is that at diagnosis, bone marrow edema or activity lesions tend to be more specific but the structural lesions tend to be sorry the bone marrow edema tends to be more sensitive but the structural lesions tend to be more specific. The interesting thing is that if you follow these people over time the diagnostic performance of the lesions doesn't really change but the specificity and the overall diagnostic performance of the structural lesions improves over time suggesting that as patients accrue more damage, specificity of MRI structural lesions becomes even higher. The second take home message looks at local readers of MRIs versus central readers of MRIs, that is slightly less experienced radiologists versus radiologists with a particular interest in MRI diagnosis of spondyloarthritis and not surprisingly they found that the local readers were slightly more likely than the central readers to overcall the presence of bone marrow oedema in early axial spondyloarthritis, suggesting that as we become more experienced in reading MRIs we become a little bit more discriminating in what we call a real or important bone marrow oedema lesion.

The third take home message is looking at the performance of plain x rays versus T1 weighted MRIs to look at structural lesions in axial spondyloarthritis. We've long known that x rays have pretty poor diagnostic performance but they're still really important to our day to day diagnosis in the clinic. This study looked at patients who had T1 weighted MRIs and x rays in the same patient and compared their structural findings. Interestingly enough there was pretty poor agreement. The capital was only 0.39 and indeed fewer than half of the x rays that were reported as meeting the modified New York criteria for sacroiliitis actually showed any structural change on the T1 weighted MRI.

So I guess what that means is that either the x rays are much more sensitive modality than MRI, which they're not, or x rays really are not a very good diagnostic tool. So what do we expect in the future? Well we expect to see the rise and rise of MRI as a tool and perhaps we expect to see the demise of plain x rays. So if you want to learn more about this and everything happening at this meeting, don't forget to go to roomnow.com.

Alright. So I'm doctor Bittancourt, here we are at ACR in Chicago in 2018. And I'm here with doctor Mark Goralek, who's associated with the Baylor College of Medicine, the Texas Biomedical Research Institute, and Children's Hospital in San Antonio. And he has some really interesting research that he's gonna present later today on Kawasaki's and Anakinra. So thank you for being with us.

Thank you. Doctor. Gorlick. So tell us a little bit just about the importance of studying Kawasaki's and how you came about looking at the IL-one receptor inhibitor.

Kawasaki disease is a disease of childhood. It's a disease where kids get fevers and a couple of other clinical signs and symptoms and then develop heart damage. And specifically the kind of heart damage they can develop is aneurysms in the heart but also scarring in the heart. And it actually is the number one cause of acquired heart disease in children in the developed world. That used to be rheumatic heart disease, but now it's Kawasaki disease.

So it is just for that reason alone, it's important to study. And what we're really trying to do is make this disease more treatable. So currently the treatment, is via something called IVIG which is a kind of a infusion of antibodies and this helps to treat about three quarters of the patients who have heart damage but another quarter of the patients who have heart damage still have persistent disease. And so there's a couple of, investigators around the world who are looking at other modalities to treat this disease and one of the modalities is, IL-one which is, interleukin one which has been found to have, an important role in inciting the initial inflammation in this disease. And so I work in collaboration with, a gentleman named Moshe Arditi who is at, Cedars Sinai Hospital in Los Angeles.

He is one of the pioneers in this area looking at the role of IL-one and together with him we were looking specifically wanted to ask a question, can we treat, Kawasaki, the mechanical dysfunction of the heart that occurs within Kawasaki with this drug Anakinna which is an IL-one blocker. So what happens in Kawasaki disease is not only is there this inflammation and damage to the heart but the heart also doesn't beat as well during the, acute part of the disease. In a small portion of patients it's potentially possible that later on down the road they may have more damage and more fibrosis due to this. We wanted to look at this and to start off looking at this we looked at it in a mouse model of the disease. So we give the mouse what looks like a kind of a Kawasaki like disease and, they develop very, very similar features.

And one thing we wanted to do first is just look, do these features of Kawasaki disease, the not pumping so well, and another feature that occurs, the swelling of the heart. Do these things also occur in the mouse? And they do. And then we wanted to see what if we treat these mice now with anakinra, can we stop those features from happening? And we can.

And so that really helps to validate the use of anti, this blocking therapy, this IL-one blocking therapy for Kawasaki disease, in potentially in humans. And then something else that we saw was also were able to kind of slow block a lot of the subsequent fibrosis or scarring that happens. So I think from here, you know, there is already quite a bit of, data from Doctor. Arditi and some others on the role of IL-one in Kawasaki disease but we're helping I think to broaden the, the idea that this drug is useful, applicable and maybe one of the those kind of drugs that we can use to help treat that quarter of patients that is currently beyond treatment.

Well, sounds like very promising, therapy in the horizon and, we're looking to learn more about

it.