ACR 2019 Day 2B Save

Hi. I'm doctor Jack Cush, and this is the ACR 2019 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, everybody. I'm Mike Putman reporting for RheumNow from ACR twenty nineteen. I want to talk about an exciting presentation I saw this morning on the 2019 guidelines for the management of giant cell arteritis. Three things in particular I wanted to highlight. The first one I think is going to be somewhat controversial.

They recommended temporal artery biopsy over temporal artery ultrasound for the diagnosis of GCA. I know our European colleagues are especially enthusiastic about temporal artery biopsy or temporary ultrasound and it's something that I myself use especially in patients who have what I consider to be a high pretest probability. The second thing that they recommended that is something I've been doing in my practice and have been advocating for is leading with tocilizumab upfront. The GIACTIA study to me was convincing that this is a steroid sparing agent that's good for our patients and the new ACR guidelines reflect that. It's interesting because that's actually not what the EULAR guidelines recommended.

They recommended a different approach up front for patients with giant cell arteritis. And last but not least, they did recommend large vessel imaging, which I thought was interesting. That's something that I have been doing in patients who have symptoms, but I think they're emphasizing the fact that a lot of patients who have large vessel imaging wind up getting missed. Very interesting guidelines and some that I think will be very useful for all of us who treat giant cell For more information, please go to the website at roomnow.com.

David Lu here for RheumNow from ACR twenty nineteen here in Atlanta, Georgia. I'd like to tell you a little bit about an abstract I saw yesterday Hepatitis C related cryoglobulinic vasculitis. It's been a big problem and been the most common cause of cryoglobulinic vasculitis in the last few years, but with the introduction of directly acting agents in Hepatitis C, it's changed the game. Patients now often, overwhelmingly get sustained viral remission and get cured of their hepatitis C. Question of course is, once you get cured of your hepatitis C, do you get cured of the vasculitis that comes along with it?

And so a large cohort of ten nineteen patients from four different registries looked at this. Two registries from Egypt where there are very high rates of hepatitis C, France and Italy as well. So looking at those patients, all of those nineteen patients who had cryoglobulin vasculitis related to hepatitis C were all cured of their hepatitis C by those directly acting agents, but eleven percent of those still had flares of the cryoglobulin vasculitis even after the cure of their hepatitis. This really reflects other data which has suggested in the past that even if you've had a cure of your hepatitis C, if you're in sustained viral remission, you can still have de novo vasculitis as well, which is a scary prospect in itself. So just one to be alert too, once you cure the hepatitis C, doesn't mean that you cure the vasculitis that goes along with it.

For more information about ACI twenty nineteen, go to roomnoww.com, and I'll see you soon.

Hi, Elaine Husney from Cleveland Clinic. Welcome to ACR twenty nineteen. I wanted to talk about, a presentation on psoriatic arthritis outcomes and remission rates. This, was from one to 02:00. Please check out RheumNow for more details.

We are focusing on domain strategy. So what does that mean? So in psoriatic arthritis, it's such a heterogeneous disease that we need to really rely on the domains and what I mean by that is looking at enthesitis, dactylitis, peripheral joints, as well as the skin. So the better we can monitor these different domains, better we can understand how to use these treatment options. We spent an hour, Phil Meese and I will be talking on domain strategies and treatments, so really highlighting what to do and not being afraid that patients can fall between domains and you may have to treat with different treatments based on the domain that's affecting them the most.

So please check out Domain Strategies in psoriatic arthritis and check out RheumNow for more details.

This is Doctor. Catherine Dow reporting for RheumNow. I'm at the ACR Conference in Atlanta, Georgia and I am in the presence of royalty and yes this is Doctor. Gwen Mountain and she is the President of Lafayette Clinic and not only that Vice President of the Association of Women in Rheumatology. So welcome Doctor.

Mountain. Thank you so much. And can you tell me a little bit about AWIR Aware?

The Association of Women in Rheumatology was begun about five years ago, but the idea occurred ten years ago when we looked around our college and saw that the college was pink, but the leadership was blue. And we decided to make everything purple.

I love that. And what exactly are the goals of, the Association for Women in Rheumatology?

So it's interesting. The association is comprised of not only women, but men that also support us. It's a society that allows women to lead will help the whole society. So what we're doing is trying to empower our ladies to be leaders, to advocate, to do some work life balance so that we can all take better care of our rheumatic patients.

Tell me about some of the successes that your association has accomplished.

So we've been very, very proud in that our growth has not only been national, local, it's also been global. So we're very proud now we have about 30 local chapters around Continental US and we've expanded globally with Brazil, Puerto Rico, Pakistan, Bangladesh, India and we have partnered with The Caribbean as well as Italy which we're going to go to next week to help support those ladies in rheumatology. Oh my gosh that's amazing and so global and just and tell me about like what do you

think the future holds for women?

It's very interesting that should ask that. It's very important that we realize that half of the human race is women, and we can and will conquer the world. But we're gonna need support, and we're going to have to be recognized for the value that we bring to society and most importantly to our rheumatic patients. What our concern is is that as we grow in our specialty that we won't be valued as well and this has to be addressed with the equity of pay that many of us are working on including the Association of Women in Rheumatology.

So if you had to give one bit of advice to our female rheumatologists, especially those who come out of training because you know it's like I remember when I came out of training I was a little bit timid not sure you know am I going to choose an academic career, a private career and it was so overwhelming And but I've had such good mentors. So what kind of advice would you give to these young female trainees?

The first thing I would do is make absolutely certain that I understand what my priorities are. If you want to have a flexible schedule, not be held down by a hospital system, you may want to try a flexible schedule in a private practice situation if you could find one. Practice. If you're interested in academia and want to pursue research interests, then you may in fact want to stay at the academic center, but realize that you have to, be allowed to be who you are and to actually get the kind of support that's needed just like your male colleagues in the academic center. If you want a flexible job in a hospital setting, go and find out if the flexibility can be transferred properly and look and see how you're going to meld all of that together with your domestic responsibilities.

Thank you so much for that. I mean, it's amazing advice. And you heard it first here at RheumNow. And you know what, Doctor. Melton, Jack Cush has been really itching to join the AWIR and you've heard Doctor.

Melton says men are welcome too. So this is Doctor. Catherine Dow reporting for RheumNow Come visit us on rheumnow.com. So this is Doctor. Catherine Dow reporting for RheumNow at the ACR twenty nineteen meeting in Atlanta, Georgia.

So I just gotten out the session that reviewed the draft guidelines for arteritis. And so the three types of arteritis vasculitis that were reviewed included GCA, included Tachyasiast arteritis as well as polyarteritis nodosum. And so some of these guidelines actually opened up doors to more questions that weren't necessarily answered by the guidelines committee but I'm just going to give you highlights of what I learned and what they recommend. For the first thing, alright if you're going to diagnose GCA in a patients that you have high clinical symptoms get a temporal artery biopsy bypass the temporal artery ultrasound. Okay so if you have a choice do that.

If you have a choice do just a unilateral biopsy and if that's negative your suspicion is high then go for the bilateral. And then when you tell the surgeon the biopsy you need at least one centimeter of temporal artery length. Okay, anything below that it's you're probably because it skipped lesions may not be able to make a diagnosis. And not only that they do recommend now this is the part that's important a baseline non invasive extracranial evaluation of the large vessels. So now this is where the guidelines committee specify of what right so they were saying of the aorta but do you use an echo do you use abdominal ultrasound CT angio what Alright that wasn't clear at all.

Okay so how do you go ahead and treat right? So the recommendation is immediately start them on high dose steroids so high dose steroids meaning a mg per kg per day of prednisone up to eighty milligrams a day with tocilizumab. Alright? And it doesn't say do they favor q week tocilizumab versus q two weeks, tocilizumab or IV tocilizumab. So and then for cranial ischemic temporal arteritis, then you really need a pulse with IV glucocorticoids.

That we all know. For extracranial complications, they can you can consider adding methotrexate if they're still having disease in patients with tocilizumab and also on glucocorticoids. And then this is the part that a lot of us found confusing because in the audience, evaluation and questions there were so many questions about this but they never answered it. It says here that if surgery is required, you need to perioperatively give them high dose steroids. So complications from GCA, surgery required for vascular complications, give them high dose glucocorticoids.

So why? We don't have the data presented on that. And then for patients who relapse when off of all therapy, can go ahead and use methotrexate with tocilizumab who have cranial symptoms without having to go back on glucocorticoids. Optimal duration of glucocorticoids, optimal duration of these non glucocorticoid therapies have not been established and has not been recommended and if patients have already been in remission for a while consider long term monitoring so that's every three to twelve months. Right?

Alright so let's talk about the other arteritis and vasculitis. So with regards to the other one let's look at Takayasu's. So with Takayasu's arteritis what they do recommend is using non evasive imaging over catheterized imaging. They also recommend high dose glucocorticoids just like

in

GCA but they say do not use tocilizumab. If you're going to do anything use a TNF inhibitor or a non biologic DMARD as methotrexate, azathioprine, leflutamide or, mycophenolate. None. None was presented. Dose?

Not presented. Duration? Not presented. Not sure. Alright, monitor the disease every three to twelve months if they're in remission and get imaging study every six to twelve months and labs must include inflammatory markers.

Which one? Didn't say. Alright imaging options that, was presented is on my Twitter feed so you can go to kdau2011. Alright keep going here sorry patients in remissions six to twelve months, you need to go ahead and taper off the steroids. The goal is zero steroids.

For asymptomatic imaging progression, observe. Don't do anything. For worsening limb ischemia, increase immunosuppression rather send them to surgery. For asymptomatic inflammation in a new vascular territory. So these patients have new involvement but they're asymptomatic.

What do you do? Alright, if it's rapidly progressing, if it's a new area, go ahead and increase your immunosuppression. And again, this is where I don't understand where the data is coming from but they recommend periprocedural high dose steroids if patients have to undergo surgery for a complication. So you know that stenosis or that ischemic, cranial involvement if they're going undergo surgery really bump up their steroids. Alright so let me go ahead and talk about, polyarteritis nodosa.

Alright, so these are the drafted guidelines recommendations. If you have, skin involvement do not get just a superficial simple skin punch biopsy. You need to do a deep skin biopsy. You want to go ahead and see if you can get the nerves. He also mentioned you can do a punch within a punch so you do an initial punch biopsy then you go even deeper.

That actually has pretty good yield is what he says. Let's say a patient has foot drop. Alright, you have the choice of getting a nerve biopsy or a nerve and muscle biopsy. Get both nerve and muscle biopsy. And then for patients with abdominal symptoms, use abdominal vascular imaging for diagnosis and also to gauge the extent of disease because people who have visceral involvement basically have an increased mortality over five years.

For active severe disease, this is where it's important here, you give IV pulse steroids and oral cyclophosphamide two mg per kg per day. Alright, they didn't say and that's a recommendation over rituximab or any other, biologic or non biologic DMARDs like Rituxan. Now for patients who have rapidly progressive disease, renal disease, they really don't recommend plasmapheresis or plasma exchange. Now the goal is to be off of all steroids by six months. Also patients who decline cyclophosphamide, you could go ahead and use one of the other steroid sparing agents such as methotrexate, but they really didn't go into a lot of detail what some of these other non steroid sparing agents are or the dose.

If the patient's in remission after eighteen months, stop all of your medications. Usually this could be a self limiting disease. Now let's say a patient presents with foot drop or some neurologic manifestations, do serial clinical neurologic exam. Don't go for serial EMG nerve conduction study because your patients probably won't come back, right? And then physical therapy is recommend for patients with weakness and deconditioning.

And then for non severe disease, they did say that you don't have to necessarily go immediately to cyclophosphamide but a non glucocorticoid, non biologic medication. And then in patients who've had abdominal involvement go ahead and do follow-up serial non invasive imaging. And now there's one more thing that they added to this guideline that I thought was really cool. Alright, patients who have the ADA2 gene mutation. So these patients are DATA2 deficient, right?

And if you have that, in a PAN patients, these patients are at high risk for stroke and so you really want patients who present with stroke, high suspicion and PAN, check them for, DATA2 deficiency. Okay, so I had posted all these in my Twitter feed, so I hope you'll check them out. Also, more information, to roomnow.com. Doctor. Catherine Dow.

This is Doctor. Arty Cavanaugh coming to you from ACR twenty nineteen for RheumNow. A lot of stuff going on at the meeting. Just came from a session, the FDA session, which has been a it's been a tradition now. We've had it for a couple of years.

The FDA sends their officers, great folks, rheumatologists who come to talk to us, this year they talked about some of the newer data on safety, of course very important, some updated information that resulted in changes to the labeling. For example, thinking of the VTE risk for the Jakinibs and some other important developments. New drug approvals and that's been proceeding really apace. A lot of new action in rheumatology and of course that involves the FDA very deeply. It's really nice to hear their input into how they approach drug approvals and things like drug safety and also some other topics like the pediatric considerations.

It's been amazing. There's been such progress in the availability of agents for pediatric rheumatology, which is great. Certainly serves a big unmet need, and that's really a dynamic area where they're thinking about study design and extrapolations and other novel methods to continue to bring new treatments to our pediatric population. The FDA session, a great session at ACR, one of the many exciting bits of information going on here. This Arti Kavanagh from UCSD talking for RheumNow.

Hi, I'm Cassie Calabrese here at ACR twenty nineteen in Atlanta, day two. I just left the poster hall and found one poster. Well, were many interesting ones, but one particularly, caught my attention. That was from my institution, the Cleveland Clinic, looking at vasculitis, in the setting of hydralazine, a kind of poorly understood, topic. This was done by Rula Hajali and two of my trainees, Sajah Almeda and Kananah Yasin.

It was abstract number sixteen sixty seven. Hydralazine is a commonly used blood pressure medicine that we know can cause a lot of problems for us in rheumatology. We know up to seventy percent of patients can have a positive ANA and vasculitis is a complication. So what they did, it's a retrospective study, spanning over fifteen years at the Cleveland Clinic, found twenty three patients who were diagnosed with vasculitis in the setting duration of being on hydralazine was thirty four months with the shortest duration being five months. They found that one hundred percent of these patients had renal involvement, renal vasculitis, with a variety of other organ complications including lung and skin.

A hundred percent of patients were ANCA positive, mostly PR3NPO. Ninety percent of patients were ANA positive, and a large proportion of patients had positive double stranded DNA and anti histone antibodies. There were thirty months median duration of follow-up. There were no relapses. This is the longest looking at the longest duration of follow-up.

Very interestingly, they had very poor outcomes. The vast majority of patients had chronic kidney disease, and there were three vasculitis related deaths out of those twenty three patients. Patients were treated with high dose steroids, some received cyclophosphamide and rituximab. Certainly, not to be forgotten, these complications of hydralazine and probably a blood pressure medicine that we should be avoiding if we can. For more, go to roomnow.com.

Hi. Elaine Husney from the Cleveland Clinic. Welcome to ACR twenty nineteen. Just wanted to highlight, an oral, abstract presentation this afternoon, from 02:30 to four, abstract number seventeen eighty nine in the cell trafficking, section. A little more of the basic translational science.

As you know, biologic therapies have really revolutionized our treatment for psoriasis and psoriatic arthritis, but only forty percent, up to forty percent actually don't respond. So we need to be better at personalized care rather than the trial and error. So this particular, oral abstract is going to focus on, having a personalized therapy. We're looking at specifically a mechanism of TNF R2 pathway. It's a DNA variant.

We're hoping that we're going to look at a defect myosin. Hopefully, genotyping this type of polymorphism could really help optimize who we should start TNF therapy first. We're looking at something that can help with TNF responsiveness.

Hi, my name is Philip Robinson and I'm coming to you from Atlanta, Georgia at the ACR meeting in 2019. I'm from Brisbane, Australia and I've come back from Desiree Van de Heide's talk on non radiographic axial spondyloarthritis for M001. Desiree went through a case, and then she emphasized the importance of not using the ASAS axial SPA criteria to make a diagnosis. She emphasized that because that's not how they were designed to be used. It's important that you take a good history, you look at the different factors, you look at the laboratory values, and you look at the imaging and you make a diagnosis based on that.

She also emphasised through a number of studies showing that the burden of disease in non radiographic axial SPA was the same as ankylosing spondylitis. So essentially contributing to the conclusion that this is one continuum. And we see that looking at disease activity based on clinical trials as well because the trials using cerdulizumab used across the range of disease and we saw response rates that were the same. So I think we should think about axial SpA not as two diseases as they have evolved to be thought about but as one disease. And I suppose the last major point to think about is the importance of imaging both for diagnosis but also in the right group.

There are certainly emerging studies showing that a huge percentage, up to eighty for example, of women who have just delivered babies have positive MRI scans, sacroiliac joint MRI scans. So it's important that you think about who you're imaging and that they make sure that you're imaging in the right clinical context, those who have a high probability of having the disease. If you do that, then you're not going to go wrong when you're making the diagnosis, and you're not going to go wrong when you're thinking about treatment. If you want to know more, I would encourage you to visit roomnow.com for further information and videos.

Hi, I'm Jack Cush here at the RheumNow booth in Atlanta, ACR 2019 for the Rheumatoid Arthritis Panel Discussion, wherein I have two experts to talk to. I'm Jack Cush from Dallas.

Artie Cavanagh, San Diego. Jonathan Kay from Massachusetts.

All right, gentlemen, we're here to talk about rheumatoid arthritis. I want each of us to bring up something that we found interesting here at the meeting. Artie, why don't you start us

off?

Well, the one thing I found interesting is the trajectory of response to rheumatoid arthritis. One thing we see in the clinic is that there are patients who do real well, real fast, But from treat to target, we're told that we should think about when to change therapy. So this showed that some people do do well very fast, some people don't do well, and then there are people in the middle. So the question is when do we wait for it? There are abstracts thirteen forty two and thirteen fifty, one with tocilizumab and one with baricitinib.

And I think it's an important question. We can't predict ahead of time who's gonna have that course. Who do we wait for? Maybe twelve weeks, maybe longer before we switch therapy.

So do you think it's finding that trajectory issue? Like who what club you belong to? Mhmm. Is that something that has clinical utility and about how whether you should stay on the drug? Or does that have long term implications?

Where is this gonna fit in in management if we could actually really identify phenotypically who someone is by this you know response trajectory?

I think it's important. Think the people who do well fast, they do great, they're the people that you can potentially taper off treatment but the people in between when do

we give up on them?

And do we go and wait four months because they're a little better? Or do we say we'll never get better with them so that we won't be able to, well, let's go switch to something else because we have other options.

That leads into a poster that I saw yesterday. Ian McGinnis looked at whole blood from patients treated with lupadacitinib and profiled the cytokine expression and other genes and found that there was down regulation of those pro inflammatory cytokines that you'd expect with JAK inhibition, JAK1 or JAK3 inhibition. But there was also a gene that was upregulated, was a master regulator of chemokine. He described it as something a sticky molecule where the chemokines would bind to it and down regulate leukocyte migration. So the reason I bring this up is that one could individualize treatment by profiling the gene expression of an patient and perhaps assigning them to one of these trajectories and determining when to change and when to hold your course.

That might play out really well especially in the Jack class. We have a number of Jacks right now, we might get more Jacks in the future. They're not quite the same, they're all a little bit different, but yet we're applying the same population without any real guidance and we do know that they are going to behave differently as far as what genes are affecting, what cytokine expression they're affecting. Maybe that would be a good way of choosing JAK inhibitors in the future. I think it's something that needs to be developed because any new drug that comes along is now the twentieth or twenty first new drug in rheumatoid arthritis and you've got to figure out how to use it when I already have a whole bunch that are working very well with.

So we need reasons to know how to use a new drug or where it's going to apply and to apply them all to people who are failures at everything is not good for the drug, it's not good for us, it's not good for our patients.

I think fitting with that, the theme I've seen in a number of posters, dozen posters at least so far, machine learning. And that is that instead of trying to think things rationally, just say, it's a complex system which we've always known. Let's figure out let the machine, let the computer, the artificial intelligence figure out the patterns of response and also the biomarkers

that

define

the patterns.

The advantage of that is it's an unbiased approach and we're all biased by our preconceptions and machine learning. There was a presentation that Ian McGinniss gave at EULAR trying to subset responses of patients with psoriatic arthritis to a drug for psoriatic arthritis based upon their gene expression as opposed to their clinical phenotype.

So you gentlemen both do research in rheumatoid arthritis, right? Yes. You've done a lot of clinical trials in your history.

Yes.

You're known for this and are responsible for some of the most major advances in RA therapy in the last decade or two. Well, abstract eleven sixty says that you are a horrible individual, both of you. It's an abstract

about There's lot more abstracts that say there.

Oh, it's not just eleven sixty.

I'm surprised it took this long for that abstract to come out.

Well, 60 is actually about the under representation of ethnicities in RA clinical trials. They looked at thousands of patients in trials in the last decade and showed that the pattern of racial representation, it's all, you know, Caucasian, Caucasian. I mean, the the bars are like this for Caucasians and everything little down here, whether you're Asian or African American, it's really kind of sad. And what's sad about it is it hasn't changed in ten years and it doesn't look like it's going to change. My question then is, is this important data?

Does it tell us a real limitation of the clinical trials that we're always talking about and teaching from?

Well, are other limitations to clinical trials. They all expect an acute phase reactant to be elevated and fifty eight percent of patients with active rheumatoid arthritis by CDI have both a normal sedimentation rate less than 28 millimeters per hour and a C reactive protein below the upper limit of normal. So those patients are not characteristic of those enrolled in clinical trials regardless of their ethnicity.

Yeah, and I think that as rheumatologists we need to treat the diversity of patients that we have. So it would be good to try to have the clinical trials population represent that. I think one thing that the FDA just made a statement on last year is that eventually we may see pregnant women allowed in studies because we have no information on pregnant women And with enough scientific rationale, the agency basically said they would consider whether or you would allow pregnant women, which would be a big advance because we're we're that's a big part of our practice. And but also clinical

trials are difficult to enroll in The United States and Western Europe, and so they're going to Eastern Europe, South America. I was just in Africa last month at the AFLAR meeting, and African rheumatologists have very few biologic agents available for their patients. Africa is an area where clinical trials would be welcome.

So let's end with a quick comment about JAK inhibitor development and what's going on in the last few years. We got a lot of new JAKs and whatnot. It looks like to me the big buzz on JAKs is going be in safety. I think we have the shing the shingles thing kinda figured out that that the issue really is VTE and thromboembolic events. Is this a big issue?

Do you think there's something that everyone should be really worried about or is this a minority issue which the company's gonna fight over whether who who who needs to worry about this and who doesn't?

The data that come from the clinical trials suggest that it's not a major problem. Although it is occurring in clinical practice, the spontaneous drug reporting for tofacitinib indicated that there was a signal, whereas there was no signal in a analysis of all of the clinical trials and all of the indications. So I think that this is a problem that really needs to be investigated further. Most importantly, the mechanism needs to be worked out. Because until we understand the mechanism for VTEs in patients treated with JAK inhibitors, we won't be able to identify which patients are at risk and intervene appropriately to prevent that from occurring.

Yeah. I think it is it's an issue. We don't know the mechanism. We really don't know the extent of it. We just had the FDA's safety session, and one of the the FDA physicians, appropriately say that I think they consider it a class effect.

Someone asked a question, why aren't the labels exactly the same? And so they they say they respond to the data as it is and as the data keeps going, and they fully anticipate that it's something across the classes even if the wording isn't the same, at least for now with the agents we have.

So last week, there was a release by the EMA on tofacitinib basically strengthening the warning and the major change being that anyone who's at risk for VTE is probably not a great candidate and you should probably think that choice in therapy. The question what do do is someone's been at risk and they've already been on a JAK inhibitor and I don't stop them although I will continue to worry about them, watch them, that sort of thing. Anyway, any final comments?

No. It's been a good meeting. Very full. Still a

lot of

stuff to come.

There are more abstracts tomorrow about things that these guys have done that we're gonna look for that'll make the news. That's it from ACR. Tune in for more videos.

Hi. It's Janet Pope. Welcome to the ACR twenty nineteen Atlanta at RheumNow. I'm a reporter for at RheumNow. I'd like to talk about a primer of comorbidities in lupus.

So at poster sessions there were three posters that stood out for me. The first one, number 607, was looking at the frequency of interstitial lung disease in lupus. My impression is it's very uncommon. That's what the author found as well. It's only two percent of patients.

What he did find though was that most of these patients even with seven to twelve years of follow-up did not progress their ILD so that's very reassuring so most weren't clinically progressive. The next one is looking at heart attacks because acute coronary syndrome or heart disease is one of our killers of patients in lupus. So looking at number six forty one, what was found, we know lupus increases coronary artery events. What this study looked at age and sex match controls in the population and what it found was that your coronary syndrome or myocardial infarction that the lupus patients did less well and it seems that they do less well because their myocardial reserve or their heart muscle is actually more damaged. So I think that's something to note and to aggressively treat risk factors, not just disease activity.

The common risk factors like hyperlipidemia, hypertension, diabetes, metabolic syndrome, etc, and smoking cessation. The last one is what do these comorbidities lead to? Poster six forty two was looking at lupus and work disability, and as you might guess, lower education, lower socioeconomic status, and older age all lead to more work disability. That is true in every disease I've ever looked at. What in addition was found, not surprisingly, was higher score on the fibromyalgia index, the FSS, led to more work disability.

So again, if we could intervene at the workplace and try to treat fibromyalgia as best as we can with pharmacologic and non pharmacologic ways, maybe we'll help our patients maintain their ability to work and improve their quality of life. Thank you. Hi. I'm doctor Janet Pope. I'm a RheumNow reporter.

Where am I? I'm at the ACR twenty nineteen in Atlanta. I'd like to talk to you about the changing faces of rheumatoid arthritis. And for this, I want to discuss three abstracts that were presented at the ACR, number 171, 172, and eight forty one. The first two abstracts, one hundred seventy one and one hundred seventy two, looked at the incidence of rheumatoid arthritis in Olmsted County, Minnesota, so a population based incidence over thirty years.

And some surprising things were found. First of all, we know there's less smoking and we would expect that, but the incidence in men and women was the same over the thirty years, not increasing as we have seen in Canada where it's increasing in the very old. The next thing that's a little bit surprising, maybe, is that there's less seronegative, or sorry. There's more seronegative RA, so less seropositive RA. And that makes sense because in early RA cohorts, now about fifty to sixty percent are RF positive, fifty sixty percent CCP positive with a huge overlap between the two.

What is surprising though with less obesity and less smoking that they found, although in some years there is more obesity and they didn't do BMI, but they found what's a little bit surprising was more erosions. Now in fairness, if you meet the twenty ten RA criteria from ACR and EULAR, you if you're seronegative, you have to have more damage or more joints to get in. So the epidemiology is to me a little bit confusing. Then if we go on to look at other risk factors for RA, number eight four one, abstract, looked at increasing ACPA positive patients before RA from the Nurses Health Study where serum were frozen serially and about a 10 times increase of COPD diagnosis before RA. Asthma and COPD were increased before RA as well as after someone got the diagnosis of RA.

So I never thought of obstructive lung disease as a risk factor. I think that's a Th2 disease. I think of RA as a Th1. So I think this story will unravel at the meeting. Thank you.

I'm Chad Diehl. I'm at ACR in Atlanta 2019 and I just attended a session, The Great Debate. The topic of debate was whether or not teriparatide should be primary therapy in patients with steroid induced osteoporosis. The impetus for this debate was the 2017 ACR guidelines, which made teriparatide only a second choice for even for high risk patients on steroids with osteoporosis. That's different from the previous guidelines that proceeded where teriparatide was choice for high risk patients.

So Doctor. Saag and Doctor. Humphrey debated this topic, and my personal feeling is that teriparatide should be primary therapy in high risk patients just like it is for all the patients we see, especially those with very low T scores and previous fractures, especially vertebral fractures and hip fractures. More information, go to RheumNow.

I'm Jonathan Kay from the University of Massachusetts in Worcester, Massachusetts here at the American College of Rheumatology meeting in Atlanta, Georgia. I heard a very interesting plenary presentation today, Abstract seventeen fifty eight, given by Doctor. Hemsfeld from the Karolinsk Institute in Stockholm, Sweden. She described the risk RA study in which two sixty eight patients were recruited who had anti citrullinated protein antibodies and joint pain but not arthritis. This is a tremendous number of patients to recruit with this pre arthritis clinical presentation.

They assessed these patients and made sure that they didn't have clinical evidence of arthritis, and then looked at various risk factors for the development of arthritis following these patients over at least two years. They found that individuals who had these antisynchronated protein antibodies and also rheumatoid factor were more likely to develop arthritis than those who had no rheumatoid factor but the antisynchronated protein antibodies alone. They looked for ultrasound detectable synovitis as their endpoint and found that about a quarter of the patients developed arthritis by two years. When they looked at risk factors, they found that the presence of tenosynovitis on ultrasound at baseline predicted the development of inflammatory arthritis with a threefold increased risk compared to those without tenosynovitis. The presence presence of antibodies to cyclinated filigrine increased the risk of developing arthritis by two point five fold, and the presence of increased levels of interleukin six increased the risk by about one and a half fold.

When they looked at the number of antigens to which citrullination was, the number of anti citrullinated protein antibodies to various citrullinated antigens, they found that the more antibodies to citrullinated antigens that were present, the more likely the patients were to develop arthritis. So this was very interesting. Patients who were double positive anti protein antibodies and rheumatoid factor were more likely to develop inflammatory arthritis as evidenced by ultrasound over the course of two years. They then took this to the lab and they injected mice with anti citrullinated protein antibodies and found that they could decrease their pain threshold so they experienced pain with tactile stimuli more than mice that were injected with control antibodies. They also found that these mice developed tenosynovitis, after the injection of these antisitronated protein antibodies.

So they were able to develop an animal model for pre rheumatoid arthritis. So not only did this group recruit two sixty eight patients with joint pain and antisiphonated antibodies that they followed for two years and found that about a quarter developed ultrasound evident inflammatory arthritis, but they created an animal model in which this condition could be studied. It'll be very interesting to see what comes out of this group in the future. I'm Jonathan Kaye. For more information, to RheumNow.

I am Fabrizio De Benedetti. I'm the head of the division of pediatric rheumatology at the Children's Hospital in Rome. I'm here at the ACR in Atlanta. Today we presented the preliminary data from a study with Emapalumab in macrophage activation syndrome. Emapalumab is an anti interferon gamma neutralizing antibody and there is plenty of evidence showing that interferon gamma may be important in MAS both in animal models and in patients with systemic JIA.

The data from the clinical trial showed significant efficacy with nine out of nine patients achieving the primary outcome of complete response. The safety, results were very reassuring. It's a shorter term treatment, maximum treatment duration was twenty eight days, all patients tapered significantly glucocorticoid with seven out of nine patients going back to less than 0.8. These results are very promising and suggest a new avenue to be pursued for tackling macrophage activation syndrome, a severe complication of both systemic GI patients and patients with adult onset Still's disease. Thank you very much for listening.

Hello everyone, I'm Olga Petrina reporting from the twenty nineteen ACR meeting. I would like to share some highlights from abstract sessions today, and from the poster hall. One abstract that draw my attention is abstract number twelve thirty seven, which speaks about treatment of gout flares with a novel inflammasome inhibitor, OLT eleven seventy seven. So in this abstract, authors highlight very nicely the pathophysiology of gout flare, and remind us that most of the gout flares happen as a result of inflammasome activation from the monosodium urate crystals, and as a result it triggers the cascade of reaction that leads to release of cytokines IL-one beta, IL-six, and, the inflammatory substances resulting in a flare of gout. So, authors propose use of inflammasome inhibitor as a potential therapeutic target for, managing patients with gout flares, and in this study they used oil T1177 in different doses, three hundred milligram, one thousand milligram, and two thousand milligram, to be administered orally for eight days from the beginning of the FLIR until full resolution of the symptoms.

During this study they assessed levels of IL-one and IL-six in the blood of the patients, as well as WBC counts. In addition to this, they, cultured the peripheral blood, monocytes of the patients, and, assessed their ability to be stimulated by monsoonuric crystals, during and after treatment. So blood of the patients was assessed on days three, seven, and 14, which is a week after treatment was completed, and not only their white cell count decreased and their interleukin one and interleukin six levels decreased, Also, the cultured PBMCs were not able, or had decreased level of production of inflammatory cytokines ex vivo, which means that medication continues to work at least a week later after flare results. So that, identifies OLT eleven seventy seven as a potential therapeutic, target for treatment of acute flares of gout. And if you like to learn more, please follow us on RheumNow.

Thank you and have a nice day.