RheumNow - ACR 2017 San Diego - Day 3b Save

Hello, I'm Alvin Wells. I'm here at the ACR National Meeting in San Diego, California. I would like to share with you some exciting areas that I've seen here at the meeting and that's actually revolving around telehealth and telemedicine. As you're looking at where the future is gonna be, I really think I'm convinced that the days of seeing a doctor in the office are gonna be limited. That many of our patients, whether in rheumatology or primary care, will be connected away with us virtually.

So look into telehealth, telemedicine, and telerheumatology. This year at the meeting there's been some showcase about several different things. Yesterday was an abstract talking about how using telehealth to look at patients with gout. They had a program when they had patients who had gout, once they were hospitalized and treated for the gout, then using the internet to connect them with nurse practitioners and nurses to show they can decrease the gout flare and other kind of long term benefits as well as far as less joint damage, kidney disease as well. There's also a poster talking about an area where there's unmet need like in Alaska.

So an abstract talking about the Alaskan native population has showed because there's not many rheumatologists there, how they've connected with other rheumatologists in the region to do things remotely. And also now one of my biggest interests is working and talking about doing tele ultrasound. This has been spearheaded by the obstetrician and gynecologist, so if you have a remote site, that a patient can take an ultrasound image, and that image can be interpreted remotely, for example, by a rheumatologist. That can be done live, that can be done also not in live time, can be done offline. So I think doing telehealth and telemedicine, particularly when it revolves around for us as rheumatologists, telerheumatology and doing tel ultrasound is going to make a dramatic difference.

So it's exciting to be here at the meeting to share this information with you. If you want some more information, I welcome you to visit roomnow.com.

Hey, this is Doctor. Arti Kavanaugh on RoomNow. And I'd just like to remind you all of an opportunity to come to an educational activity, that is RWCS, the Rheumatology Winter Clinical Symposium. This will be February 2018 in Maui. We've got a great lineup of faculty, great chance to catch up with colleagues, discuss clinical issues, talk to the people who are doing the research in the field, learn a lot, and enjoy and relax and remember why you liked rheumatology in

the first place. So we'll see

you at RWCS twenty eighteen. This is Artie Cavanagh for RheumNow.

I'm Cassie Calabrese coming to you from day three of ACR twenty seventeen in San Diego. I just left the poster hall where there are many excellent abstracts on immune related adverse events from checkpoint inhibitor therapy, a topic near and dear to my heart. I was in particular interested in an abstract, by Noha Abdelwahab from MD Anderson. Her and her group presented a study that was a systematic review of patients with preexisting rheumatic autoimmune diseases who go on to get checkpoint inhibitor therapy, a very important topic, very luposity of data. And they did a systematic review of the literature from 30 patients with rheumatic diseases, mostly rheumatoid arthritis.

All of them had melanoma. Most of them went on to get ipilimumab, a CTLA four inhibitor, for their cancer, and they looked at who flared, who didn't. And turns out a third of them flared their underlying rheumatic disease. A quarter of them went on to get IRAEs in other systems, and about thirteen percent of them experienced both. It seems that if the rheumatic disease was not well controlled at the time of checkpoint inhibitor initiation, they had a higher chance of flaring their disease, and there was no increased risk of getting an IRAE whether they had an underlying rheumatic disease or not.

There was a small number of patients, but this is such an interesting topic and a great need for further studies, and I think this will help us manage these patients down the road. For more, go to roomnow.com.

Hi. I'm Jack Cush, executive editor of roomnow.com. I'm coming to you from ACR 2017 here in San Diego. We're on the Exhibit Floor and we're at the RheumNow booth and I'm here with Pete Salzman. Pete is vice president of US immunology at Eli Lilly and Company.

I've asked Pete to come by so we could talk about, I think what I think is a really interesting issue. So, Pete, this issue, in my mind, has come up with this new data about pain as a differentiator with Jack Cush, that you're developing, baricitinib. And, you know, when drugs are being developed, we as advisors and leaders in the community often are looking for distinguishing features, just as you are. Yeah. And we look at the safety data, we look at the efficacy data, we look, we ask about cost, you know, and it ends up being yet another a long list.

So just recently, you know, there's this new data that's come up about pain as a differentiator, which is, I find surprising for this disease modifying drug, baricitinib. So tell me the story behind it and how you think it's gonna play out.

Yeah. Thanks for the question. So first of all, the data that you're referring to is from our pivotal phase three trial, which compared baricitinib to adalimumab to placebo in CD MARRED IR patients. So that was a population. And it had all the standard, scales that you would think of, ACR scores, CDAI, all those kind of things, lab values.

What we noticed as we looked at the components of the ACR was differentially positive effect in pain, we thought. So, Peter Taylor and others at, Lilly conducted a post hoc analysis where they really tried to tease that out. Mhmm. And what we found is that compared to adalimumab and also compared to placebo, baricitinib resulted in a larger decrease in pain, and that decrease in pain happened faster. And interestingly, for those patients who had the most pain at baseline, they had the largest improvement.

So when you looked at those who had a pain response, was there anything about that group that was distinguishing compared to other patients? Did they have more inflammatory disease? Did they have more damage? They have more disability? Was there anything that distinguished them?

Yeah. Great question. So, the people who had, higher pain at baseline, I already mentioned that. And certainly people this was a group that was, you know, a pretty active disease if you look at the inclusion criteria. But you're right.

Among those people who had the most active inflammation, they also had the most pain and therefore the most pain relief. But among people who had their inflammatory signs improve, so just all the typical things as simple as swollen joints or CRP, We controlled or Peter Taylor and his group controlled for that. And when you when you took out that, which they called the sort of direct pain reduction, because you'd assume that if you reduce inflammation, you reduce pain. Right? Right.

There was still this component that was unexplained that was the indirect pain relief, and that part, that pain relief was pretty substantial. It's about 50% of the pain relief could not be explained by the improvement in, inflammation.

So I would guess at Lilly, when you see these kind of results, you say, quick, let's look at our past data. Let's look at dose related effects on pain. And does this extrapolate to other studies? How does this play out by dose?

Yeah. So the differences by dose so this particular study only had the four milligram, but you can look in other studies and you typically see that baricitinib relative to placebo in the other studies is gonna show this impact. We haven't yet teased out the difference two milligram versus four milligram. Okay. But but it's an important question.

I agree.

Do you think this actually is going to tell you maybe this is a drug that will do something for pain and work in pain models like dysmenorrhea, dental extraction, post operative pain, whatever? Is that something that you wanna look at at this point or right now it's still just a curiosity?

I would say it's not a it's neither a curiosity nor a broad based pain development program. I think, you know, pain in RA is an important topic. Think you'd agree. And, you know, during the q and a after Peter's presentation, someone mentioned, you know, a rheumatologist mentioned, you know, we all have these patients who their swelling gets a lot better on exam, but they still have a fair amount of pain. And, you know, that could be the type of patient who's really gonna benefit from this differential impact to baricitinib.

So we do plan to further explore how baricitinib can help patients with rheumatoid arthritis with pain, also psoriatic arthritis because we're studying in psoriatic arthritis where you may have a similar situation.

So from a practitioner standpoint and one who represents a lot of rheumatologists can tell you that, we do get frustrated when trying to find the distinguishing features and often wonder, it even possible? So this is a novel finding, one that's encouraging, and I congratulate you for finding it. The question is going to be how far can you take it? We're gonna wait and see.

Yeah. Absolutely. I agree, Jack.

Thank you.

Thank you.

Hi. I'm doctor Janet Pope. I'm at the ACR twenty seventeen at the RheumNow booth. We're starting to wind down today, and I have a really interesting abstract to talk to you about, number 3,377. This is from the early RA cohort, Esquire, from France, and there's over 400 patients in this cohort.

And what they wanted to do is look at radiographic change when they're using various drugs. We know that if we get the disease under control that anything could be a DMARD. If we suppress inflammation, we might improve joint damage. What's different about this study and contradictory to a lot of other things we've heard is that corticosteroids actually were a poor predictor and had more X-ray damage. We could explain it by the fact that only the worst patients got corticosteroids, but if you look at the EULAR guidelines, corticosteroids have been used as an add on in early RA for a long time in Europe even though the guidelines are recent.

So I really wonder if they're channeling bias or confounding by indication, but it makes us think twice, try to control the inflammation with our proper DMARDs and maybe save the steroids for later. Who knows? Thanks from RheumNow. Hi. It's doctor Janet Pope.

I'm back at RheumNow, ACR twenty seventeen. I wanted to talk about interstitial lung disease and rheumatoid arthritis. So there's several, abstracts at this meeting, and they're saying things like in about a hundred and fifty six patients, up to one in four of them have ILD, and cytokines are increased, such as MMP three and some other cytokines. Interestingly, IL six are isn't increased. But if you really think of how common interstitial lung disease is in our rheumatoid arthritis patients that's clinically relevant, I think it's far lower than that, and I look forward to you having a poll on that and giving us the answer.

However, along that vein, there were two studies of looking at after RA a billing code of interstitial lung disease and one seemed to suggest that interstitial lung disease incidence in rheumatoid arthritis, although low, was the same in TNF inhibitors as abadacept. However, there was another study that looked at a large database market scan and some of the large big data and found that abadacept seemed to have less new interstitial lung disease compared to TNFs and compared to some of the other comparators. So I think the word's not out. We do have patients with interstitial lung disease, and I think more will come over time. Thank you.

Morning everyone. This is Doctor. Julio Gonzalez reporting live from the American College of Rheumatology meeting in San Diego, California. And now, it's been a great congress so far, especially on the topic of psoriatic arthritis. We've heard great articles and I'd like to continue that trend here.

I'd like to report a couple of papers that have been published, actually three studies on the topic of psoriatic arthritis and radiographic progression. The first one is Late Breaker that was just presented this morning. It's a future five study on secukinumab. This was a very large study, nine ninety six patients that were randomized to receive either 300, 150 with loading and 150 without loading, 300 with loading of secukinumab. These patients were, around thirty percent of them were TNF failure, so those patients were included in the study.

The study was carried out to twenty four weeks to monitor structural progression at 16 as expected. Tegucinemab had better scores as compared to placebo and at twenty four weeks radiographic progression was significantly inhibited in Tegucinemab as compared to placebo. The second study I want to talk about is on another IL-seventeen inhibitor, this time it's tegucinemab. There was another study this time carried out to fifty two weeks. This study was presented by Doctor.

Vanderheit yesterday and they showed that at fifty two weeks in both the every two weeks and the every four weeks doses of execizumab, radiographic progression was halted significantly. These patients were initially on either placebo or adalimumab and were switched to execizumab and then they got the measurements at fifty two weeks. The third study that I want to talk about on radiographic progression is on tofacitinib. So this is a lot of news around this in the field of psoriatic arthritis. And this study was interesting in the way that they had an Alimumab arm up to fifty two weeks.

And they also grouped their patients between CRP levels. So patients with high CRPs and patients with low CRPs or normal CRPs. What they did is that they looked at their radiographic data at 52 and what they saw was significant diminishing or altering of progression at fifty two weeks in the three arms, the TOFA-five BID, the TOFA-ten BID, and the adalimumab arm. So as expected, up to fifty two weeks diminished radiographic progression in the three studies. So great news in the field of psoriatic arthritis.

We keep hearing good things. It's been a great congress in this field and specifically we're anxious ly waiting the release of the new American College of Rheumatology and National Steroids Foundation criteria for psoriatic arthritis today at 1PM. So if you're here, sure to go check it out and if you want to learn more, make sure to go to roomnow.com to get the latest and greatest information as it happens.

This is Len Calabrese. I'm coming at you from ACR San Diego. It's been an incredible meeting. I'd like to talk to you for a minute about, herpes zoster. A lot of activity here.

We know the risk factors for drugs, particularly the jackotinibs. A lot of this was overshadowed by the introduction of Shingrix, the new GSK killed vaccine coupled to a adjuvant system. I've talked to a lot of people about it and we're very excited to use it, but we are cautiously concerned about assessing the potential for adjuvants to aggravate autoimmune disease across the image spectrum. I have no reason to suspect this other than from the data. I'm looking forward to robust studies, on behalf of the company that will explore this, and, I look forward to, offering this to my patients in a sense of shared and informed decision making.

Thanks.

Hi. I'm Doctor. Rachel Tate from Dallas, Texas presenting today for you from ACR twenty seventeen in San Diego, California. I love the plenary sessions. I think that they are the most high yield and they give you a lot of information in very, very small subsets, is really nice for me.

It's digestible. So I just attended a really great plenary session with Landewey on the safety and efficacy of sustained remission in patients on adalimumab versus placebo. So that's something we all talk about, right? We want to know not only how do we achieve remission for our patients, but can we sustain that remission? And if so, can we do it off of medication?

So this study actually is called the ABILITY-three, if you're interested in more information. And realistically, what they looked at is they had patients who had non radiographic SPA. So that's using the ASAS criteria, not the New York criteria. And why is that important? That's important because we are looking at non radiographic spondyloarthritis, not radiographic spondyloarthritis.

So in general, they took three zero five patients who had been on adalimumab every two weeks for twenty eight weeks. Of those three zero five patients who had achieved remission, they then broke it down into a placebo group of 153 patients versus a non placebo group with continued adalimumab every two weeks, one hundred and fifty two patients. So we looked at a couple of things. Number one, we wanted to make sure that the safety data was still there for the patients. So there were no new safety indications for Humira based on what we'd already known.

So that's really important. But we also wanted to know, of the patients who had achieved remission, can we sustain that remission? Well, we found that seventy percent of the patients who had already achieved remission on adalimumab and who stayed on adalimumab, seventy percent of those patients did very well, but thirty percent had flares. So what about the remission group that had achieved it, then had to be off of the medication who were within the withdrawal placebo group? We actually found that only thirty percent of those patients had no flares.

So that's seventy percent of those patients had flares and could be reintroduced to adalimumab. So here's the caveat to that though. Once they achieved remission, they were taken off of drug in the withdrawal phase of the study, and then they were put back on adalimumab, it wasn't as effective. So it's twofold information. It goes to show that maybe we do need to reconsider the way that we approach these patients.

We need to make sure they hit clinical but it's really important to have sustained remission. And partly, this may be keeping them on drug for the extended period of time. So I hope that you learned something from this session. I know I did. I always send patients and people to plenary sessions because personally, that's where I learn the most bang for my buck.

So I hope you enjoy roomnow.com and keep checking us out for up to date information from ACR twenty seventeen in San Diego, California. Hi, I'm Doctor. Rachel Tate from Dallas, Texas, and I'm coming to you live from ACR twenty seventeen in San Diego, California. So I just saw a really great poster, abstract number fifteen oh five from Doctor. Dugum and his group and they were looking at gender biases for ankylosing spondylitis and particularly patterns of inheritance.

They looked at two different cohorts of 105 HLA B27 positive parent and offspring pairs to look not only at patterns of inheritance but if there's a gender bias. So historically we know that we think that mothers really do transmit this disease to patients, whether that be male or female offspring. But what we actually found was that the fathers had the increased rate of transmission to patients. Also, it seems to be that the sons are more affected in this particular subset than daughters. So this goes against our conventional wisdom.

So it seems that not only HLA B27 positive patients who meet New York criteria for AS, as well as radiographic damage, and gender are also transmitted with a male bias. I hope you learned something from this. I think that realistically we need to be looking into more inheritance patterns because this challenges our conventional wisdom. More from ACR twenty seventeen with rheumnow.com and I hope you're enjoying the coverage. I know I am.

Hi, I'm Doctor. Rachel Tate from Dallas, Texas coming to you live from ACR twenty seventeen in San Diego, California. There are two things that I really like to talk about when it comes to rheumatology, particularly education in addition to actual use of ultrasound, which is something that I practice in clinical practice as well. But realistically, can we integrate those? So Doctor.

Sterling West did a fantastic year interview update for medical education this week. And something that he found in his study and research in this is that of the 113 rheumatology fellowship programs, these are both adult and pediatrics, that 103 of those programs actually believe that we should be training our future rheumatologists with ultrasound, musculoskeletal ultrasound for diagnostics as well as for doing intra articular injections. But interestingly, when we looked at that data further, 30 out of 74, so not all of the programs participated in the second part of the study, but 74 of them said that, Wait a second, we don't have a core curriculum. So there's a vast majority of program directors who believe that we should be using musculoskeletal ultrasound as part of our core curriculum for rheumatology, but only 30 out of those 74 and possibly out of 113 programs are actually developing those core curriculums. So I think this is a really important part of what we do in rheumatology.

We pride ourselves on being innovators and thinkers about things that we can do to improve our patients' quality of life, but also now to improve our fellowship program. So I encourage you if you're a program director or if you have any ideas for the supporting program directors, especially if you are the fellows, to develop some of these core curriculums. I think it's really important. This is the wave of the future. It helps us with diagnosis.

It helps to ensure we're putting steroids in the right spots. And I think that that's the wave of the future regardless of reimbursement. So more from rheumnow.com. Check us out. We'll be here all week at ACR twenty seventeen in San Diego.

Hello, friends. Doctor Akhirkar from Mumbai, India here at ACR twenty seventeen. I was particularly looking at the data about new molecules in psoriatic arthritis, arthritis, and ACR was really not disappointing in that respect. We have a lot of data about new molecules in psoriatic arthritis here presented. The first molecule on the horizon, tofacitinib.

The Opel Broaden and Opel Beyond data presented, showing good efficacy in terms of significant difference in the patient related outcomes. The Opel balanced study, thirty six months data about the safety of tofacitinib. No new safety signals there. And doctor Vanderheit presented the Opel Broaden study, a study with active psoriatic arthritis patients, those who are refracted to dBERTS, TNF alpha nine, four twenty two patients, and the study duration of twelve months. More than ninety percent of the patients did not have any significant radiological progression.

I'm sure one year is not that bigger duration for radiological progression, but it's the step in that right direction. Coming to the second molecule on the horizon in psoriatic arthritis, execizumab. Another study, a phase three SPIRIT two study data presented with good efficacy with significant difference in the patient related outcomes. Some data about abarticept in psoriatic arthritis, promising data, but but long way to go for abarticept. As far as the established molecules are concerned, Aprim last four years safety and efficacy data with Aprimilast as monotherapy in psoriatic arthritis.

Good efficacy with ACR twenty, fifty, seventy of sixty eight percent, forty three percent, twenty three percent respectively, and a PASI seventy five and fifty score of forty and sixty seven percent respectively. So so good things as far as Eprimulast is concerned. And lastly, not to forget, secukinumab, safety data of seven seven six nine patient years of exposure presented here at the ACR. So all in all, as things stand today, good data for psoriatic arthritis and molecules. A lot of things to expect in the future for psoriatic arthritis patients.

Thank you.

Hi, I'm Bill Scherge. I'm talking to you from the American College of Rheumatology meeting in San Diego 2017, and just left a very exciting seminar on giant cell arteritis. From, the take home messages from this meeting, and this session in particular, giant cell arteritis is really a hot area of interest. We had three great speakers in Drs. Wyand, Karmani, Grayson, who covered the basic pathophysiology, current treatment recommendations, and imaging studies.

These lectures were all superb. Learned some interesting take home points on the pathogenesis, and one of the really take home points that I thought about afterwards was that you really are losing privileged sensitivity of the aorta in these giant cell arteritis disorders. And between the combination of increased CD four cells, leaky portals into the vessels, failure of checkpoints, lead to the vascular damage. But equally important for the patients in evaluating is what they happen to see in the periphery. And these are manifestations primarily generated by acute inflammatory products from the liver, and this is the PMR type of features that we've come to recognize.

When we move into treatments, certainly steroids have remained the mainstay of treatment, but over the last few months, we've had the first medication actually approved for the treatment of giant cell arteritis and tocilizumab, and this has really become a very important topic. But one interesting area that we've come to see is this seems to focus primarily on the acute phase reactants, the PMR activity. Even Doctor. Wyand was a little uncertain as to what is going to happen long term to vascular manifestations and how closely we are going to need to follow these patients. It's a great addition to our armamentarium.

We control the disorder. We can minimize steroid use, but we still need to follow the patients, particularly for some vascular complications. There was some sobering data of patients actually having vascular complications five to ten years out from being, disease free. And lastly, what we're certainly looking for, in the diagnostic arena is imaging modalities over an invasive temporal artery biopsy. We've been real excited about the ultrasound.

Some initial reports on ultrasounds really showed sensitivity and specificities in the sixty-ninety range, but other studies have not come up with this. Also, there's MRI and PET scanning, and these two have very variable sensitivities and specificities. But in the certain study that compared biopsy to imaging modalities, it really appeared that the imaging modalities may help more than the biopsy. And their current suggestion is if you have a firm diagnosis or a very good looking diagnosis on an imaging study in a classic clinical presentation, then perhaps you can skip the biopsy entirely. If there is a negative ultrasound or other imaging in the setting of a classic clinical history, pursue the biopsy, and if it's a negative imaging and not a classic story, then once again you're free from doing the biopsy.

So, with that, I will close and say for more information, go to RheumNow.

Hello, I'm Alvin Wells. I'm here at the ACR National Meeting in San Diego, California. I would like to share with you some exciting areas that I've seen here at the meeting and that's actually revolving around telehealth and telemedicine. As you're looking at where the future is going to be, I really think I'm convinced that the days of seeing a doctor in the office are going to be limited. That many of our patients, whether in rheumatology or primary care, will be connected with us virtually.

So look into telehealth, telemedicine, and telerheumatology. This year at the meeting there's been some showcase about several different things. Yesterday was an abstract talking about how using telehealth to look at patients with gout. They had a program when they had patients who had gout, once they were hospitalized and treated for the gout, then using the internet connecting with nurse practitioners and nurses to show they can decrease the gout flare and other kind of long term benefits as well as far as less joint damage, kidney disease as well. There's also a poster talking about in areas where there's unmet need like in Alaska.

So talk about the Alaskan native population that showed because there's not many rheumatologists there how they've connected with other rheumatologists in the region to do things remotely. And also now one of my biggest interests is working and talking about doing tele ultrasound. This has been spearheaded by the obstetrician and gynecologist, so if you have a remote site, that a patient can take an ultrasound image and that image can be interpreted remotely, for example, by a rheumatologist. That can be done live, that can be done also, not in live time, it can be done offline. So I think doing telehealth and telemedicine, particularly when it revolves around for us as rheumatologists, telerheumatology and doing tel ultrasound is going make a dramatic difference.

So it's exciting to be here at the meeting to share this information with you. If you want some more information, I welcome you to visit roomnow.com.

Hey, this is Doctor. Arti Kavanaugh on RoomNow. And I'd just like to remind you all of an opportunity to come to an educational activity, that is RWCS, the Rheumatology Winter Clinical Symposium. This will be February 2018 in Maui. We've got a great lineup of faculty, great chance to catch up with colleagues, discuss clinical issues, talk to the people who are doing the research in the field, learn a lot, and enjoy and relax and remember why you liked rheumatology in the

first place. So we'll see you

at RWCS twenty eighteen. This is Arti Kavanaugh for RheumNow.

I'm Cassie Calabrese coming to you from day three of ACR twenty seventeen in San Diego. I just left the poster hall where there are many excellent abstracts on immune related adverse events from checkpoint inhibitor therapy, a topic near and dear to my heart. And I was in particular interested in an abstract by Noha Abdelwahab from MD Anderson. Her and her group presented a study that was a systematic review of patients with preexisting rheumatic autoimmune diseases who go on to get checkpoint inhibitor therapy, a very important topic, very luposity of data. And they did a systematic review of the literature from 30 patients with rheumatic diseases, mostly rheumatoid arthritis.

All of them had melanoma. Most of them went on to get ipilimumab, a CTLA four inhibitor, for their cancer, and they looked at who flared, who didn't. And turns out, a third of them flared their underlying rheumatic disease. A quarter of them went on to get IRAEs in other systems, and about thirteen percent of them experienced both. It seems that if the rheumatic disease was not well controlled at the time of checkpoint inhibitor initiation, they had a higher chance of flaring their disease, and there was no increased risk of getting an IRAE whether they had underlying rheumatic disease or not.

There was a small number of patients, but this is such an interesting topic and a great need for further studies, and I think this will help us manage these patients down the road. For more, go to roomnow.com.

Hi. I'm Jack Cush, executive editor of roomnow.com. I'm coming to you from ACR two thousand seventeen here in San Diego. We're on the Exhibit Floor and we're at the RheumNow booth and I'm here with Pete Salzman. Pete is vice president of US immunology at Eli Lilly and Company.

I've asked Pete to come by so we could talk about, I think, what I think is a really interesting issue. So, Pete, this issue, in my mind has come up with this new data about pain as a differentiator with, Jack Cush, that you're developing, baricitinib. And, you know, when drugs are being developed, we as advisers and and leaders in the community often are looking for distinguishing features, just as you are. Yeah. And we look at the safety data, we look at the efficacy data, we look, we ask about cost, you know, and it ends up being yet another a long list.

So just recently, there's this new data that's come up about pain as a differentiator, which is, I find surprising for this disease modifying drug, baricitinib. So tell me the story behind it and how you think it's gonna play out.

Yeah. Thanks for the question. So first of all, the data that you're referring to is from our pivotal phase three trial, which compared baricitinib to adalimumab to placebo in CD MARRED IR patients. So that was a population. Mhmm.

And it had all the standard, scales that you would think of, ACR score, CDAI, all those kind of things, lab values. What we noticed as we looked at the components of the ACR was a differentially positive effect in pain, we thought. So, Peter Taylor and, others at, Lilly conducted a post hoc analysis where they really tried to tease that out. Mhmm. And what we found is that compared to adalimumab and also compared to placebo, baricitinib resulted in a larger decrease in pain and that decrease in pain happened faster.

And interestingly, for those patients who had the most pain at baseline, they had the largest improvement.

So when you looked at those who had a pain response, was there anything about that group that was distinguishing compared to other patients? Did they have more inflammatory disease? Did they have more damage? They have more disability? Was there anything that distinguished

Yeah. Great question. So, the people who had, higher pain at baseline, I already mentioned that, and certainly people this was a group that was, you know, a pretty active disease if you look at the inclusion criteria. But you're right. Among those people who had the most active, inflammation, they also had the most pain and therefore the most pain relief, but among people who, had their inflammatory signs improve, so just all the typical things as simple as, swollen joints or CRP, We controlled or Peter Taylor and his group controlled for that.

And when you when you took out that, which they called the sort of direct pain reduction, because you'd assume that if you reduce inflammation, you reduce pain. Right? Right. There was still this component that was unexplained that was the indirect pain relief and that part, that pain relief was pretty substantial. It's about 50% of the pain relief could not be explained by the improvement in, inflammation.

So I would guess at Lilly when you see these kind of results, say quick, let's look at our past data. Let's look at dose related effects on pain. And does this extrapolate to other studies? How does this play out by dose?

Yeah. So the differences by dose so this particular study only had the four milligram, but you can look in other studies and you typically see that baricitinib relative to placebo in the other studies is gonna show this impact. We haven't yet teased out the difference two milligram versus four milligram. But but it's an important question. I agree.

Do you think this actually is going to tell you maybe this is a drug that will do something for pain and work in pain models like dysmenorrhea, dental extraction, postoperative pain, whatever. Is that something that you wanna look at at this point? Right now, it's still just a curiosity?

I would say it's not it's neither a curiosity nor a broad based, pain development program. I think, you know, pain in RA is an important topic. I think you'd agree. And, you know, during the q and a, after Peter's presentation, someone mentioned, you know, a rheumatologist mentioned, you know, we all have these patients who their swelling gets a lot better on exam, but they still have a fair amount of pain. Mhmm.

And, you know, that could be the type of patient who's really gonna benefit from this differential impact of baricitinib. So we do plan to further explore how baricitinib can help patients with rheumatoid arthritis with pain, also psoriatic arthritis because we're studying in psoriatic arthritis where you may have a similar situation.

So from a practitioner standpoint and one who represents a lot of rheumatologists can tell you that, you know, we do get frustrated when trying to find the distinguishing features and and often wonder, it even possible? So this is a novel finding, one that's encouraging, and I congratulate you for finding it finding it. The question is going to be how far can you take it? We're gonna wait and see.

Yeah. Absolutely. I agree, Jack.

Thank you.

Thank you.

Hi. I'm doctor Janet Pope. I'm at the ACR twenty seventeen at the RheumNow booth. We're starting to wind down today, and I have a really interesting abstract to talk to you about, number 3377. This is from the early RA cohort, Esquire, from France, and there's over 400 patients in this cohort.

And what they wanted to do is look at radiographic change when they're using various drugs. We know that if we get the disease under control, that anything could be a DMARD. If we suppress inflammation, we might improve joint damage. What's different about this study and contradictory to a lot of other things we've heard is that corticosteroids actually were a poor predictor and had more X-ray damage. We could explain it by the fact that only the worst patients got corticosteroids, but if you look at the EULAR guidelines, corticosteroids have been used as an add on in early RA for a long time in Europe even though the guidelines are recent.

So I really wonder if they're channeling bias or confounding by indication, but it makes us think twice, try to control the inflammation with our proper DMARDs and maybe save the steroids for later. Who knows? Thanks from RheumNow. Hi. It's doctor Janet Pope.

I'm back at RheumNow, ACR twenty seventeen. I wanted to talk about interstitial lung disease and rheumatoid arthritis. So there's several, abstracts at this meeting, and they're saying things like in about a hundred and fifty six patients, up to one in four of them have ILD, and cytokines are increased, such as MMP three and some other cytokines. Interestingly, IL six are isn't increased. But if you really think of how common interstitial lung disease is in our rheumatoid arthritis patients as clinically relevant, think it's far lower than that, and I look forward to you having a poll on that and giving us the answer.

However, along that vein, there were two studies of looking at after RA, a billing code of interstitial lung disease. And one seemed to suggest that interstitial lung disease incidence in rheumatoid arthritis, although low, was the same in TNF inhibitors as abidacept. However, there was another study that looked at a large database market scan and some of the large big data and found that abatacept seemed to have less new interstitial lung disease compared to TNFs and compared to some of the other comparators. So I think the word's not out. We do have patients with interstitial lung disease, and I think more will come over time.

Thank you.

Small molecule JAK inhibitor. Morning everyone, this is Doctor. Julio Gonzalez reporting live from the American College of Rheumatology meeting in San Diego, California. And it's been a great congress so far, especially on the topic of psoriatic arthritis. We've heard great articles and I'd like to continue that trend here.

I'd like to report a couple papers that have been published, actually three studies on the topic of psoriatic arthritis and radiographic progression. The first one is Late Breaker that was just presented this morning. It's a future five study on secukinumab. This was a very large study, nine ninety six patients that were randomized to receive either three hundred, one hundred fifty with loading and one hundred fifty without loading, three hundred with loading of secukinumab. These patients were, around thirty percent of them were TNF failures.

Those patients were included in the study. The study was carried out to twenty four weeks to monitor structural progression at sixteen weeks as expected. Segucinemab had better scores as compared to placebo. And at twenty four weeks radiographic progression was significantly inhibited in secukinumab as compared to placebo. The second study I want to talk about is on another IL-seventeen inhibitor, this time it's secukinumab.

There was another study this time carried out to fifty two weeks. This study was presented by Doctor. Vanderheit yesterday and they showed that at fifty two weeks in both the every two weeks and the every four weeks doses of execizumab, execizumab, radiographic progression was halted significantly. These patients were initially on either placebo or adalimumab and were switched to execisumab and then they got the measurements at fifty two weeks. The third study that I want to talk about on radiographic progression is on tofacitinib.

So this is a lot of news around this in the field of psoriatic arthritis. And this study was interesting in the way that they had an Alimumab arm up to fifty two weeks. And they also grouped their patients between CRP levels. So patients with high CRPs and patients with low CRPs or normal CRPs. What they did is that they looked at their radiographic data at fifty two weeks and what they saw was significant diminishing or altering of progression at fifty two weeks in the three arms, the TOFA-five BID, the TOFA-ten BID, and the adalimumab arm.

So as expected, up to fifty two weeks, diminished radiographic progression in the three studies. So great news in the field of psoriatic arthritis. We keep hearing good things. It's been a great congress in this field and specifically we're anxiously waiting the release of the new American College of Rheumatology and National Thoracic Foundation criteria for psoriatic arthritis today at 1PM. So if you're here, make sure to go check it out.

If you want to learn more, make sure to go to roomnow.com to get the latest and greatest information as it happens.

This is Len Calabrese. I'm coming at you from ACR San Diego. It's been an incredible meeting. I'd like to talk to you for a minute about, herpes zoster. A lot of activity here.

We know the risk factors, for drugs, particularly the jackotinibs. A lot of this was over shadowed by the introduction of Shingrix, the new GSK, killed vaccine, coupled to a, adjuvant system. I've talked to a lot of people about it and we're very excited to use it, but we are cautiously concerned about assessing the potential for adjuvants to aggravate autoimmune disease across the image spectrum. I have no reason to suspect this other than from the data. I'm looking forward to robust studies, on behalf of the company that will explore this.

And, I look forward to, offering this to my patients in a sense of shared and informed decision making. Thanks.

Hi. I'm doctor Rachel Tate from Dallas, Texas presenting today for you from ACR twenty seventeen in San Diego, California. I love the plenary sessions. I think that they are the most high yield and they give you a lot of information in very, very small subsets, is really nice for me. It's digestible.

So I just attended a really great plenary session with Doctor. Glenn Dewey on the safety and efficacy of sustained remission in patients on adalimumab versus placebo. So that's something we all talk about, right? We want to know not only how do we achieve remission for our patients, but can we sustain that remission? If so, we do it off of medication?

So this study actually is called the ABILITY-three, if you're interested in more information, and realistically what they looked at is they had patients who had non radiographic SPA, so that's using the ASAS criteria, not the New York criteria. Why is that important? That's important because we are looking at non radiographic spondyloarthritis, not radiographic spondyloarthritis. So in general, they took three zero five patients who had been on adalimumab every two weeks for twenty eight weeks. Of those three zero five patients who had achieved remission, they then broke it down into a placebo group of one hundred and fifty three patients versus a non placebo group with continued adalimumab every two weeks, one hundred and fifty two patients.

So we looked at a couple of things. Number one, we wanted to make sure that the safety data was still there for the patients. So there were no new safety indications for Humira based on what we'd already known. That's really important. But we also wanted to know of the patients who had achieved remission, can we sustain that remission?

Well, we found that seventy percent of the patients who had already achieved remission on adalimumab and who stayed on adalimumab, seventy percent of those patients did very well, but thirty percent had flares. So what about the remission group that had achieved it, then had to be off of the medication who were within the withdrawal placebo group? We actually found that only thirty percent of those patients had no flares. So that's seventy percent of those patients had flares and could be reintroduced to adalimumab. So here's the caveat to that though.

Once they achieved remission, they were taken off of the drug in the withdrawal phase of the study, and then they were put back on to adalimumab, it wasn't as effective. So it's twofold information. So it goes to show that maybe we do need to reconsider the way that we approach these patients. We need to make sure they hit clinical remission, but it's really important to have sustained remission. And partly, this may be keeping them on drug for the extended period of time.

So I hope that you learned something from this session. I know I did. I always send patients and people to plenary sessions because personally, that's where I learned the most bang for my buck. So I hope you enjoy roomnow.com and keep checking us out for up to date information from ACR twenty seventeen in San Diego, California. Hi, I'm Doctor.

Rachel Tate from Dallas, Texas and I'm coming to you live from ACR twenty seventeen in San Diego, California. So I just saw a really great poster, abstract fifteen oh five, from Doctor. Dugum and his group. And they were looking at gender biases for ankylosing spondylitis and particularly patterns of inheritance. They looked at two different cohorts of 105 HLA B27 positive parent and offspring pairs to look not only at patterns of inheritance but if there's a gender bias.

So historically we know that we think that mothers really do transmit this disease to patients, whether that be male or female offspring. But what we actually found was that the fathers had the, increased rate of transmission to patients. Also, it seems to be that the sons are more affected in this particular subset than daughters. So this goes against our conventional wisdom. So it seems that not only HLA B27 positive patients who meet New York criteria for AS, as well as radiographic damage and gender are also transmitted with a male bias.

So I hope you learned something from this. I think that realistically we need to be looking into more inheritance patterns because this challenges our conventional wisdom. So more from ACR twenty seventeen with roomnow.com and I hope you're enjoying the coverage. I know I am. Hi, I'm Doctor.

Rachel Tate from Dallas, Texas coming to you live from ACR twenty seventeen in San Diego, California. There are two things that I really like to talk about when it comes to rheumatology, particularly education in addition to actual use of ultrasound, which is something that I practice in clinical practice as well. But realistically, can we integrate those? So Doctor. Sterling West did a fantastic year interview update for medical education this week, and something that he found in his study and research in this is that of the 113 rheumatology fellowship programs, these are both adult and pediatrics, that 103 of those programs actually believe that we should be training our future rheumatologists with ultrasound, musculoskeletal ultrasound, for diagnostics as well as for doing intra articular injections.

But interestingly, when we looked at that data further, 30 out of 74, so not all of the programs participated in the second part of the study, but 74 of them said that, Wait a second, we don't have a core curriculum. So there's a vast majority of program directors who believe that we should be using musculoskeletal ultrasound as part of our core curriculum for rheumatology, but only 30 out of those 74 and possibly out of 113 programs are actually developing those core curriculums. So I think this is a really important part of what we do in rheumatology. We pride ourselves on being innovators and thinkers about things that we can do to improve our patient's quality of life, but also now to improve our fellowship programs. So I encourage you, if you're a program director or if you have any ideas for supporting program directors, especially if you are the fellows, to develop some of these core curriculums.

I think it's really important. This is the wave of the future. It helps us with diagnosis. It helps to ensure we're putting steroids in the right spots. And I think that that's the wave of the future regardless of reimbursement.

So more from rheumnow.com. Check us out. We'll be here all week at ACR twenty seventeen in San Diego.

Hello, friends. Doctor. Akhirkar from Mumbai, India here at ACR twenty seventeen. I was particularly looking at the data about new molecules in psoriatic arthritis, and ACR was really not disappointing in that respect. We have a lot of data about new molecules in psoriatic arthritis here presented.

The first molecule on the horizon, tofacitinib. The Opel broaden and Opel beyond data presented showing good efficacy in terms of significant difference in the patient related outcomes. The Opel balance study, thirty six months data about the safety of tofacitinib. No new safety signals there. And doctor Vanderheit presented the Opel broaden study, a study with active psoriatic arthritis patients, those who are refracted to dBERTS, TNF alpha nine, four twenty two patients, and the study duration of twelve months.

More than ninety percent of the patients did not have any significant radiological progression. I'm sure one year is not that bigger duration for radiological progression, but it's the step in that right direction. Coming to the second molecule on the horizon in psoriatic arthritis, execizumab. Another study, a phase three SPIRIT two study data presented with good efficacy with significant difference in the patient related outcomes. Some data about abarticept in psoriatic arthritis, promising data, but but long way to go for abarticept.

As far as the established molecules are concerned, Aprimilast, four years safety and efficacy data with Aprimilast as monotherapy in psoriatic arthritis. Good efficacy with ACR twenty, fifty, 70 of 68, forty three percent, twenty three percent respectively, and a PASI 75 and 50 score of forty and sixty seven percent respectively. So so good things as far as Eprimulast is concerned. And lastly, not to forget, secukinumab, safety data of seven seven six nine patient years of exposure presented here at the ACR. So all in all, as things stand today, good data for psoriatic arthritis and molecules.

Lot of things to expect in the future for psoriatic arthritis patients. Thank you.

Hi. I'm Bill Shergy. I'm talking to you from the American College of Rheumatology meeting in San Diego 2017, and just left a very exciting seminar on giant cell arteritis. From, the take home messages from this meeting and this session in particular, giant cell arteritis is really a hot area of interest. We had three great speakers in Drs.

Wyand, Karmani, and Grayson who covered the basic pathophysiology, current treatment recommendations, and imaging studies. These lectures were all superb. Learned some interesting take home points on the pathogenesis, and one of the really take home points that I thought about afterwards was that you really are losing privileged sensitivity of the aorta in these giant cell arteritis disorders, Between the combination of increased CD4 cells, leaky portals into the vessels, failure of checkpoints, all lead to the vascular damage. Equally important for the patients in evaluating is what they happen to see in the periphery. These are manifestations primarily generated by acute inflammatory products from the liver.

This is the PMR type of features that we've come to recognize. When we move into treatments, certainly steroids have remained the mainstay of treatment, but over the last few months, we've had the first medication actually approved for the treatment of giant cell arteritis and tocilizumab, and this has really become a very important topic. But one interesting area that we've come to see is this seems to focus primarily on the acute phase reactants, the PMR type activity. And even doctor Wyand was a little uncertain as to what is gonna happen long term to vascular manifestations and how closely we are going to need to follow these patients. So it's a great addition to our armamentarium.

We can control the disorder. We can minimize steroid use, but we still need to follow the patient, particularly for some vascular complications. There was some sobering data of patients actually having vascular complications five to ten years out from being disease free. Lastly, what we're certainly looking for in the diagnostic arena is imaging modalities over an invasive temporal artery biopsy. And we've been real excited about the ultrasound.

Some initial reports on ultrasounds really showed sensitivity and specificities in the 60 to 90 kind of range, but other studies have not come up with this. Also, there's MRI and PET scanning, and these two have very variable sensitivities and specificities, but in the certain study that compared biopsy to imaging modalities, it really appeared that the imaging modalities may help more than the biopsy, and their current suggestion is if you have a firm diagnosis or a very good looking diagnosis on an imaging study in a classic clinical presentation, then perhaps you can skip the biopsy entirely. If there is a negative ultrasound or other imaging in the setting of a classic clinical history, pursue the biopsy. If it's a negative imaging and not a classic story, once again you're free from doing the biopsy. So, with that, I will close and say for more information, go to RheumNow.