ACR 2019 Day 2A Save
ACR 2019 Day 2A by Dr. Cush
Transcription
Hi. I'm doctor Jack Cush, and this is the ACR two thousand nineteen podcast. We're coming to you from the annual meeting in Atlanta, Georgia. This episode is a collection of our faculty reports, interviews, and panel discussions recorded live from the RheumNow booth. I hope you enjoy and learn.
Hi. I'm David Liu from Melbourne, Australia reporting from RheumNow from ACI twenty nineteen here in Atlanta. Some really interesting anchor associated vasculitis abstracts on the floor today and really practice changing kind of stuff. The first one was reporting the results from the RITASA REM trial which looked at Rituximab versus Azathioprine as maintenance for ANCA associated vasculitis following Rituximab induction. Multi center study, really important study and the results were fairly clear in that Rituximab really did outperform azathioprine as maintenance therapy.
Really impressively though, the safety profile comparing between rituximab and azathioprine was pretty similar even in terms of hypergammaglobulinemia, the kind of thing that you might worry about if you're giving rituximab every four months like they were doing in the study. Second practice changing study on ANCA associated vasculitis today was actually from the French from a large French collaborative that's been collecting vasculitis data since 1983. They looked at seven hundred and ninety five GPA vasculitis patients, and it was really examining the question, do we ever cure patients, and do those cured patients ever do better than the ones who aren't supposedly cured, the ones that stay on therapy versus the ones who have a sustained remission off therapy. And comparing these patients at three years, five years, greater than seven years, they didn't find any difference between the two groups. Really comes down to the fact that anchor associated vasculitis is one of those conditions that you often have to treat ongoingly with maintenance therapy on an ongoing basis to really get the best outcomes.
So really thought provoking stuff in ankle associated vasculitis today. There's some interesting abstracts from the French group in coming days as well. Log on to the roomnow.com for for more data from this whole meeting, and I'll see you there.
This is doctor Catherine Dow reporting for RheumNow. I'm at the ACR twenty nineteen meeting in Atlanta, Georgia, and I just got out of a very interesting session. This is on clinical infection risk and safety profile for RA therapeutics and there were several posters that were or abstracts that were presented and so I'm just gonna summarize what I found out. The first one was looking at, hypogammaglobulinemia in patients who've received rituximab. Now there are certain patients who, have underlying hypogammaglobulinemia who then have developed infection.
But what about those patients who actually had a normal immunoglobulin level and then received rituximab and then developed hypogammaglobinemia? What is the profile of those patients and what happened to those patients? Well in this one retrospective trial, they looked at these patients in particular. They found that about twenty four percent of patients on rituximab can develop hypogammaglobinemia. And they found that those patients at risk for developing it were number one, with ANCA patients associated vasculitis, patients who received cyclophosphamide in the past, and three, patients who have been exposed to high dose steroids.
So those patients are at risk. Not only that, these patients have a higher rate of infection, though non clinically significant. And then the other abstract that was presented was also the rate of major adverse cardiovascular events, MACE, and VTE in patients across upadacitinib. So these are based on phase three trials and they found that actually there's no increased risk for MACE or VTEs with OOPA. Alright, so this is kind of different from all the other JAK inhibitors.
Why that? Well, the author was saying, first of all, the follow-up is short compared to some of the other JAK inhibitors. It's only two years. They didn't find any correlation with OOPA with dosing. So higher doses of OOPA didn't increase the risk for cardiovascular events VTEs.
They didn't find any correlation with lipid numbers and they didn't find any correlation with platelets. Alright, so another abstract. This one is looking at the Medicare database. This is Jeff Curtis's study and they were wanting to see what happened to patients who received long term low dose steroids. So they were divided up into mg, less than five mg, five-ten mg, and greater than ten mg.
And there were over 246,000 patients studied. Forty seven percent of them with rheumatoid arthritis were on, or I'm sorry, rheumatic diseases were on glucocorticoids. They found that patients who required long term glucocorticoids actually had higher use of narcotics. They also had an increased rate of hospitalized infections. And this also correlated with, prior studies where the higher the milligrams per day of steroids, the higher the rates of hospitalized infection.
Patients requiring long term glucocorticoids were also patients who had rheumatoid arthritis.
They also had less follow-up with their physicians. Take home point, minimize steroids, and also see your patients quickly and frequently. And then the last abstract that was presented during this session was evaluating the risk for cancer in patients with biologics compared to patients who are on traditional synthetic DMARDs. This is a French database study. They found that when they evaluated 83,659 patients long term, they didn't find any risk for increase in solid malignancy, just like in the other studies.
And the hazard ratio for lymphoma is 1.35 non significant p value, and there's really no difference in cancer whether or not you're on biologics therapy or biologics plus DMAR. So this actually just confirms what we know that biologics really don't increase the risk for cancer or lymphoma. So if you want more information please go to roomnow.com acr19. Roomnow.com. Doctor.
Catherine Dow reporting.
Hi everyone my name is Kanika Manga and I'm with RheumNow and we are at the American College of Rheumatology Annual Meeting and wow what a great start it's been and I'm extremely excited to have Doctor. Ravelle here with me right now. Can't wait to ask him lots of questions for us. Hi Doctor. Ravelle how are you Good
to see you.
Nice to see you. So first off congratulations for being ACR master. That's amazing.
Well I sort of feel a question of having survived that long. Mean given the alternative but it's an honor. It truly is an honor. I've been working with the ACR for, Lord, nearly forty years, and this is a very great honor to have been selected for this.
Well, it's my honor to be here with you right now. What advice would you have for people that want to pursue a career in rheumatology?
Well this is a very good time to be going to rheumatology. We have a much clearer concept of pathogenesis, better aids in diagnosis and by all means more and effective treatments albeit expensive. We really can now do something for our patients. We are taught diagnosis and to be skilled therein and we know that early diagnosis and early initiation of effective therapy is very important in outcome and that we have the tools now for that early diagnosis with genetics, with biomarkers, with new imaging techniques and the like.
That's extremely true and of course I'm biased and I love rheumatology as well. So Doctor. Ravelle how do you feel the field has changed over the years?
Well when I joined, we were called the American Rheumatism Association when I first joined this organization. Actually, first meeting I attended was in as a medical student in 1976. So that that it goes back quite a ways. Things have changed a great deal. Especially has grown enormously.
The awareness of what it is and of the diseases involved they're in and especially like I said with this growing awareness we can diagnose earlier. The technology has remarkably moved forward and the ACR has more
and
more been enabled to really help us in our mission.
That's actually very, yeah, very true. Now what are you most excited to see at this year's meeting? What session are you most excited to attend?
Well, the plenaries are are remarkable, and they they're they're they're especially highlighting novel treatments and novel pathogenesis. The the I'm just completely bowled over how fast the scene the scenery is changing and and how much that we're going to be able to do. And it it makes this especially all the more exciting. I think there's so many different sessions that that one can attend, so many ways that appeal to an individual's own focus or expertise that it's like being a kid in a candy store. The only danger is getting diabetic.
That's true. It's a Disney world for a rheumatologist. Rheumatologist. So I am extremely excited about the Hench lecture that you're going to give us on Tuesday morning. Can you tell us a little bit more about what's in store for us?
Well that's a special passion of mine. Chronic back pain is a major challenge in this country. It's the leading cause of disability. Huge billions of dollars in lost productivity, work wages, disability funding and all that kind of stuff. And it's not well managed by the community, especially by rheumatology community, where looking at some insurance databases, fourteen percent of patients with chronic back pain ever even encounter a rheumatologist.
The problem is that one third in the NHANES study, twenty percent of The US population, twenty percent has chronic back pain. One third of them have chronic inflammatory back pain. And of course that's a symptom and raises suspicion high for spondyloarthritis. With the diminishing manpower we have in rheumatology, which will turn around, this represents a special challenge because mostly people don't counter rheumatologists because some of the novel terminology like that ankylosing spondylitis is now synonymous with radiographic axial spondyloarthritis. All this is unknown to primary care practitioners.
And this is very troubling because spondyloarthritis represents a group of diseases where so many novel and effective treatments have come forward, but they work by far the best and do their best job preventing disability and deformity if initiated early in the disease course. So this is a big focus of mine. We're gonna start with looking at the specter of chronic back pain in United States, to chronic inflammatory back pain, talking about non radiographic axial spondyloarthritis, the challenge that it represents, especially in women, because the majority of people with non radiographic are women and and too many are called fibromyalgia and again it's an issue we know that these medications work very well even before the x rays turned positive which seven to ten years after the onset of symptoms So I'm going to really be focused on that and finally to where we've gone with this with some of the new advances in genetics where we're understanding more and more what causes disease and especially where you got a gene, you've got a drug. I mean the genes predict the drugs that are going to work. All the novel treatments have been planned by genetics and so this is important knowledge to have.
I just wish that we had the manpower and the focus to better address this at a national level from the denominator of chronic back pain.
Thank you so much for that explanation. I'm now even more excited and thrilled about the lecture. Once again, thank you so much for talking to us at RheumNow. And for everyone watching this, please log on to roomnow.com for more information. Thank you.
Thank you.
Hi. I'm Philip Rumson. I'm from Brisbane in Australia, and I've just come back from Dan Claw's session on fibromyalgia, which was a fantastic summary on how to think about fibromyalgia and how to treat fibromyalgia. One of the things that he reminded us is that there are lots of chronic pain syndromes that we don't necessarily think about. Things like dry eye, necessarily that's also like a fibromyalgia of the eye in a lot of people.
And think about these other syndromes in the patients that you're seeing. He reminded us that potentially the relevance of tender points isn't that relevant now and that you can ask questions like, are you uncomfortable when people hug you? Are you uncomfortable when people do your blood pressure? Are much more relevant because these are chronic widespread pain disorders, not just focal pain disorders. He also reminded us that people really don't often have just one type of pain, they have mixed pain.
And so you've got to think about the proportion of pain that each person has. Do they have an amount of nociceptive pain, which you would expect from say rheumatoid, neuropathic pain, and then central pain, because you're never going to make progress unless you actually target the cause of their pain. Finally, he reminded us that opiates, well, they often work to start with the longer you are on them and the higher doses that patients end up on, the less effective they are. And he reminded us that there are more effective therapies including SNRIs and gabapentinoids and simple tricyclics, that, have evidence. And he also reminded us of the burgeoning amount of evidence for non pharmacological treatments like CBT and regular activity.
And you're going to make progress with your patients when you actually put together a combination of these treatments because not each one of them is very effective, but when you combine them together, they often create a package that's actually effective for patients. So if you want to know more about this, I recommend you go to roomnow.com.
Hello, my name is Torkel Ellington and I'm from Odinson University Hospital in Denmark and I've been asked to add a few comments on poster five sixty three which is data from one of our PhD students, Rick Asmussen, who is unfortunately not able to be here. And it's about sex differences in ankylosing spondylitis and non radiographic axSpA where Rege collected 100 patients consecutively from a university clinic setting in Swedenborg and Odense, Denmark. And we decided to focus on pain parameter that we not usually collect when we evaluate disease activity in ankylosing spondylitis and non radiographic axSpA. And the two main findings are that the Basti among females with non radiographic axSpA was significantly higher than in the males and that in both ankylosing spondylitis and non radiographic axSpA we found significant higher number of tender points when evaluated clinically. And this is interesting because obviously pain is a challenge for both the patient and the physician when you deal with ankylosing spondylitis.
But when you see sex differences like this then you need to be very cautious when you make decisions on when you intensify or make evaluations that are needed for treatment changes. Rege will evaluate this further in her coming papers and the poster just presented is last week published in Arthritis and Research Care, so please check it up there.
Hi. I'm David Liu from Melbourne, Australia reporting from RheumNow from ACI twenty nineteen here in Atlanta. Really interesting poster on the floor today from the IgG4 related disease clinic at MassGen. Obviously, these guys have been collecting a lot of data over time and they've got a large cohort looking at their 205 patients. They wanted to see whether there was a mortality difference between the patients that they had versus age age and disease match controls.
And so they looked at the standardized mortality rates between their patients and comparing that to normative data. The really interesting thing, and I wouldn't have expected this, is the fact that, in fact, these patients it's not a life limiting condition in these patients, that these patients have at least short term mortality, which is comparable to what they would look like otherwise. It didn't matter how you splice or dice it, if you looked at criteria positive patients, male patients, patients with internal organ involvement, they all seem to do okay. Now is this because Mastroon are really good at treating IgG4 related disease, or is this because that this isn't a life limiting condition or somewhere in between? That question still remains to be answered.
And really what we need to do is get broader data, longer term data, data from more centers, and data from places where they're maybe not giving as much rituximab upfront where steroids steroid first line therapy is more common. So more data needed in this space really starts to ask question though, is IgG4 related disease a life limiting condition or not? I'm David Liu and for more information go to rheumnow.com.
Hi, I'm Doctor. Rachel Tate coming to you from Atlanta for ACR twenty nineteen. I just attended a really great poster session, so I'm going to tell you a little bit about Abstract eleven sixty three. So, number one, we know that inflammatory pain is often a cause for patients coming to a rheumatology office. And we also know that in terms of ASAS criteria, we need MRI changes as well as an HLA B27 positivity as part of that criteria.
Not for every patient though. This is a Belgian study that looked at 138 patients and they wanted to understand if inflammatory back pain was actually predisposing patients to have MRI changes. They took these one hundred and thirty eight patients and they did MRIs on everyone and found that those patients who had inflammatory back pain symptoms as well as HLA B27 positivity in these newly diagnosed ACSPA patients who all were TNF naive, they found that inflammatory back pain was actually probably a harbinger for severity of disease. On MRI, the most common finding were erosions, but predominantly in the patient population that had experienced inflammatory back pain symptoms. So, though even this means that inflammatory back pain is something we need to be worried about, I argue that because this is a small study, non inflammatory back pain symptoms may also be something we need to really look at.
So we need to make sure we're properly imaging patients based on their symptomatology, not just for ASAS criteria. Check us out on roomnow.com and RoomNow on Twitter. We can't wait to give you more information from this meeting. It's been a great one. Hi, I'm Doctor.
Rachel Tate from West Palm Beach, Florida coming to you from Atlanta for ACR twenty nineteen. I just got out of a great session this morning. The CSRO did a small legislative update, which I'll be blogging on later at roomnow.com. But I wanted to share one piece of really vital information for you if you are unaware. In rheumatology, we're really good at advocating for our patients, but we need to be better advocates for our self.
Politically, legislatively, we need some help in this particular regard. So the CSRO decided to update their website this year. It's csro.info. Why I'm telling you this is because down the next few months we're going to see a huge change on the website. They're putting together an interactive state map that allows you to go to click on your state and you will see all of the legislature and how it affects you clinically as a physician.
And also how it affects the patients. Why is this tool useful? Well, a couple of things. Number one, if you want to stay up to date and with your legislators, this is a way to do it. But also, if you have a patient who's invested in their own advocacy and wants more information, it's another way for them to do that.
So if you have legislature coming down the pipeline, they will also have direct links of how to interact with that, what to say, who to talk to, all of it will be done for you. Now it's not out yet, but it will be on csro.info and I highly recommend you check it out. For me, I think this is a game changer. We need to be advocates for ourselves. So in addition to what you do in clinical practice, this is a way to do it.
So keep checking us out on roomnow.com. Handle for Twitter is roomnow. We're going to send you more updates from ACR twenty nineteen in Atlanta.
Hello,
I'm Jonathan Kay from of Massachusetts Medical School in Worcester, Massachusetts. I'm at ACR twenty nineteen in Atlanta, and I just heard an interesting presentation by Doctor. Ernest Choi about major adverse cardiovascular events and venous thromboembolic events in patients with rheumatoid arthritis from the integrated safety database of upadacitinib. He presented data from the five clinical trials in the phase three program of upadacitinib looking at two doses, fifteen and thirty milligrams, as well as the comparators, methotrexate, adalimumab, forty milligrams every other week, and placebo. What he presented was that the rates of major adverse cardiovascular events and venous thromboembolic events overlapped for all of the treatment groups.
Upadacitinib at fifteen and thirty mg taken by mouth daily, adalimumab forty mg taken subcutaneously every other week, methotrexate, and placebo. All of the patients with major adverse cardiovascular events had at least one cardiovascular risk factor, and patients with venous thromboembolic events also had risk factors for venous thromboembolic events, such as a prior deep venous thrombosis, knee replacement, or other risk factors. The conclusion of the study was that there was no dose relationship between upadacitinib and the occurrence of these events, and the rate of these events was similar for upadacitinib with the comparators adalimumab, methotrexate, and placebo. What this does not answer is the question as to why patients treated with JAK inhibitors are developing venous thromboembolic events. It's not related to platelet counts since platelet counts did not change significantly throughout the time period that patients were treated with upadacitinib, and patients on placebo also developed these events.
It will be very important to understand the mechanism whereby venous thromboembolic events occur in patients treated with JAK inhibitors so that we can predict which patients are at risk and treat them appropriately to prevent this devastating adverse effect, which may be an effect of this class of medications and may be completely unrelated. For more information, go to RheumNow. I'm Jonathan Kaye. Thanks.
Great. Okay.
You're always first take Doctor. Kaye. Okay.
Arthur Lau reporting, from ACR two thousand nineteen from Atlanta for our roomnow.com. I want to talk to you an interesting study I, just saw on the poster hall, abstract number fourteen twelve, the, oral shift study, where which was an open label, global phase three b four study, where patients with methotrexate inadequate response were initially started on, ZALGEN's, MR eleven milligrams for, twenty four weeks as open label. And then if the if these patients were able to achieve, low disease activity based on C. Dye, they were then randomized to either go on monotherapy of these Zalogens MR11 milligrams or to stay on their methotrexate. You have to be on fifteen to twenty five milligrams of methotrexate oral, at the beginning to be included in this study, and the mean dose was somewhere between sixteen and seventeen milligrams in each group.
What the study showed is that after another twenty four weeks, of either mono therapy or continuing methotrexate, there was very little difference for health related quality of life for both the mental and the physical component of the SF-thirty six. So overall, what this shows is that if you were able to achieve low disease activity for, after starting on a JAK inhibitor, Xaljanz MR in this instance, you can actually do relatively well and discontinue methotrexate, and the patients can still maintain good quality of life. This is important because, you know, I have many patients with rheumatoid, with comorbidities that are either unable or unwilling to continue on methotrexate. So this just reassures me that once they, initially do well, I can discontinue their methotrexate, and likely, will continue to do well in the future. Thanks for, tuning in here.
And for more information, log on to, roomnow.com for further informations and to see their extended coverage for ACR.
This is Doctor. Catherine Dow reporting for RheumNow. I'm at the ACR twenty nineteen meeting here in Atlanta, Georgia. And I just got out of an exciting lecture. It's the Klimper Lecture with Doctor.
James who presented The Winding Road to Lupus. So what are the main take home points here? Well, as you know, there are a lot of patients who are positive ANA. In fact, up to twenty five percent of people in the healthy population will have a positive ANA. But yet, only five to eight percent of these patients actually develop lupus.
Well, can we predict who will develop lupus? And what about those twenty percent of patients who don't develop lupus? What's so special about them? So Doctor. James, who works for the OMRF, basically has a database that is accessing the Department of Defense.
And essentially, what was found was that number one, these patients who develop and transition into lupus have actually a few risk factors. They're typically first degree relatives of family members who have lupus. Not only that, they probably have a lot of autoantibodies. The more autoantibodies you have, actually, and also an interferon signature, that means you're more likely to progress to lupus. What she also found was that other risk factors traditionally that we've seen also predispose patients to develop lupus.
That's tobacco smoking, that is hormones, so that's either an oral contraceptive or else hormone replacement therapy. In addition to that, vitamin D deficiency and sleep deprivation. That would be me, right? So if you sleep under seven hours a night, that puts you at risk. Now what's also interesting is that alcohol, moderate alcohol could be protective against developing lupus.
So, I didn't see that one coming. But anyways, when they compared patients who are positive ANA to patients who are negative ANA and patients who are lupus. They found that these positive ANA patients who are healthy actually have suppressive cytokines as well as inflammatory cytokines. They're not at all as healthy as we thought. So there are these triggers that may have patients progress and there's currently a study.
In fact, one of our study sites is at UT Southwestern. That's where I am faculty at. And what we're looking at right now is patients who are ANA positive who also have one sleep criteria positive. And we want to know whether or not these patients will develop lupus if given hydroxychloroquine. So the study is in progress.
If you have patients who are interested in enrolling, you can always contact us. And for more information please go to roomnow.com or acr19.roomnow.com. Doctor. Catherine Dow reporting.
Everyone. I'm Olga reporting from the annual ACR meeting here in Atlanta. Today, would like to talk about the abstract number three zero one, which speaks about pamela recommendations on use of imaging studies in gout. So there is a lot been told about guiding our treatment based on serum uric acid, but there is not really a clear recommendation how we could use imaging modalities in monitoring and guiding treatment of, gout patients. So, Pamela's ultrasound study group included rheumatologists, radiologists, statisticians, and methodologists to develop recommendations in this regard.
After reviewing all available, evidence, they graded most of their recommendations at level two and three and oh, based on the all the evidence in the literature, and then they developed following recommendations. Recommendation number one is that we can use ultrasound to detect the elementary deposits in the joints, and we could use dual energy CT scan to detect monosodium murine crystals in patients with gout. The same group suggests that both ultrasound and dual energy CT scan can be not so sensitive in detecting monosodium urate crystals in damage in patients who had disease duration of less than two years, but is very specific, so that justifies the use of those modalities. It also says that patients with gout, do not present with very clear, imaging results on X-ray and CT scan in terms of joint damage, but based on low cost of the study and high sensitivity, it is recommended to still use x-ray and CT scan as initial, imaging study in patients with gout. As it comes to an MRI and ultrasound, these modalities are considered very effective in detecting synovitis and tenosynovitis, but they're not very useful in assessing for crystal deposition and gouty erosions in patients with gout.
And, also, there is, no sufficient evidence to support using these modalities in, guiding treatment choices or in monitoring patients over time, and it says it's best to use these modalities for initial diagnosis only. Although, it can be used as a complementary monitoring techniques in most of the cases. If you would like to learn more, can read about us more on RheumNow, and also continue following us online. Thank you, and have a nice day.
Okay. Sarah Cushman, from Northwestern University in Chicago. I'm coming to you live from the ACR meeting in Atlanta, for RheumNow. What's going on today on Sunday? Well, one of the exciting abstracts we're going to see today is the first of the phase three trials of guzelkabab in psoriatic arthritis.
We've seen progression of treatment options in psoriatic arthritis looking at different approaches, different pathways and now we've got the first phase three data for an interleukin twenty three inhibitor. These drugs are really hot in the psoriasis space. We've seen phase two data in psoriatic arthritis and now we're seeing two trials at this meeting. The first of which is a plenary session today in phase three data for gazelkumab, very effective in psoriatic arthritis, effective at two different dose arms either given every eight weeks as is, conventional for psoriasis and every four weeks, thinking that perhaps psoriatic arthritis would need a higher dose. The trial today looked at patients who are both biologic naive and a small percentage of patients who are biologic experienced.
There was a slight difference, in dosing arms with the four week, patients getting a little bit better numerical response, though not statistically different. We're going to see the second phase three trial later in the week in which there wasn't a real difference between arms. The key point of the second trial, which includes patients who are all biologic naive, is that there was radiographic benefit statistically significant at the highest dose arm. Really cool data, the safety profile of this pathway is tremendous. It does appear that we're going to see fewer infections, fewer adverse events than we've seen with other cytokine inhibitors.
So, we're really looking forward to having IL-twenty three inhibitors in our armamentarium for psoriatic arthritis as rheumatologists. Our psoriatic our dermatologist friends have been using it for psoriasis for a while and we're excited to get on the bandwagon.
Hi, I'm Mike Putman coming to you from ACR twenty nineteen reporting from RheumNow. I wanted to talk briefly about the ACR urine review today. It was a wonderful lecture. And the select monotherapy came up. With trials like this, I think there's something important for you to remember.
That trial was run on patients who were methotrexate non responders and went on to either continue methotrexate or get upadacitinib. The implication when you hear the trial discussed is that upadacitinib was better than methotrexate. However, this isn't a population of patients who already didn't respond to methotrexate so it's not surprising that a new drug would perform better than the old drug that already wasn't performing. It's a very different question than saying I have a patient with rheumatoid arthritis, should I give them methotrexate or upadacitinib? In a blank slate population it may be that they're equivalent, may be that methotrexate even works better than upadacitinib.
We're still waiting for a trial that's going to assess that question. I think it's important to remember that a trial assessing a new therapy in non responders, continuing therapy, doesn't necessarily prove that point. Thank you so much. I hope you're all enjoying the meeting. If you're looking for more information, please go to RheumNow Live.
RheumNow.
Hi, I'm Doctor. Rachel Tate coming to you from Atlanta 2019 for ACR twenty nineteen. So I just got through an amazing poster session. Check them out if you haven't, and definitely follow us at RheumNow for Twitter and roomnow.com. But I wanna tell you a little bit about this year.
So 2019 and 2020 is gonna be a huge year for gout. In fact, on Wednesday, we're going to have the updated gout guidelines or gout lines as I like to call them. And what I wanted to share with you as a little appetizer are the actual panlar recommendations for 2019. So panlar decided to put together a task force of nine rheumatologists, musculoskeletal radiologists, ultrasonographers, statisticians and methodologists. And they looked at a huge literature review to determine how we can best utilize imaging for our patients.
So they came up with eight particular recommendations, and I will refer you to abstract three zero one or poster three zero one for further information, but I wanna highlight two things. The entire task force went together on two. There was a consensus on two of these recommendations. The first is for those difficult patients. So when you have a patient who is difficult to diagnose, you think that they're Galpa, perhaps they are not.
The group unanimously decided that ultrasound or scanning would be appropriate for these particular patients. The other subset is when you have patients who you believe have MSU or uric acid deposition in crystals in other tissues besides the joints, they again recommend ultrasound and scanning. So they looked at all of the literature that they could to determine between x rays, CT scans, MRIs, and ultrasounds, and this is what they came up with. So if you want to look at it a little bit further, a little more in-depth, I recommend abstract number three zero one, poster three zero one. And thank you for coming to to share some time with us in Atlanta for ACR twenty nineteen.
And check us out on Twitter. The handle is at room now or room now dot com. And more will come from gout. I promise you. So stay tuned.
Hey. Hi. I'm doctor Janet Pope. I'm a roving reporter for RheumNow at the ACR twenty nineteen conference in sunny but cool Atlanta. I'd like to talk to you about abstract four sixty four.
This is a Japanese study, and the reason I'm talking about it, even though it's a little study, is because it answers a clinically relevant question. The question is if you're seropositive and you have rheumatoid arthritis and you're treated with a TNF inhibitor, will reduction of the rheumatoid factor independent of improvement on your disease activity score affect erosions? So this was a small study and they only looked at seropositive patients. The mean, positivity was a level of one hundred and four at the beginning, over fifty patients, and they looked at four months and twelve months. And patients who became lower in the rheumatoid factor positivity by at least thirty percent had less erosions at the end of a year even if you adjusted for DAS score.
So lowering your rheumatoid factor with a TNF inhibitor interestingly seems to give less erosions even if it was an equal change in DAS. I picked this paper because it's really important when we know that anti CCP has been looked at a lot, and we know that as a, for instance, adalimumab doesn't lower anti CCP as much as say abatacep, this is looking at rheumatoid factor within people on TNF inhibitors. Will this change my practice repeating RF factors over and over? No, but it gives me a hint that there's a pathway independent of disease activity that causes joint erosions in RA. Thank you.
Hi. I'm David Liu from Melbourne, Australia reporting from RheumNow from ACI twenty nineteen here in Atlanta. Some really interesting anchor associated vasculitis abstracts on the floor today and really practice changing kind of stuff. The first one was reporting the results from the RITASA REM trial which looked at Rituximab versus Azathioprine as maintenance for ANCA associated vasculitis following Rituximab induction. Multi center study, really important study and the results were fairly clear in that Rituximab really did outperform azathioprine as maintenance therapy.
Really impressively though, the safety profile comparing between rituximab and azathioprine was pretty similar even in terms of hypergammaglobulinemia, the kind of thing that you might worry about if you're giving rituximab every four months like they were doing in the study. Second practice changing study on ANCA associated vasculitis today was actually from the French from a large French collaborative that's been collecting vasculitis data since 1983. They looked at seven hundred and ninety five GPA vasculitis patients, and it was really examining the question, do we ever cure patients, and do those cured patients ever do better than the ones who aren't supposedly cured, the ones that stay on therapy versus the ones who have a sustained remission off therapy. And comparing these patients at three years, five years, greater than seven years, they didn't find any difference between the two groups. Really comes down to the fact that anchor associated vasculitis is one of those conditions that you often have to treat ongoingly with maintenance therapy on an ongoing basis to really get the best outcomes.
So really thought provoking stuff in ankle associated vasculitis today. There's some interesting abstracts from the French group in coming days as well. Log on to the roomnow.com for for more data from this whole meeting, and I'll see you there.
This is doctor Catherine Dow reporting for RheumNow. I'm at the ACR twenty nineteen meeting in Atlanta, Georgia, and I just got out of a very interesting session. This is on clinical infection risk and safety profile for RA therapeutics and there were several posters that were or abstracts that were presented and so I'm just gonna summarize what I found out. The first one was looking at, hypogammaglobulinemia in patients who've received rituximab. Now there are certain patients who, have underlying hypogammaglobulinemia who then have developed infection.
But what about those patients who actually had a normal immunoglobulin level and then received rituximab and then developed hypogammaglobinemia? What is the profile of those patients and what happened to those patients? Well in this one retrospective trial, they looked at these patients in particular. They found that about twenty four percent of patients on rituximab can develop hypogammaglobinemia. And they found that those patients at risk for developing it were number one, with ANCA patients associated vasculitis, patients who received cyclophosphamide in the past, and three, patients who have been exposed to high dose steroids.
So those patients are at risk. Not only that, these patients have a higher rate of infection, though non clinically significant. And then the other abstract that was presented was also the rate of major adverse cardiovascular events, MACE, and VTE in patients across upadacitinib. So these are based on phase three trials and they found that actually there's no increased risk for MACE or VTEs with OOPA. Alright, so this is kind of different from all the other JAK inhibitors.
Why that? Well, the author was saying, first of all, the follow-up is short compared to some of the other JAK inhibitors. It's only two years. They didn't find any correlation with OOPA with dosing. So higher doses of OOPA didn't increase the risk for cardiovascular events VTEs.
They didn't find any correlation with lipid numbers and they didn't find any correlation with platelets. Alright, so another abstract. This one is looking at the Medicare database. This is Jeff Curtis's study and they were wanting to see what happened to patients who received long term low dose steroids. So they were divided up into mg, less than five mg, five-ten mg, and greater than ten mg.
And there were over 246,000 patients studied. Forty seven percent of them with rheumatoid arthritis were on, or I'm sorry, rheumatic diseases were on glucocorticoids. They found that patients who required long term glucocorticoids actually had higher use of narcotics. They also had an increased rate of hospitalized infections. And this also correlated with, prior studies where the higher the milligrams per day of steroids, the higher the rates of hospitalized infection.
Patients requiring long term glucocorticoids were also patients who had rheumatoid arthritis.
They also had less follow-up with their physicians. Take home point, minimize steroids, and also see your patients quickly and frequently. And then the last abstract that was presented during this session was evaluating the risk for cancer in patients with biologics compared to patients who are on traditional synthetic DMARDs. This is a French database study. They found that when they evaluated 83,659 patients long term, they didn't find any risk for increase in solid malignancy, just like in the other studies.
And the hazard ratio for lymphoma is 1.35 non significant p value, and there's really no difference in cancer whether or not you're on biologics therapy or biologics plus DMAR. So this actually just confirms what we know that biologics really don't increase the risk for cancer or lymphoma. So if you want more information please go to roomnow.com acr19. Roomnow.com. Doctor.
Catherine Dow reporting.
Hi everyone my name is Kanika Manga and I'm with RheumNow and we are at the American College of Rheumatology Annual Meeting and wow what a great start it's been and I'm extremely excited to have Doctor. Ravelle here with me right now. Can't wait to ask him lots of questions for us. Hi Doctor. Ravelle how are you Good
to see you.
Nice to see you. So first off congratulations for being ACR master. That's amazing.
Well I sort of feel a question of having survived that long. Mean given the alternative but it's an honor. It truly is an honor. I've been working with the ACR for, Lord, nearly forty years, and this is a very great honor to have been selected for this.
Well, it's my honor to be here with you right now. What advice would you have for people that want to pursue a career in rheumatology?
Well this is a very good time to be going to rheumatology. We have a much clearer concept of pathogenesis, better aids in diagnosis and by all means more and effective treatments albeit expensive. We really can now do something for our patients. We are taught diagnosis and to be skilled therein and we know that early diagnosis and early initiation of effective therapy is very important in outcome and that we have the tools now for that early diagnosis with genetics, with biomarkers, with new imaging techniques and the like.
That's extremely true and of course I'm biased and I love rheumatology as well. So Doctor. Ravelle how do you feel the field has changed over the years?
Well when I joined, we were called the American Rheumatism Association when I first joined this organization. Actually, first meeting I attended was in as a medical student in 1976. So that that it goes back quite a ways. Things have changed a great deal. Especially has grown enormously.
The awareness of what it is and of the diseases involved they're in and especially like I said with this growing awareness we can diagnose earlier. The technology has remarkably moved forward and the ACR has more
and
more been enabled to really help us in our mission.
That's actually very, yeah, very true. Now what are you most excited to see at this year's meeting? What session are you most excited to attend?
Well, the plenaries are are remarkable, and they they're they're they're especially highlighting novel treatments and novel pathogenesis. The the I'm just completely bowled over how fast the scene the scenery is changing and and how much that we're going to be able to do. And it it makes this especially all the more exciting. I think there's so many different sessions that that one can attend, so many ways that appeal to an individual's own focus or expertise that it's like being a kid in a candy store. The only danger is getting diabetic.
That's true. It's a Disney world for a rheumatologist. Rheumatologist. So I am extremely excited about the Hench lecture that you're going to give us on Tuesday morning. Can you tell us a little bit more about what's in store for us?
Well that's a special passion of mine. Chronic back pain is a major challenge in this country. It's the leading cause of disability. Huge billions of dollars in lost productivity, work wages, disability funding and all that kind of stuff. And it's not well managed by the community, especially by rheumatology community, where looking at some insurance databases, fourteen percent of patients with chronic back pain ever even encounter a rheumatologist.
The problem is that one third in the NHANES study, twenty percent of The US population, twenty percent has chronic back pain. One third of them have chronic inflammatory back pain. And of course that's a symptom and raises suspicion high for spondyloarthritis. With the diminishing manpower we have in rheumatology, which will turn around, this represents a special challenge because mostly people don't counter rheumatologists because some of the novel terminology like that ankylosing spondylitis is now synonymous with radiographic axial spondyloarthritis. All this is unknown to primary care practitioners.
And this is very troubling because spondyloarthritis represents a group of diseases where so many novel and effective treatments have come forward, but they work by far the best and do their best job preventing disability and deformity if initiated early in the disease course. So this is a big focus of mine. We're gonna start with looking at the specter of chronic back pain in United States, to chronic inflammatory back pain, talking about non radiographic axial spondyloarthritis, the challenge that it represents, especially in women, because the majority of people with non radiographic are women and and too many are called fibromyalgia and again it's an issue we know that these medications work very well even before the x rays turned positive which seven to ten years after the onset of symptoms So I'm going to really be focused on that and finally to where we've gone with this with some of the new advances in genetics where we're understanding more and more what causes disease and especially where you got a gene, you've got a drug. I mean the genes predict the drugs that are going to work. All the novel treatments have been planned by genetics and so this is important knowledge to have.
I just wish that we had the manpower and the focus to better address this at a national level from the denominator of chronic back pain.
Thank you so much for that explanation. I'm now even more excited and thrilled about the lecture. Once again, thank you so much for talking to us at RheumNow. And for everyone watching this, please log on to roomnow.com for more information. Thank you.
Thank you.
Hi. I'm Philip Rumson. I'm from Brisbane in Australia, and I've just come back from Dan Claw's session on fibromyalgia, which was a fantastic summary on how to think about fibromyalgia and how to treat fibromyalgia. One of the things that he reminded us is that there are lots of chronic pain syndromes that we don't necessarily think about. Things like dry eye, necessarily that's also like a fibromyalgia of the eye in a lot of people.
And think about these other syndromes in the patients that you're seeing. He reminded us that potentially the relevance of tender points isn't that relevant now and that you can ask questions like, are you uncomfortable when people hug you? Are you uncomfortable when people do your blood pressure? Are much more relevant because these are chronic widespread pain disorders, not just focal pain disorders. He also reminded us that people really don't often have just one type of pain, they have mixed pain.
And so you've got to think about the proportion of pain that each person has. Do they have an amount of nociceptive pain, which you would expect from say rheumatoid, neuropathic pain, and then central pain, because you're never going to make progress unless you actually target the cause of their pain. Finally, he reminded us that opiates, well, they often work to start with the longer you are on them and the higher doses that patients end up on, the less effective they are. And he reminded us that there are more effective therapies including SNRIs and gabapentinoids and simple tricyclics, that, have evidence. And he also reminded us of the burgeoning amount of evidence for non pharmacological treatments like CBT and regular activity.
And you're going to make progress with your patients when you actually put together a combination of these treatments because not each one of them is very effective, but when you combine them together, they often create a package that's actually effective for patients. So if you want to know more about this, I recommend you go to roomnow.com.
Hello, my name is Torkel Ellington and I'm from Odinson University Hospital in Denmark and I've been asked to add a few comments on poster five sixty three which is data from one of our PhD students, Rick Asmussen, who is unfortunately not able to be here. And it's about sex differences in ankylosing spondylitis and non radiographic axSpA where Rege collected 100 patients consecutively from a university clinic setting in Swedenborg and Odense, Denmark. And we decided to focus on pain parameter that we not usually collect when we evaluate disease activity in ankylosing spondylitis and non radiographic axSpA. And the two main findings are that the Basti among females with non radiographic axSpA was significantly higher than in the males and that in both ankylosing spondylitis and non radiographic axSpA we found significant higher number of tender points when evaluated clinically. And this is interesting because obviously pain is a challenge for both the patient and the physician when you deal with ankylosing spondylitis.
But when you see sex differences like this then you need to be very cautious when you make decisions on when you intensify or make evaluations that are needed for treatment changes. Rege will evaluate this further in her coming papers and the poster just presented is last week published in Arthritis and Research Care, so please check it up there.
Hi. I'm David Liu from Melbourne, Australia reporting from RheumNow from ACI twenty nineteen here in Atlanta. Really interesting poster on the floor today from the IgG4 related disease clinic at MassGen. Obviously, these guys have been collecting a lot of data over time and they've got a large cohort looking at their 205 patients. They wanted to see whether there was a mortality difference between the patients that they had versus age age and disease match controls.
And so they looked at the standardized mortality rates between their patients and comparing that to normative data. The really interesting thing, and I wouldn't have expected this, is the fact that, in fact, these patients it's not a life limiting condition in these patients, that these patients have at least short term mortality, which is comparable to what they would look like otherwise. It didn't matter how you splice or dice it, if you looked at criteria positive patients, male patients, patients with internal organ involvement, they all seem to do okay. Now is this because Mastroon are really good at treating IgG4 related disease, or is this because that this isn't a life limiting condition or somewhere in between? That question still remains to be answered.
And really what we need to do is get broader data, longer term data, data from more centers, and data from places where they're maybe not giving as much rituximab upfront where steroids steroid first line therapy is more common. So more data needed in this space really starts to ask question though, is IgG4 related disease a life limiting condition or not? I'm David Liu and for more information go to rheumnow.com.
Hi, I'm Doctor. Rachel Tate coming to you from Atlanta for ACR twenty nineteen. I just attended a really great poster session, so I'm going to tell you a little bit about Abstract eleven sixty three. So, number one, we know that inflammatory pain is often a cause for patients coming to a rheumatology office. And we also know that in terms of ASAS criteria, we need MRI changes as well as an HLA B27 positivity as part of that criteria.
Not for every patient though. This is a Belgian study that looked at 138 patients and they wanted to understand if inflammatory back pain was actually predisposing patients to have MRI changes. They took these one hundred and thirty eight patients and they did MRIs on everyone and found that those patients who had inflammatory back pain symptoms as well as HLA B27 positivity in these newly diagnosed ACSPA patients who all were TNF naive, they found that inflammatory back pain was actually probably a harbinger for severity of disease. On MRI, the most common finding were erosions, but predominantly in the patient population that had experienced inflammatory back pain symptoms. So, though even this means that inflammatory back pain is something we need to be worried about, I argue that because this is a small study, non inflammatory back pain symptoms may also be something we need to really look at.
So we need to make sure we're properly imaging patients based on their symptomatology, not just for ASAS criteria. Check us out on roomnow.com and RoomNow on Twitter. We can't wait to give you more information from this meeting. It's been a great one. Hi, I'm Doctor.
Rachel Tate from West Palm Beach, Florida coming to you from Atlanta for ACR twenty nineteen. I just got out of a great session this morning. The CSRO did a small legislative update, which I'll be blogging on later at roomnow.com. But I wanted to share one piece of really vital information for you if you are unaware. In rheumatology, we're really good at advocating for our patients, but we need to be better advocates for our self.
Politically, legislatively, we need some help in this particular regard. So the CSRO decided to update their website this year. It's csro.info. Why I'm telling you this is because down the next few months we're going to see a huge change on the website. They're putting together an interactive state map that allows you to go to click on your state and you will see all of the legislature and how it affects you clinically as a physician.
And also how it affects the patients. Why is this tool useful? Well, a couple of things. Number one, if you want to stay up to date and with your legislators, this is a way to do it. But also, if you have a patient who's invested in their own advocacy and wants more information, it's another way for them to do that.
So if you have legislature coming down the pipeline, they will also have direct links of how to interact with that, what to say, who to talk to, all of it will be done for you. Now it's not out yet, but it will be on csro.info and I highly recommend you check it out. For me, I think this is a game changer. We need to be advocates for ourselves. So in addition to what you do in clinical practice, this is a way to do it.
So keep checking us out on roomnow.com. Handle for Twitter is roomnow. We're going to send you more updates from ACR twenty nineteen in Atlanta.
Hello,
I'm Jonathan Kay from of Massachusetts Medical School in Worcester, Massachusetts. I'm at ACR twenty nineteen in Atlanta, and I just heard an interesting presentation by Doctor. Ernest Choi about major adverse cardiovascular events and venous thromboembolic events in patients with rheumatoid arthritis from the integrated safety database of upadacitinib. He presented data from the five clinical trials in the phase three program of upadacitinib looking at two doses, fifteen and thirty milligrams, as well as the comparators, methotrexate, adalimumab, forty milligrams every other week, and placebo. What he presented was that the rates of major adverse cardiovascular events and venous thromboembolic events overlapped for all of the treatment groups.
Upadacitinib at fifteen and thirty mg taken by mouth daily, adalimumab forty mg taken subcutaneously every other week, methotrexate, and placebo. All of the patients with major adverse cardiovascular events had at least one cardiovascular risk factor, and patients with venous thromboembolic events also had risk factors for venous thromboembolic events, such as a prior deep venous thrombosis, knee replacement, or other risk factors. The conclusion of the study was that there was no dose relationship between upadacitinib and the occurrence of these events, and the rate of these events was similar for upadacitinib with the comparators adalimumab, methotrexate, and placebo. What this does not answer is the question as to why patients treated with JAK inhibitors are developing venous thromboembolic events. It's not related to platelet counts since platelet counts did not change significantly throughout the time period that patients were treated with upadacitinib, and patients on placebo also developed these events.
It will be very important to understand the mechanism whereby venous thromboembolic events occur in patients treated with JAK inhibitors so that we can predict which patients are at risk and treat them appropriately to prevent this devastating adverse effect, which may be an effect of this class of medications and may be completely unrelated. For more information, go to RheumNow. I'm Jonathan Kaye. Thanks.
Great. Okay.
You're always first take Doctor. Kaye. Okay.
Arthur Lau reporting, from ACR two thousand nineteen from Atlanta for our roomnow.com. I want to talk to you an interesting study I, just saw on the poster hall, abstract number fourteen twelve, the, oral shift study, where which was an open label, global phase three b four study, where patients with methotrexate inadequate response were initially started on, ZALGEN's, MR eleven milligrams for, twenty four weeks as open label. And then if the if these patients were able to achieve, low disease activity based on C. Dye, they were then randomized to either go on monotherapy of these Zalogens MR11 milligrams or to stay on their methotrexate. You have to be on fifteen to twenty five milligrams of methotrexate oral, at the beginning to be included in this study, and the mean dose was somewhere between sixteen and seventeen milligrams in each group.
What the study showed is that after another twenty four weeks, of either mono therapy or continuing methotrexate, there was very little difference for health related quality of life for both the mental and the physical component of the SF-thirty six. So overall, what this shows is that if you were able to achieve low disease activity for, after starting on a JAK inhibitor, Xaljanz MR in this instance, you can actually do relatively well and discontinue methotrexate, and the patients can still maintain good quality of life. This is important because, you know, I have many patients with rheumatoid, with comorbidities that are either unable or unwilling to continue on methotrexate. So this just reassures me that once they, initially do well, I can discontinue their methotrexate, and likely, will continue to do well in the future. Thanks for, tuning in here.
And for more information, log on to, roomnow.com for further informations and to see their extended coverage for ACR.
This is Doctor. Catherine Dow reporting for RheumNow. I'm at the ACR twenty nineteen meeting here in Atlanta, Georgia. And I just got out of an exciting lecture. It's the Klimper Lecture with Doctor.
James who presented The Winding Road to Lupus. So what are the main take home points here? Well, as you know, there are a lot of patients who are positive ANA. In fact, up to twenty five percent of people in the healthy population will have a positive ANA. But yet, only five to eight percent of these patients actually develop lupus.
Well, can we predict who will develop lupus? And what about those twenty percent of patients who don't develop lupus? What's so special about them? So Doctor. James, who works for the OMRF, basically has a database that is accessing the Department of Defense.
And essentially, what was found was that number one, these patients who develop and transition into lupus have actually a few risk factors. They're typically first degree relatives of family members who have lupus. Not only that, they probably have a lot of autoantibodies. The more autoantibodies you have, actually, and also an interferon signature, that means you're more likely to progress to lupus. What she also found was that other risk factors traditionally that we've seen also predispose patients to develop lupus.
That's tobacco smoking, that is hormones, so that's either an oral contraceptive or else hormone replacement therapy. In addition to that, vitamin D deficiency and sleep deprivation. That would be me, right? So if you sleep under seven hours a night, that puts you at risk. Now what's also interesting is that alcohol, moderate alcohol could be protective against developing lupus.
So, I didn't see that one coming. But anyways, when they compared patients who are positive ANA to patients who are negative ANA and patients who are lupus. They found that these positive ANA patients who are healthy actually have suppressive cytokines as well as inflammatory cytokines. They're not at all as healthy as we thought. So there are these triggers that may have patients progress and there's currently a study.
In fact, one of our study sites is at UT Southwestern. That's where I am faculty at. And what we're looking at right now is patients who are ANA positive who also have one sleep criteria positive. And we want to know whether or not these patients will develop lupus if given hydroxychloroquine. So the study is in progress.
If you have patients who are interested in enrolling, you can always contact us. And for more information please go to roomnow.com or acr19.roomnow.com. Doctor. Catherine Dow reporting.
Everyone. I'm Olga reporting from the annual ACR meeting here in Atlanta. Today, would like to talk about the abstract number three zero one, which speaks about pamela recommendations on use of imaging studies in gout. So there is a lot been told about guiding our treatment based on serum uric acid, but there is not really a clear recommendation how we could use imaging modalities in monitoring and guiding treatment of, gout patients. So, Pamela's ultrasound study group included rheumatologists, radiologists, statisticians, and methodologists to develop recommendations in this regard.
After reviewing all available, evidence, they graded most of their recommendations at level two and three and oh, based on the all the evidence in the literature, and then they developed following recommendations. Recommendation number one is that we can use ultrasound to detect the elementary deposits in the joints, and we could use dual energy CT scan to detect monosodium murine crystals in patients with gout. The same group suggests that both ultrasound and dual energy CT scan can be not so sensitive in detecting monosodium urate crystals in damage in patients who had disease duration of less than two years, but is very specific, so that justifies the use of those modalities. It also says that patients with gout, do not present with very clear, imaging results on X-ray and CT scan in terms of joint damage, but based on low cost of the study and high sensitivity, it is recommended to still use x-ray and CT scan as initial, imaging study in patients with gout. As it comes to an MRI and ultrasound, these modalities are considered very effective in detecting synovitis and tenosynovitis, but they're not very useful in assessing for crystal deposition and gouty erosions in patients with gout.
And, also, there is, no sufficient evidence to support using these modalities in, guiding treatment choices or in monitoring patients over time, and it says it's best to use these modalities for initial diagnosis only. Although, it can be used as a complementary monitoring techniques in most of the cases. If you would like to learn more, can read about us more on RheumNow, and also continue following us online. Thank you, and have a nice day.
Okay. Sarah Cushman, from Northwestern University in Chicago. I'm coming to you live from the ACR meeting in Atlanta, for RheumNow. What's going on today on Sunday? Well, one of the exciting abstracts we're going to see today is the first of the phase three trials of guzelkabab in psoriatic arthritis.
We've seen progression of treatment options in psoriatic arthritis looking at different approaches, different pathways and now we've got the first phase three data for an interleukin twenty three inhibitor. These drugs are really hot in the psoriasis space. We've seen phase two data in psoriatic arthritis and now we're seeing two trials at this meeting. The first of which is a plenary session today in phase three data for gazelkumab, very effective in psoriatic arthritis, effective at two different dose arms either given every eight weeks as is, conventional for psoriasis and every four weeks, thinking that perhaps psoriatic arthritis would need a higher dose. The trial today looked at patients who are both biologic naive and a small percentage of patients who are biologic experienced.
There was a slight difference, in dosing arms with the four week, patients getting a little bit better numerical response, though not statistically different. We're going to see the second phase three trial later in the week in which there wasn't a real difference between arms. The key point of the second trial, which includes patients who are all biologic naive, is that there was radiographic benefit statistically significant at the highest dose arm. Really cool data, the safety profile of this pathway is tremendous. It does appear that we're going to see fewer infections, fewer adverse events than we've seen with other cytokine inhibitors.
So, we're really looking forward to having IL-twenty three inhibitors in our armamentarium for psoriatic arthritis as rheumatologists. Our psoriatic our dermatologist friends have been using it for psoriasis for a while and we're excited to get on the bandwagon.
Hi, I'm Mike Putman coming to you from ACR twenty nineteen reporting from RheumNow. I wanted to talk briefly about the ACR urine review today. It was a wonderful lecture. And the select monotherapy came up. With trials like this, I think there's something important for you to remember.
That trial was run on patients who were methotrexate non responders and went on to either continue methotrexate or get upadacitinib. The implication when you hear the trial discussed is that upadacitinib was better than methotrexate. However, this isn't a population of patients who already didn't respond to methotrexate so it's not surprising that a new drug would perform better than the old drug that already wasn't performing. It's a very different question than saying I have a patient with rheumatoid arthritis, should I give them methotrexate or upadacitinib? In a blank slate population it may be that they're equivalent, may be that methotrexate even works better than upadacitinib.
We're still waiting for a trial that's going to assess that question. I think it's important to remember that a trial assessing a new therapy in non responders, continuing therapy, doesn't necessarily prove that point. Thank you so much. I hope you're all enjoying the meeting. If you're looking for more information, please go to RheumNow Live.
RheumNow.
Hi, I'm Doctor. Rachel Tate coming to you from Atlanta 2019 for ACR twenty nineteen. So I just got through an amazing poster session. Check them out if you haven't, and definitely follow us at RheumNow for Twitter and roomnow.com. But I wanna tell you a little bit about this year.
So 2019 and 2020 is gonna be a huge year for gout. In fact, on Wednesday, we're going to have the updated gout guidelines or gout lines as I like to call them. And what I wanted to share with you as a little appetizer are the actual panlar recommendations for 2019. So panlar decided to put together a task force of nine rheumatologists, musculoskeletal radiologists, ultrasonographers, statisticians and methodologists. And they looked at a huge literature review to determine how we can best utilize imaging for our patients.
So they came up with eight particular recommendations, and I will refer you to abstract three zero one or poster three zero one for further information, but I wanna highlight two things. The entire task force went together on two. There was a consensus on two of these recommendations. The first is for those difficult patients. So when you have a patient who is difficult to diagnose, you think that they're Galpa, perhaps they are not.
The group unanimously decided that ultrasound or scanning would be appropriate for these particular patients. The other subset is when you have patients who you believe have MSU or uric acid deposition in crystals in other tissues besides the joints, they again recommend ultrasound and scanning. So they looked at all of the literature that they could to determine between x rays, CT scans, MRIs, and ultrasounds, and this is what they came up with. So if you want to look at it a little bit further, a little more in-depth, I recommend abstract number three zero one, poster three zero one. And thank you for coming to to share some time with us in Atlanta for ACR twenty nineteen.
And check us out on Twitter. The handle is at room now or room now dot com. And more will come from gout. I promise you. So stay tuned.
Hey. Hi. I'm doctor Janet Pope. I'm a roving reporter for RheumNow at the ACR twenty nineteen conference in sunny but cool Atlanta. I'd like to talk to you about abstract four sixty four.
This is a Japanese study, and the reason I'm talking about it, even though it's a little study, is because it answers a clinically relevant question. The question is if you're seropositive and you have rheumatoid arthritis and you're treated with a TNF inhibitor, will reduction of the rheumatoid factor independent of improvement on your disease activity score affect erosions? So this was a small study and they only looked at seropositive patients. The mean, positivity was a level of one hundred and four at the beginning, over fifty patients, and they looked at four months and twelve months. And patients who became lower in the rheumatoid factor positivity by at least thirty percent had less erosions at the end of a year even if you adjusted for DAS score.
So lowering your rheumatoid factor with a TNF inhibitor interestingly seems to give less erosions even if it was an equal change in DAS. I picked this paper because it's really important when we know that anti CCP has been looked at a lot, and we know that as a, for instance, adalimumab doesn't lower anti CCP as much as say abatacep, this is looking at rheumatoid factor within people on TNF inhibitors. Will this change my practice repeating RF factors over and over? No, but it gives me a hint that there's a pathway independent of disease activity that causes joint erosions in RA. Thank you.
If you are a health practitioner, you may Login/Register to comment.
Due to the nature of these comment forums, only health practitioners are allowed to comment at this time.