RheumNow - ACR 2017 San Diego - Day 2 Save
RheumNow - ACR 2017 San Diego - Day 2 by Dr. Cush
Transcription
Hi. I'm Cassie Calabrese here at ACR twenty seventeen in San Diego, and I just came from the poster hall where I saw an interesting poster from the gout section by Ken Saag and all, looking at a tolerizing regimen of peglodecase, in the triple study. Peglodecase is a mammalian, recombinant uricase that's reserved for chronic gout patients that are refractory to traditional urate lowering therapies. While we know it can drop your uric acid levels very quickly, patients develop anti drug antibodies, patients have infusion reactions, anaphylaxis, and a lot of patients will have gout flares during the first couple months of treatment. Pharmacokinetic data has shown that with the biweekly dosing, the drug levels might not be high enough during the two weeks, contributing to the immunogenicity, immunogenicity.
And that pharmacokinetic data has also shown that possibly adding a biweekly infusion might improve this. This enter the triple study, where they enrolled patients, with chronic gout who had uric acid levels above six and gave, one dose of peglodecase, in the middle of the biweekly dosing. They enrolled 50 patients and they looked at, serum uric acid levels as a primary outcome. They looked at infusion reactions and gout flares. They found that the incidence of gout flares was lower.
They found that only one patient of the 50 had an infusion reaction and it was mild. But they found that about the same number of patients had a persistent uric acid lowering, about, forty four percent compared to low 40s in the registry trials. So very interesting. We'll see what comes of this. If you wanna hear more, go to roomnow.com.
I'm doctor David Borenstein. I'm a clinical professor of medicine at the George Washington University, Washington DC, and I'm partner at Arthritis and Rheumatism Associates in Washington and Maryland. It's been a very exciting time here at the American College of Rheumatology annual meeting in San Diego, and I've had interest in looking at the back pain abstracts. Though there are only a few, there are a couple that were of particular interest to me at this meeting. One was from actually Toulouse, France, which looked at the inflammatory changes that occur in MRI in people who have back pain, both in the anterior component of the spine as well as the posterior elements.
And what they were looking at in these, majority who were female was looking to see if there were changes in MRI both in the anterior component, which is like the vertebral body, and whether the modic changes, occur there, were associated with pain, and whether you also found the posterior elements like the facet joints and the spinous process, whether they were associated with pain and was there a differentiation. And lo and behold, the answer once again is that there is no specific correlation with what you see and what the patient complains of. So in fact, MRI can show you anatomy, but it does not show functional changes. So you once again need to think very carefully about what the patient complains of and what is on the MRI to see if rather it actually correlates. Because if you just do blind MRIs, you will find changes.
Other very interesting abstract in the, back pain group was actually a nice study done by the University Hospital in University of Oregon where they did a study of their patients over a 150 with diffuse idiopathic skeletal hyperostosis. It's a disease that rheumatologists know because many times it's confused with ankylosing spondylitis, but it is a disease we see. And they did a very nice group study of these individuals, and what it ends up is that, unfortunately, elderly men who are obese seem to be at greatest risk of developing this disease. What's interesting, however, is only about sixty three percent ended up having back pain even though they had characteristic changes of DSH. So DSH may exist in a significant number of individuals who don't really have back pain.
So it's something we need to think about in people who may have stiffness. Some of the other things that we find that we usually associate, like diabetes and hypertension and all, weren't necessarily components of what we see with dish. So once again, I think when we think about this disease, we need to think about it with people who are older, men, who may be overweight, who may be particularly stiff.
We should think about dish. So look at these abstracts, and I
think you'll get a very good view of what's happening at the ACR annual meeting in regard to back pain. I'm doctor David Borenstein. I'm a clinical professor of, rheumatology at the George Washington University Medical Center, and I'm also a partner at Arthritis and Rheumatism Associates in Washington DC. I was the, part of the abstract group that looked at the pain abstracts here at the meeting, and there's some very important abstracts that were presented here regarding pain and rheumatic diseases. And there's an overall theme that I think we we can take away from this meeting, and that has to do, one, with an abstract that will be at the plenary session, which looks at central sensitization as part of upregulation of pain in some of our patients with rheumatoid arthritis.
There was also another interesting, abstract that was presented looking at baricitinib as an a Janus one and two inhibitor, which not only decreased rheumatoid arthritis activity like adalimumab but also had an improvement in pain above what was shown in regard to control of disease. And whether this has something to do with the interferon effect of this medicine is something that's very interesting and may also play into this central sensitization story. If
we have
to take something away from the, pain abstracts that were presented at this meeting, I would say the following, that our musculoskeletal pain is complicated, that it may in fact have no susceptive, neuropathic, and central sensitization components. So even though we control the inflammatory disease associated with these problems, if we don't take care of the central sensitization, we may be short changing these patients in regard to their problem. And then in regards to some of these other difficulties with patients, the central sensitization can have psychologic components to it. So not only do we need to think about the pharmacologic therapies that these patients need, but we also may need to think about the non pharmacologic therapies that they need in regard to stress management, sleep problems, and sleep hygiene. And those kind of components and exercise which really make an important component to really taking care of the whole pain picture.
So I think as an as someone who's been very much interested in pain as a component of the diseases we take care of, I'm really pleased with the number of abstracts that were presented here at the ACR Annual Meeting, making our understanding of pain and our rheumatic diseases much more understandable.
So my name's Erwin Lim. I'm a rheumatologist from Sydney, Australia. I just attended a wonderful lecture on checkpoint inhibitors by Doctor. Bingham. Checkpoint inhibitors are a wonderful new therapy for oncology, where these new agents actually turn on the immune system to treat otherwise poorly treatable cancers.
Why is it relevant for Rheumatologists? Well, by turning on the immune system, you then end up having autoimmune diseases. And these diseases cause all sorts of rheumatic manifestations, including terribly difficult to control inflammatory arthritis, sicker symptoms, polymyalgia, rheumatica, you name it, it seems to be able to create and occur. Why else is it important? It's poorly recognized at the moment, but because these agents are going to be used more and more, we're all going to need to learn how to treat these diseases.
Come back to roomnow.com for further information about ACR seventeen.
Hi. I'm Jack Cush, executive editor of rheumnow.com. I'm here at ACR two thousand seventeen in San Diego with my best friend and mentor, doctor Ted Pincus. I wanna tell you that I started out in 1984. Ted was one of the first big time guys to engage me, and he was so kind then.
He's been kind for, like, the last thirty five years. And he's here to take to tell me about damage in rheumatoid arthritis. We we have lot we've over the years, we have lots of discussions about what we're not doing right, what we should do better. And, something that's come to your attention that you may come brought to my attention is this whole issue of damage. How did this first come up?
Well, thank you, Jack, and thanks for those kind words. The way it first came up was, as you know, in rheumatoid arthritis, we have seven core dataset measures. One of them is Physician Global on a zero to 10 scale using a visual analog scale. And I noticed that sometimes I would have a patient who had no swollen joints and had a sedimentation rate that was perfectly normal. And yet, I felt uncomfortable to say they have a physician global of zero or even one when they had a pain score of eight, and they had deformed joints.
Mhmm. So I thought, well, how am I gonna account for this? And I decided what we have on our Rheumatrix scale, which I think I can show you here Sure. Has the physician global, but also has three globals for inflammation, damage Mhmm. And distress, which is fibromyalgia and depression, which also impacts our patients, many of our patients, and can contribute to, management issues.
So inflammation, damage, and distress is filled out by the physician?
This is by the physician. It's not easy to get the physician to do any work. I don't have to tell you, Jack. And
It's not a muffin or a domino
to attach
to it. You know?
The only thing you can count on is is clicking the billing statement. But And you'll notice that we have instead of a 10 centimeter line, we have 21 circles because we found that physicians, at least in the exam room who are rheumatologists, don't know how to use this advanced implement called the ruler. Uh-huh. So and and it's actually act easier because then you don't have to worry about if when you photocopy when you photocopy 10 centimeters, sometimes it becomes 9.8 or 10.2.
So where does this play? I mean, so you find that Well that this explains some of the issue, and now you can kinda quantify it.
Well
How should this be playing out?
Well, we are just beginning to do this, and we are still in the process of validating some of these concepts. But I can tell you, we have one poster here at the ACR meeting that says in all of our diseases, which are thought to result from inflammation and which we think we treat only inflammation to control damage, that the scores for damage are higher than for inflammation. For example, in rheumatoid arthritis, it's about, three versus 2.2. And in lupus, ankylosing spondylitis, psoriatic arthritis, gout, polymyalgia rheumatica, the scores for damage are higher than inflammation. I think what this suggests is we should be measuring in some way quantitative, damage and distress as well as inflammation.
All of our measures traditionally, are directed to inflammation, but that may not be enough to figure out what's going on with our patients.
So quantifying and identifying damage, you taught me a long time ago that HAC predicts damage. HAC predicts everything.
Yeah. Absolutely. But You got it, Jack.
Well, I
You're a good student.
I was a I was a young dog then. Yeah. You know? Yeah. The tricks came easy.
Yeah.
But the the question is, is this being picked up by HAC, or is this still something different
than HAC? It's picked up by HAC, but it's also picked up by DOS 28 and by CDAI. So it's buried in there. Because if Patient Global is part of all these indices and a Patient Global of somebody with a lot of damage or a lot of fibromyalgia may be six or seven. And, actually, Jack, that's one of the reasons you can't get into remission and even can't get an ACR 20 in a clinical trial, which is probably more important than why we only see sixty percent ACR twenties in clinical trials than the target is not correct.
And is this somewhat validated as well by the common practice observation that even though you've got a great drug biologic DMARD, still need to use Tylenol or prednisone in low doses or some nonsteroidal or actual narcotic medicines to manage the patient.
That's true except don't use narcotics.
Absolutely. I agree.
If you can help it. Yeah. But but that's right, that the patients and we know that even in the best clinics in the world using any index we have that we see fewer than thirty percent of people in remission sustained. And so that means there may be something about the the measure that's picking up damage even if the patient has no swollen joints in normal laboratory tests.
So this is the rest of the equation. I think what you're doing is you're putting a spotlight on it so people pay more attention to it. And hopefully, it'll lead to paying not just attention to it that it's there, but we gotta do something about this.
Absolutely. And I will say also that using this scale and actually the rapid three scale shows that osteoarthritis today is a more severe problem than rheumatoid arthritis in usual rheumatology care. When the patients come in, they're similar. But since we have such good treatments now for RA, the mean rapid three score goes from 15 to 11 in RA over the next few months. And in OA, it only goes from 15 to 13 and a half.
And that becomes statistically significant or also clinically significant.
So now as an old dog, I'm still learning new tricks from the master. Well That's it for the
moment. Jack.
Hi. I'm Jack Cush, executive editor of rheumnow.com. It's ACR two thousand seventeen. I'm here in San Diego with all my friends. I just got back from a nice so this is what?
Monday afternoon, 03:00 session on on gout and hyperuricemia and a really interesting lecture by doctor Michael Pillinger from NYU. Michael is sort of a leader in the gout field, and he did a thirty minutes on, the impact of, asymptomatic hyperuricemia. And it was a nice review. And while he showed fairly impressive data that elevated uric acid levels really is not a very good thing in children, at least the hypertension. And when you use your rate lowering therapy, hypertension goes away.
When they gave those kids, same kids who had hypertension and elevated uric acid placebo. They didn't go away. But when the same kind of studies are done in adults, it's not there. He showed other really good data about levels of uric acid in populations in the highest quartiles actually having higher risk of cardiovascular disease and poor cardiovascular outcomes. But, again, there's an inconsistency to that.
And then, again, there are a number of different lines of evidence to show the hazards imposed by hyperyasthenia, yet the research does not yet show and prove that this is an independent risk factor for either hypertension or renal disease that, in and of itself, merits individual specific therapy. So such therapies are such studies are flawed by the fact that the prospective ones have too little data. The retrospective ones are flawed in design. The studies that are most convincing are done in kids but don't hold up in adults. So the bottom line is that there is not yet a full and clear message about when asymptomatic hyperuricemia should be treated.
Michael sort of concluded by it should be treated when you think that the benefits would outweigh the potential hazards of giving such therapy. You know, I commented that it used to be that I would only treat asymptomatic hyperuricemia at 14, and then it was maybe 12 or 11, and mainly to reduce the risk of stones and nephrolithiasis and other chronic kidney disease. More recently, I view it almost as a metabolic syndrome co factor. And so I am treating, asymptomatic hyperuricemia, especially in patients who I think may be at risk and especially in patients who I think can safely take urate lowering therapy. So that's the takeaway message from that nice session, again, run by Michael Pillinger.
You could probably look at it at, ACR Select online. Tune in to room more RheumNow for more good news and videos.
Hi. I'm Janet Pope. I'm here at RheumNow, and I wanna tell you some hashtag game changers. I looked at some posters on gout, and there's three important take home messages. If a patient has gout, they are more apt to be admitted to hospital for congestive heart failure, including repeat admissions.
And I think the take home could be if they have gout, they might be on more diuretics like furosemide, but it might really be all the heavy burden of comorbidities they have. We should really be conscious of that, look for gout, treat it effectively. The second game changer is that patients with both gout and diabetes have more extra articular such as TOFI and have more erosions. And I don't know what that means, but I thought that was a really interesting thing that can be explored because it's not something I could easily clinically put together. However, when you treat gout and diabetes, there are some new oral hypoglycemic that give glycosuria and some of them will decrease purine metabolism, exacerbate gout and then act more like allopurinol.
The final game changer is that if your patient is not treated to target with gout, don't blame the patient, blame the doctor. The adherence of medications for gout medications such as uric acid lowering are actually far higher than the usual meds that have poor adherence such as antihypertensives and some of the other medications. So it's really the doctor that has to treat to target and encourage the patient to take the meds because they are filling their prescriptions. Thanks from RheumNow. Hi.
I'm Janet Pope coming to you from RheumNow. I wanted to talk about something controversial at this meeting. So for the JAK inhibitors, it's been found in two of the JAKs, that there's increased VTE, venous thromboembolic events. So tofasidenib has a study where they've looked in their safety and haven't found it. But in baricitinib and upar, upasidenib, they have some signals.
And I'd like to compare it to what we found when TNFs first came out. In Fred Wolf's database, there was certainly concern about lymphoma. The first publication showed it, and the second one actually didn't show it. Now you see it. Now you don't.
I'm not sure what's going to happen, and I think this is a topic we'll all follow carefully. Thank you. Hi. I'm doctor Janet Pope, and I'm helping out with RheumNow, and I'm a newbie at tweeting. I actually have three followers now, which excites me.
I've started a new area, which is hashtag game changers and I'd like to tell you about one area that might be game changers. I've looked at a few abstracts at this meeting and they were on what to do for pre op of total hip or knee, plan joint replacements and usually rheumatoid arthritis. And what studies have seen to show is that we always know steroids, corticosteroids have an increased risk, but it looks like holding the biologics such as a TNF inhibitor is not at all necessary necessary and doesn't increase the risk. And if you hold drugs too long and patients flare, then we have a big problem. There's another abstract that again demonstrates that prosthetic infections, how we are actually diagnosing them with respect to imaging hasn't changed.
So if you suspect a joint replacement in the hardware of a prosthetic joint replacement, obviously, orthopedics should be involved, and you're probably gonna look at a high CRP. So the game changer for me is I don't have to hold biologics for scheduled joint replacements at this point in time. Thank you.
Hi. I'm Ken Sag from the University of Alabama at Birmingham. Today is an exciting day at the ACR. A lot of great posters and presentations on gout. Gout as we know is perhaps the most common inflammatory arthritis affecting about five percent of adults up to eight percent of men in their later years get gout.
Yet it's been one of the diseases that rheumatologists really have not embraced as actively as many other diseases. Within the gout arena, particularly in places like mine, down in the South where we have a lot of people with obesity and comorbidities, we see really bad gout and we need some very therapies to manage that. One of the drugs that's really been fairly underutilized in the gout field is peglidicase. Peglidicase is a recombinant uricase, pegylated uricase that essentially is replacing what we're missing. We don't make uricase as human beings and by providing this, it can be quite effective in debulking the disease and dissolving TOFI and helping people with severe chronic refractory gout get better.
We've had quite a bit experience using this therapy in our very severe gout patients and I would say that of all the patients I see, I have some of the most gratified patients who have had a good response to uricase, to pegylated uricase. The problem with it is that many patients, if not most patients, over time will develop immunogenicity. The drug will lose its effectiveness due to the development of anti PEG and anti pegloticase antibodies and that will be manifest by a rise in the serum urate levels that should indicate when it's time to stop the drug. We have a poster today at the meeting which looks at the idea of giving a tolerizing dose of pegloticase, an additional dose, early on. And the idea is that if you can induce immune tolerance to pegloticase, you may be able to use it longer.
In our study, we were pleased to not see infusion reactions. We saw only about half the patients getting flares of gout, we thought seemed reasonably good. Regrettably, forty plus percent of patients were responders. We'd hoped that would have been a little higher, but additional investigations and analyses of that data is underway. It does though set us up to think about other strategies and we've heard anecdotally of clinicians using things like azathioprine, maybe methotrexate in addition to the pegloticase as a way to block the development of these antibodies.
And we're actually getting ready to start a study now looking at mycophenolate, mafetil, as an adjunct to the administration of pegloticase in a controlled pilot study to see whether that may be effective in reducing the development of these PEG and pegloticase antibodies and hopefully allowing people to use the drug longer. There's gonna be additional studies looking at Imuran, Azathioprine, other drugs as well. So we're hopeful that over time we'll find a way to use this drug even better.
Good morning, everyone. I'm Olga Petrina, and I'm reporting from the ACR meeting in San Diego. This morning, I had the pleasure of moderating a great session where doctor Mencket presented data on cardiovascular comorbidities in inflammatory and autoimmune conditions. Doctor Mencket is a cardiologist at the Mayo Clinic, and she also runs a center for cardiovascular women's health. And in this session, she emphasized on the importance of screening patients with autoimmune and inflammatory conditions for cardiovascular comorbidities.
Apparently, patients with inflammatory conditions such as rheumatoid arthritis, lupus, ankylosing spondylitis are all at a higher risk of both structural and functional cardiovascular disease. And such complications as valvular dysfunction, pericarditis and pericardial effusions, as well as cardiovascular ischemic disease are very common. For unknown to us reason, in lupus patients, inflammatory markers don't tend to correlate with the risk of cardiovascular disease. And in a lot of RA patients, Framington risk scores are not really reliable. And there is no known reason for that.
It is known that patients who are treated with biologic DMARDs have better cardiovascular outcomes and lesser risk of cardiovascular disease as opposed to non biologic DMARD therapy. Long term chronic steroid use is negative factor increasing the risk of cardiovascular disease again. And interestingly enough, use of statins tends to attenuate this long term steroid effect. All in all, it was suggested that patients with rheumatoid arthritis, lupus, and other autoimmune conditions be screened for underlying cardiovascular disease, even if they don't have obvious and severe manifestations of the disease or signs suggestive of active disease, as early treatment and prevention may have an important role in their outcomes. Oftentimes joint cardiology and rheumatology clinics are a great idea for this type of screening.
Thank you. If you would like to know more, please follow us on roomnow.com and have a nice day.
Hi. This is Paul Cushka coming to you live from ACR 17 in San Diego. I just came out of a session that was talking about how physicians and scientists should can manage their online reputation and distribute their research from what people read it. The first step to do this is to have a main hub, so your blog or your research site where your things are published. And you're gonna use all the other social networking tools like Twitter and Facebook and everything else, to, bring your people to your main hub.
So important to have a main hub to bring people to. Second, be aware that there are research and science specific social networks. So one that might be worth checking out is ResearchGate, and one that might surprise you is fairly useful for scientists is actually LinkedIn. We think a lot that one is more of a business site, but scientists are big on there too. And then last, make your information very easy to share.
So, if you produce an infographic or something that can be shared and looked at graphically, it makes it easier for other people to distribute your content. And then, again, bring it back to your your main hub and, bring more attention to yourself. So if you so, some good ways for scientists to get more people to read their articles. And for more information, go to RheumNow.
Hello. My name is Philip Meese. I'm here at the ACR meeting in San Diego. I'm a rheumatologist from Seattle, Washington. I'm very excited about one of the late breakers, that's being presented here, which is known as the Future Five Study.
This is a study that is the largest that has been conducted in psoriatic arthritis using the drug secukinumab in two different dosages and one dose arm without a load. As you may know, secukinumab is approved three hundred milligrams or one hundred fifty milligrams, given five weekly doses and then monthly thereafter. And in this study, in which we were testing to see if it would inhibit radiographic progression, there was also a, no load dose, that was given at baseline and monthly. So what did we learn? Well, not a surprise, we learned that giving secukinumab did inhibit evidence of progressive structural damage in joints as measured by x-ray.
So that was a key outcome from the study. It also confirmed previously known results in terms of very high ACR responses, for example, ACR 20 at the primary endpoint of week sixteen of about sixty three percent, which is very high, and correspondingly high ACR fiftyseventy, responses and very high skin responses. We also saw significant inhibition of dactylitis and enthesitis at week sixteen. If we turn to what we learned about loading versus not loading, we learned that the load is better. There were numerically higher responses with the 300 and one hundred and fifty milligram doses when given a load, than with no load, and the responses were faster.
We also saw differences in enthesitis and dactylitis response. So my take home message is that it's better to follow, the current, recommended dosing of giving a load, and then in patients with moderate to severe psoriasis giving three hundred milligrams, one hundred and fifty is also an option because that did show like the three hundred milligram dose evidence of inhibition of radiographic progression, all supporting, the effectiveness of secukinumab in treating psoriatic arthritis with this IL17A inhibitor.
So my name is Ian Bruce. I'm professor of rheumatology at the University of Manchester, and I'm here at ACR in San Diego 2017. '17, and this is a RheumNow podcast. I've been looking at lot of posters in lupus and vasculitis, and there's been a number of posters this year from the Toronto group looking at a rare adverse event in patients with prolonged antimalarial therapy, cardiac toxicity. First of all, it's important to emphasize that these are rare uncommon events, but they seem to present either as a dysrhythmia or with cardiac failure, shortness of breath, etcetera.
What you see is a hypertrophic restrictive type of cardiomyopathy. And several of these patients have actually had endomyocardial biopsies done showing evacuated, myopathy, which would be typical of antimalarial toxicity. Several have also been diagnosed with highly suggestive patterns on cardiac MR. I think one of the key take home messages from this is that when you think about patients who are on very long term antimalarial therapy, that if they have a cardiac issue, whether that's a dysrhythmia, heart failure, etcetera, obviously, ischemic heart disease, atherosclerotic heart disease is much more common in this population. But one should always bear in mind the possibility that this could be related to antimalarial drugs and speak to the cardiologist about doing the precise investigations that would help reveal this if it was there.
Of note within the posters that they showed, a number of these patients actually were free of epicardial coronary heart disease, which raises more the possibility that this may have been related to antimalarial drugs. The good news in some of these situations was that when you withdraw the drug, there is a slow gradual improvement in cardiac function over time, but that can take at least two years to reverse. Sadly, in one or two patients, they, succumb to sepsis or other issues as well. So that's important, but I think the balance of risk means that antimalarial drugs still remain overwhelmingly beneficial in the vast majority of patients with SLE. And therefore, because of the many benefits that they have, we should continue to use these.
But we just need to pay, respect and attention to this drug, particularly on long term cumulative use. This is, on behalf of RheumNow, and RheumNow will be here for the rest of the week. Thank you very much.
Hi. This is Paul Sufka coming to you live from, ACR seventeen in San Diego. I just came out of a session that was talking about how physicians and scientists should can, manage their online reputation and, distribute their research so more people read it. The first step, to do this is to have a main hub, so your blog or your research site where your things are published. And you're gonna use all the other social networking tools like Twitter and Facebook and everything else, to, bring your people to your main hub.
So important to have a main hub to bring people to. Second, be aware that there are research and science specific, social networks. So one that might be worth checking out is ResearchGate, and one that might surprise you is fairly, useful for scientists is actually LinkedIn. We think a lot that one is more of a business site, but scientists are big on there too. And then last, make your information very easy to share.
So, if you produce an infographic or something that can be shared and looked at graphically, it makes it easier for other people to distribute your content. And then, again, bring it back to your your main hub and, bring more attention to yourself. So a few so, some good ways for scientists to get more people to read their articles. And for more information, go to RheumNow.
This is Catherine Dow from San Diego ACR twenty seventeen conference. I just wanna share with you some interesting updates that I've learned today. First of all, FDA updates from this morning. Something you have to know about. Do not prescribe tramadol or codeine to children or pregnant women.
Now this isn't just a box warning. This is a contraindication. This is stronger than a box ed And the FDA issued a letter and a warning back in April 2017. They are saying it again today. Do not do that.
And the reason why is because there are some individuals who have CYP two d six. This is a gene that causes hyper metabolism of these kind of compounds and particularly in children, if they have too much of this, type of metabolite which you know codeine obviously to morphine, they can go into respiratory distress as well as have death. Where we find this to be a big problem are patients like children who undergo tonsillectomies and they require, narcotics to control their pain or mothers who are breastfeeding and what happens is that they breastfeed and then, had taken their hydrocodone or their codeine or their tramadol and it goes into the milk and the baby gets them. So again, strong warnings, and contraindications from the FDA. Do not prescribe tramadol or codeine products to patients who are pregnant and children under the age of 18.
Alright. Second thing. So I attended a lecture by Virginia Pasquale. As you know, she's this great immunologist, and she spoke about precision medicine. And previously, we've known about the interferon signature in lupus.
In fact as a fellow, I had done research in microarray analysis looking at the interferon signature in lupus. Well take home points from her study, number one interferon signatures are not unique to lupus. In fact, you can find it in type one diabetes, can find it in scleroderma, you can find it in Sjogren's and also a subset of rheumatoid arthritis patients and the subset of rheumatoid arthritis patients who have it actually respond to TNF inhibitors. The other thing that is a take home message is that she has defined seven types of lupus based on their genotypes. Three different kinds of signature besides, so which are interferon signature, the plasma blast as well as the neutrophil signature and she found that the plasma blast and the neutrophil signature may actually be more of an important player for lupus.
So basically in the future we can define precision medicine so treating patients with, targeted therapy that would correspond to their gene type as something of the wave of the future and we are currently on its threshold. So this is Doctor. Dow reporting for RheumNow. Come visit us on our website and read my blogs.
And that pharmacokinetic data has also shown that possibly adding a biweekly infusion might improve this. This enter the triple study, where they enrolled patients, with chronic gout who had uric acid levels above six and gave, one dose of peglodecase, in the middle of the biweekly dosing. They enrolled 50 patients and they looked at, serum uric acid levels as a primary outcome. They looked at infusion reactions and gout flares. They found that the incidence of gout flares was lower.
They found that only one patient of the 50 had an infusion reaction and it was mild. But they found that about the same number of patients had a persistent uric acid lowering, about, forty four percent compared to low 40s in the registry trials. So very interesting. We'll see what comes of this. If you wanna hear more, go to roomnow.com.
I'm doctor David Borenstein. I'm a clinical professor of medicine at the George Washington University, Washington DC, and I'm partner at Arthritis and Rheumatism Associates in Washington and Maryland. It's been a very exciting time here at the American College of Rheumatology annual meeting in San Diego, and I've had interest in looking at the back pain abstracts. Though there are only a few, there are a couple that were of particular interest to me at this meeting. One was from actually Toulouse, France, which looked at the inflammatory changes that occur in MRI in people who have back pain, both in the anterior component of the spine as well as the posterior elements.
And what they were looking at in these, majority who were female was looking to see if there were changes in MRI both in the anterior component, which is like the vertebral body, and whether the modic changes, occur there, were associated with pain, and whether you also found the posterior elements like the facet joints and the spinous process, whether they were associated with pain and was there a differentiation. And lo and behold, the answer once again is that there is no specific correlation with what you see and what the patient complains of. So in fact, MRI can show you anatomy, but it does not show functional changes. So you once again need to think very carefully about what the patient complains of and what is on the MRI to see if rather it actually correlates. Because if you just do blind MRIs, you will find changes.
Other very interesting abstract in the, back pain group was actually a nice study done by the University Hospital in University of Oregon where they did a study of their patients over a 150 with diffuse idiopathic skeletal hyperostosis. It's a disease that rheumatologists know because many times it's confused with ankylosing spondylitis, but it is a disease we see. And they did a very nice group study of these individuals, and what it ends up is that, unfortunately, elderly men who are obese seem to be at greatest risk of developing this disease. What's interesting, however, is only about sixty three percent ended up having back pain even though they had characteristic changes of DSH. So DSH may exist in a significant number of individuals who don't really have back pain.
So it's something we need to think about in people who may have stiffness. Some of the other things that we find that we usually associate, like diabetes and hypertension and all, weren't necessarily components of what we see with dish. So once again, I think when we think about this disease, we need to think about it with people who are older, men, who may be overweight, who may be particularly stiff.
We should think about dish. So look at these abstracts, and I
think you'll get a very good view of what's happening at the ACR annual meeting in regard to back pain. I'm doctor David Borenstein. I'm a clinical professor of, rheumatology at the George Washington University Medical Center, and I'm also a partner at Arthritis and Rheumatism Associates in Washington DC. I was the, part of the abstract group that looked at the pain abstracts here at the meeting, and there's some very important abstracts that were presented here regarding pain and rheumatic diseases. And there's an overall theme that I think we we can take away from this meeting, and that has to do, one, with an abstract that will be at the plenary session, which looks at central sensitization as part of upregulation of pain in some of our patients with rheumatoid arthritis.
There was also another interesting, abstract that was presented looking at baricitinib as an a Janus one and two inhibitor, which not only decreased rheumatoid arthritis activity like adalimumab but also had an improvement in pain above what was shown in regard to control of disease. And whether this has something to do with the interferon effect of this medicine is something that's very interesting and may also play into this central sensitization story. If
we have
to take something away from the, pain abstracts that were presented at this meeting, I would say the following, that our musculoskeletal pain is complicated, that it may in fact have no susceptive, neuropathic, and central sensitization components. So even though we control the inflammatory disease associated with these problems, if we don't take care of the central sensitization, we may be short changing these patients in regard to their problem. And then in regards to some of these other difficulties with patients, the central sensitization can have psychologic components to it. So not only do we need to think about the pharmacologic therapies that these patients need, but we also may need to think about the non pharmacologic therapies that they need in regard to stress management, sleep problems, and sleep hygiene. And those kind of components and exercise which really make an important component to really taking care of the whole pain picture.
So I think as an as someone who's been very much interested in pain as a component of the diseases we take care of, I'm really pleased with the number of abstracts that were presented here at the ACR Annual Meeting, making our understanding of pain and our rheumatic diseases much more understandable.
So my name's Erwin Lim. I'm a rheumatologist from Sydney, Australia. I just attended a wonderful lecture on checkpoint inhibitors by Doctor. Bingham. Checkpoint inhibitors are a wonderful new therapy for oncology, where these new agents actually turn on the immune system to treat otherwise poorly treatable cancers.
Why is it relevant for Rheumatologists? Well, by turning on the immune system, you then end up having autoimmune diseases. And these diseases cause all sorts of rheumatic manifestations, including terribly difficult to control inflammatory arthritis, sicker symptoms, polymyalgia, rheumatica, you name it, it seems to be able to create and occur. Why else is it important? It's poorly recognized at the moment, but because these agents are going to be used more and more, we're all going to need to learn how to treat these diseases.
Come back to roomnow.com for further information about ACR seventeen.
Hi. I'm Jack Cush, executive editor of rheumnow.com. I'm here at ACR two thousand seventeen in San Diego with my best friend and mentor, doctor Ted Pincus. I wanna tell you that I started out in 1984. Ted was one of the first big time guys to engage me, and he was so kind then.
He's been kind for, like, the last thirty five years. And he's here to take to tell me about damage in rheumatoid arthritis. We we have lot we've over the years, we have lots of discussions about what we're not doing right, what we should do better. And, something that's come to your attention that you may come brought to my attention is this whole issue of damage. How did this first come up?
Well, thank you, Jack, and thanks for those kind words. The way it first came up was, as you know, in rheumatoid arthritis, we have seven core dataset measures. One of them is Physician Global on a zero to 10 scale using a visual analog scale. And I noticed that sometimes I would have a patient who had no swollen joints and had a sedimentation rate that was perfectly normal. And yet, I felt uncomfortable to say they have a physician global of zero or even one when they had a pain score of eight, and they had deformed joints.
Mhmm. So I thought, well, how am I gonna account for this? And I decided what we have on our Rheumatrix scale, which I think I can show you here Sure. Has the physician global, but also has three globals for inflammation, damage Mhmm. And distress, which is fibromyalgia and depression, which also impacts our patients, many of our patients, and can contribute to, management issues.
So inflammation, damage, and distress is filled out by the physician?
This is by the physician. It's not easy to get the physician to do any work. I don't have to tell you, Jack. And
It's not a muffin or a domino
to attach
to it. You know?
The only thing you can count on is is clicking the billing statement. But And you'll notice that we have instead of a 10 centimeter line, we have 21 circles because we found that physicians, at least in the exam room who are rheumatologists, don't know how to use this advanced implement called the ruler. Uh-huh. So and and it's actually act easier because then you don't have to worry about if when you photocopy when you photocopy 10 centimeters, sometimes it becomes 9.8 or 10.2.
So where does this play? I mean, so you find that Well that this explains some of the issue, and now you can kinda quantify it.
Well
How should this be playing out?
Well, we are just beginning to do this, and we are still in the process of validating some of these concepts. But I can tell you, we have one poster here at the ACR meeting that says in all of our diseases, which are thought to result from inflammation and which we think we treat only inflammation to control damage, that the scores for damage are higher than for inflammation. For example, in rheumatoid arthritis, it's about, three versus 2.2. And in lupus, ankylosing spondylitis, psoriatic arthritis, gout, polymyalgia rheumatica, the scores for damage are higher than inflammation. I think what this suggests is we should be measuring in some way quantitative, damage and distress as well as inflammation.
All of our measures traditionally, are directed to inflammation, but that may not be enough to figure out what's going on with our patients.
So quantifying and identifying damage, you taught me a long time ago that HAC predicts damage. HAC predicts everything.
Yeah. Absolutely. But You got it, Jack.
Well, I
You're a good student.
I was a I was a young dog then. Yeah. You know? Yeah. The tricks came easy.
Yeah.
But the the question is, is this being picked up by HAC, or is this still something different
than HAC? It's picked up by HAC, but it's also picked up by DOS 28 and by CDAI. So it's buried in there. Because if Patient Global is part of all these indices and a Patient Global of somebody with a lot of damage or a lot of fibromyalgia may be six or seven. And, actually, Jack, that's one of the reasons you can't get into remission and even can't get an ACR 20 in a clinical trial, which is probably more important than why we only see sixty percent ACR twenties in clinical trials than the target is not correct.
And is this somewhat validated as well by the common practice observation that even though you've got a great drug biologic DMARD, still need to use Tylenol or prednisone in low doses or some nonsteroidal or actual narcotic medicines to manage the patient.
That's true except don't use narcotics.
Absolutely. I agree.
If you can help it. Yeah. But but that's right, that the patients and we know that even in the best clinics in the world using any index we have that we see fewer than thirty percent of people in remission sustained. And so that means there may be something about the the measure that's picking up damage even if the patient has no swollen joints in normal laboratory tests.
So this is the rest of the equation. I think what you're doing is you're putting a spotlight on it so people pay more attention to it. And hopefully, it'll lead to paying not just attention to it that it's there, but we gotta do something about this.
Absolutely. And I will say also that using this scale and actually the rapid three scale shows that osteoarthritis today is a more severe problem than rheumatoid arthritis in usual rheumatology care. When the patients come in, they're similar. But since we have such good treatments now for RA, the mean rapid three score goes from 15 to 11 in RA over the next few months. And in OA, it only goes from 15 to 13 and a half.
And that becomes statistically significant or also clinically significant.
So now as an old dog, I'm still learning new tricks from the master. Well That's it for the
moment. Jack.
Hi. I'm Jack Cush, executive editor of rheumnow.com. It's ACR two thousand seventeen. I'm here in San Diego with all my friends. I just got back from a nice so this is what?
Monday afternoon, 03:00 session on on gout and hyperuricemia and a really interesting lecture by doctor Michael Pillinger from NYU. Michael is sort of a leader in the gout field, and he did a thirty minutes on, the impact of, asymptomatic hyperuricemia. And it was a nice review. And while he showed fairly impressive data that elevated uric acid levels really is not a very good thing in children, at least the hypertension. And when you use your rate lowering therapy, hypertension goes away.
When they gave those kids, same kids who had hypertension and elevated uric acid placebo. They didn't go away. But when the same kind of studies are done in adults, it's not there. He showed other really good data about levels of uric acid in populations in the highest quartiles actually having higher risk of cardiovascular disease and poor cardiovascular outcomes. But, again, there's an inconsistency to that.
And then, again, there are a number of different lines of evidence to show the hazards imposed by hyperyasthenia, yet the research does not yet show and prove that this is an independent risk factor for either hypertension or renal disease that, in and of itself, merits individual specific therapy. So such therapies are such studies are flawed by the fact that the prospective ones have too little data. The retrospective ones are flawed in design. The studies that are most convincing are done in kids but don't hold up in adults. So the bottom line is that there is not yet a full and clear message about when asymptomatic hyperuricemia should be treated.
Michael sort of concluded by it should be treated when you think that the benefits would outweigh the potential hazards of giving such therapy. You know, I commented that it used to be that I would only treat asymptomatic hyperuricemia at 14, and then it was maybe 12 or 11, and mainly to reduce the risk of stones and nephrolithiasis and other chronic kidney disease. More recently, I view it almost as a metabolic syndrome co factor. And so I am treating, asymptomatic hyperuricemia, especially in patients who I think may be at risk and especially in patients who I think can safely take urate lowering therapy. So that's the takeaway message from that nice session, again, run by Michael Pillinger.
You could probably look at it at, ACR Select online. Tune in to room more RheumNow for more good news and videos.
Hi. I'm Janet Pope. I'm here at RheumNow, and I wanna tell you some hashtag game changers. I looked at some posters on gout, and there's three important take home messages. If a patient has gout, they are more apt to be admitted to hospital for congestive heart failure, including repeat admissions.
And I think the take home could be if they have gout, they might be on more diuretics like furosemide, but it might really be all the heavy burden of comorbidities they have. We should really be conscious of that, look for gout, treat it effectively. The second game changer is that patients with both gout and diabetes have more extra articular such as TOFI and have more erosions. And I don't know what that means, but I thought that was a really interesting thing that can be explored because it's not something I could easily clinically put together. However, when you treat gout and diabetes, there are some new oral hypoglycemic that give glycosuria and some of them will decrease purine metabolism, exacerbate gout and then act more like allopurinol.
The final game changer is that if your patient is not treated to target with gout, don't blame the patient, blame the doctor. The adherence of medications for gout medications such as uric acid lowering are actually far higher than the usual meds that have poor adherence such as antihypertensives and some of the other medications. So it's really the doctor that has to treat to target and encourage the patient to take the meds because they are filling their prescriptions. Thanks from RheumNow. Hi.
I'm Janet Pope coming to you from RheumNow. I wanted to talk about something controversial at this meeting. So for the JAK inhibitors, it's been found in two of the JAKs, that there's increased VTE, venous thromboembolic events. So tofasidenib has a study where they've looked in their safety and haven't found it. But in baricitinib and upar, upasidenib, they have some signals.
And I'd like to compare it to what we found when TNFs first came out. In Fred Wolf's database, there was certainly concern about lymphoma. The first publication showed it, and the second one actually didn't show it. Now you see it. Now you don't.
I'm not sure what's going to happen, and I think this is a topic we'll all follow carefully. Thank you. Hi. I'm doctor Janet Pope, and I'm helping out with RheumNow, and I'm a newbie at tweeting. I actually have three followers now, which excites me.
I've started a new area, which is hashtag game changers and I'd like to tell you about one area that might be game changers. I've looked at a few abstracts at this meeting and they were on what to do for pre op of total hip or knee, plan joint replacements and usually rheumatoid arthritis. And what studies have seen to show is that we always know steroids, corticosteroids have an increased risk, but it looks like holding the biologics such as a TNF inhibitor is not at all necessary necessary and doesn't increase the risk. And if you hold drugs too long and patients flare, then we have a big problem. There's another abstract that again demonstrates that prosthetic infections, how we are actually diagnosing them with respect to imaging hasn't changed.
So if you suspect a joint replacement in the hardware of a prosthetic joint replacement, obviously, orthopedics should be involved, and you're probably gonna look at a high CRP. So the game changer for me is I don't have to hold biologics for scheduled joint replacements at this point in time. Thank you.
Hi. I'm Ken Sag from the University of Alabama at Birmingham. Today is an exciting day at the ACR. A lot of great posters and presentations on gout. Gout as we know is perhaps the most common inflammatory arthritis affecting about five percent of adults up to eight percent of men in their later years get gout.
Yet it's been one of the diseases that rheumatologists really have not embraced as actively as many other diseases. Within the gout arena, particularly in places like mine, down in the South where we have a lot of people with obesity and comorbidities, we see really bad gout and we need some very therapies to manage that. One of the drugs that's really been fairly underutilized in the gout field is peglidicase. Peglidicase is a recombinant uricase, pegylated uricase that essentially is replacing what we're missing. We don't make uricase as human beings and by providing this, it can be quite effective in debulking the disease and dissolving TOFI and helping people with severe chronic refractory gout get better.
We've had quite a bit experience using this therapy in our very severe gout patients and I would say that of all the patients I see, I have some of the most gratified patients who have had a good response to uricase, to pegylated uricase. The problem with it is that many patients, if not most patients, over time will develop immunogenicity. The drug will lose its effectiveness due to the development of anti PEG and anti pegloticase antibodies and that will be manifest by a rise in the serum urate levels that should indicate when it's time to stop the drug. We have a poster today at the meeting which looks at the idea of giving a tolerizing dose of pegloticase, an additional dose, early on. And the idea is that if you can induce immune tolerance to pegloticase, you may be able to use it longer.
In our study, we were pleased to not see infusion reactions. We saw only about half the patients getting flares of gout, we thought seemed reasonably good. Regrettably, forty plus percent of patients were responders. We'd hoped that would have been a little higher, but additional investigations and analyses of that data is underway. It does though set us up to think about other strategies and we've heard anecdotally of clinicians using things like azathioprine, maybe methotrexate in addition to the pegloticase as a way to block the development of these antibodies.
And we're actually getting ready to start a study now looking at mycophenolate, mafetil, as an adjunct to the administration of pegloticase in a controlled pilot study to see whether that may be effective in reducing the development of these PEG and pegloticase antibodies and hopefully allowing people to use the drug longer. There's gonna be additional studies looking at Imuran, Azathioprine, other drugs as well. So we're hopeful that over time we'll find a way to use this drug even better.
Good morning, everyone. I'm Olga Petrina, and I'm reporting from the ACR meeting in San Diego. This morning, I had the pleasure of moderating a great session where doctor Mencket presented data on cardiovascular comorbidities in inflammatory and autoimmune conditions. Doctor Mencket is a cardiologist at the Mayo Clinic, and she also runs a center for cardiovascular women's health. And in this session, she emphasized on the importance of screening patients with autoimmune and inflammatory conditions for cardiovascular comorbidities.
Apparently, patients with inflammatory conditions such as rheumatoid arthritis, lupus, ankylosing spondylitis are all at a higher risk of both structural and functional cardiovascular disease. And such complications as valvular dysfunction, pericarditis and pericardial effusions, as well as cardiovascular ischemic disease are very common. For unknown to us reason, in lupus patients, inflammatory markers don't tend to correlate with the risk of cardiovascular disease. And in a lot of RA patients, Framington risk scores are not really reliable. And there is no known reason for that.
It is known that patients who are treated with biologic DMARDs have better cardiovascular outcomes and lesser risk of cardiovascular disease as opposed to non biologic DMARD therapy. Long term chronic steroid use is negative factor increasing the risk of cardiovascular disease again. And interestingly enough, use of statins tends to attenuate this long term steroid effect. All in all, it was suggested that patients with rheumatoid arthritis, lupus, and other autoimmune conditions be screened for underlying cardiovascular disease, even if they don't have obvious and severe manifestations of the disease or signs suggestive of active disease, as early treatment and prevention may have an important role in their outcomes. Oftentimes joint cardiology and rheumatology clinics are a great idea for this type of screening.
Thank you. If you would like to know more, please follow us on roomnow.com and have a nice day.
Hi. This is Paul Cushka coming to you live from ACR 17 in San Diego. I just came out of a session that was talking about how physicians and scientists should can manage their online reputation and distribute their research from what people read it. The first step to do this is to have a main hub, so your blog or your research site where your things are published. And you're gonna use all the other social networking tools like Twitter and Facebook and everything else, to, bring your people to your main hub.
So important to have a main hub to bring people to. Second, be aware that there are research and science specific social networks. So one that might be worth checking out is ResearchGate, and one that might surprise you is fairly useful for scientists is actually LinkedIn. We think a lot that one is more of a business site, but scientists are big on there too. And then last, make your information very easy to share.
So, if you produce an infographic or something that can be shared and looked at graphically, it makes it easier for other people to distribute your content. And then, again, bring it back to your your main hub and, bring more attention to yourself. So if you so, some good ways for scientists to get more people to read their articles. And for more information, go to RheumNow.
Hello. My name is Philip Meese. I'm here at the ACR meeting in San Diego. I'm a rheumatologist from Seattle, Washington. I'm very excited about one of the late breakers, that's being presented here, which is known as the Future Five Study.
This is a study that is the largest that has been conducted in psoriatic arthritis using the drug secukinumab in two different dosages and one dose arm without a load. As you may know, secukinumab is approved three hundred milligrams or one hundred fifty milligrams, given five weekly doses and then monthly thereafter. And in this study, in which we were testing to see if it would inhibit radiographic progression, there was also a, no load dose, that was given at baseline and monthly. So what did we learn? Well, not a surprise, we learned that giving secukinumab did inhibit evidence of progressive structural damage in joints as measured by x-ray.
So that was a key outcome from the study. It also confirmed previously known results in terms of very high ACR responses, for example, ACR 20 at the primary endpoint of week sixteen of about sixty three percent, which is very high, and correspondingly high ACR fiftyseventy, responses and very high skin responses. We also saw significant inhibition of dactylitis and enthesitis at week sixteen. If we turn to what we learned about loading versus not loading, we learned that the load is better. There were numerically higher responses with the 300 and one hundred and fifty milligram doses when given a load, than with no load, and the responses were faster.
We also saw differences in enthesitis and dactylitis response. So my take home message is that it's better to follow, the current, recommended dosing of giving a load, and then in patients with moderate to severe psoriasis giving three hundred milligrams, one hundred and fifty is also an option because that did show like the three hundred milligram dose evidence of inhibition of radiographic progression, all supporting, the effectiveness of secukinumab in treating psoriatic arthritis with this IL17A inhibitor.
So my name is Ian Bruce. I'm professor of rheumatology at the University of Manchester, and I'm here at ACR in San Diego 2017. '17, and this is a RheumNow podcast. I've been looking at lot of posters in lupus and vasculitis, and there's been a number of posters this year from the Toronto group looking at a rare adverse event in patients with prolonged antimalarial therapy, cardiac toxicity. First of all, it's important to emphasize that these are rare uncommon events, but they seem to present either as a dysrhythmia or with cardiac failure, shortness of breath, etcetera.
What you see is a hypertrophic restrictive type of cardiomyopathy. And several of these patients have actually had endomyocardial biopsies done showing evacuated, myopathy, which would be typical of antimalarial toxicity. Several have also been diagnosed with highly suggestive patterns on cardiac MR. I think one of the key take home messages from this is that when you think about patients who are on very long term antimalarial therapy, that if they have a cardiac issue, whether that's a dysrhythmia, heart failure, etcetera, obviously, ischemic heart disease, atherosclerotic heart disease is much more common in this population. But one should always bear in mind the possibility that this could be related to antimalarial drugs and speak to the cardiologist about doing the precise investigations that would help reveal this if it was there.
Of note within the posters that they showed, a number of these patients actually were free of epicardial coronary heart disease, which raises more the possibility that this may have been related to antimalarial drugs. The good news in some of these situations was that when you withdraw the drug, there is a slow gradual improvement in cardiac function over time, but that can take at least two years to reverse. Sadly, in one or two patients, they, succumb to sepsis or other issues as well. So that's important, but I think the balance of risk means that antimalarial drugs still remain overwhelmingly beneficial in the vast majority of patients with SLE. And therefore, because of the many benefits that they have, we should continue to use these.
But we just need to pay, respect and attention to this drug, particularly on long term cumulative use. This is, on behalf of RheumNow, and RheumNow will be here for the rest of the week. Thank you very much.
Hi. This is Paul Sufka coming to you live from, ACR seventeen in San Diego. I just came out of a session that was talking about how physicians and scientists should can, manage their online reputation and, distribute their research so more people read it. The first step, to do this is to have a main hub, so your blog or your research site where your things are published. And you're gonna use all the other social networking tools like Twitter and Facebook and everything else, to, bring your people to your main hub.
So important to have a main hub to bring people to. Second, be aware that there are research and science specific, social networks. So one that might be worth checking out is ResearchGate, and one that might surprise you is fairly, useful for scientists is actually LinkedIn. We think a lot that one is more of a business site, but scientists are big on there too. And then last, make your information very easy to share.
So, if you produce an infographic or something that can be shared and looked at graphically, it makes it easier for other people to distribute your content. And then, again, bring it back to your your main hub and, bring more attention to yourself. So a few so, some good ways for scientists to get more people to read their articles. And for more information, go to RheumNow.
This is Catherine Dow from San Diego ACR twenty seventeen conference. I just wanna share with you some interesting updates that I've learned today. First of all, FDA updates from this morning. Something you have to know about. Do not prescribe tramadol or codeine to children or pregnant women.
Now this isn't just a box warning. This is a contraindication. This is stronger than a box ed And the FDA issued a letter and a warning back in April 2017. They are saying it again today. Do not do that.
And the reason why is because there are some individuals who have CYP two d six. This is a gene that causes hyper metabolism of these kind of compounds and particularly in children, if they have too much of this, type of metabolite which you know codeine obviously to morphine, they can go into respiratory distress as well as have death. Where we find this to be a big problem are patients like children who undergo tonsillectomies and they require, narcotics to control their pain or mothers who are breastfeeding and what happens is that they breastfeed and then, had taken their hydrocodone or their codeine or their tramadol and it goes into the milk and the baby gets them. So again, strong warnings, and contraindications from the FDA. Do not prescribe tramadol or codeine products to patients who are pregnant and children under the age of 18.
Alright. Second thing. So I attended a lecture by Virginia Pasquale. As you know, she's this great immunologist, and she spoke about precision medicine. And previously, we've known about the interferon signature in lupus.
In fact as a fellow, I had done research in microarray analysis looking at the interferon signature in lupus. Well take home points from her study, number one interferon signatures are not unique to lupus. In fact, you can find it in type one diabetes, can find it in scleroderma, you can find it in Sjogren's and also a subset of rheumatoid arthritis patients and the subset of rheumatoid arthritis patients who have it actually respond to TNF inhibitors. The other thing that is a take home message is that she has defined seven types of lupus based on their genotypes. Three different kinds of signature besides, so which are interferon signature, the plasma blast as well as the neutrophil signature and she found that the plasma blast and the neutrophil signature may actually be more of an important player for lupus.
So basically in the future we can define precision medicine so treating patients with, targeted therapy that would correspond to their gene type as something of the wave of the future and we are currently on its threshold. So this is Doctor. Dow reporting for RheumNow. Come visit us on our website and read my blogs.
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