RheumNow - RWCS 2018 - Day 4 Save

RheumNow is pleased to present the RWCS Daily podcast from the twenty eighteen meeting here in Maui. These podcasts are a compilation of each day's presentations by our featured faculty and presenters. We hope you enjoy these presentations from RWCS.

Thank you.

I'm Leslie Bellello, an emergency medicine physician coming from Boston, Beth Israel Deaconess Medical Center, where I serve as an emergency medicine attending as well as the assistant program director for the Harvard affiliated emergency medicine residency. I'm here at RWCS twenty eighteen presenting on updates in critical care and emergency medicine. The clinical pearls we talked about in my discussion today include respiratory failure, specifically oxygenation and ventilation, as well as intubation techniques and ventilator management. We talked about sepsis and septic shock, specifically the use of IV fluids, pressors, antibiotic therapy. We also discussed hemorrhage, hemorrhagic shock, and the massive transfusion protocol, as well as use for reversal agents and anticoagulation.

And finally, we talked about extracorporeal mechanical oxygenation in the ECMO patient, as a further bridge to cardiovascular stability. Thank you so much having me and we're looking forward to more exciting talks at RWCS twenty eighteen. Thank you.

Hi, I'm Alvin Wells from Franklin, Wisconsin. I'm here in Maui at the twenty eighteen RWCS meeting. This has been an exciting meeting. Earlier we shared with you some of our thoughts about a year in review for gout, osteoarthritis, and scleroderma. I would also like to showcase some of the things we're going to be talking about in imaging and what's the evidence behind imaging.

Many of you who are doing advanced imaging, whether ultrasound or MRR or CT scans, you know that for Rheumatoid Arthritis it plays a significant role in your management of your patients. I'm highlighting data at the meeting to show not only with Rheumatoid Fighters but other rheumatic diseases. Whether we're talking about lupus, we're talking about gout, whether talking about Sjogren's Syndrome, advanced imaging can help with the diagnosis, the monitoring and the treatment of your patients. So stay tuned and look for these exciting changes here at this meeting and at future events.

Hi, I'm Doctor. Rachel Tate coming to you from Rheumatology Winter Clinical Symposium in Maui, Hawaii, and I have the pleasure today of interviewing Doctor. Anna Pasilova about her poster. Anna, thanks for joining us, and what brings you to Maui? What's your poster about?

Thanks so much, Rachel. So my poster is about a retrospective review of granulomatous mastitis that we did in our clinic. Over a ten year period, we were able to find actually 34 patients, nineteen of which came back for an appointment, so we had clinical data. For those who are unfamiliar with granulomatous mastitis, a disease, because as rheumatologists we don't really see a lot of breast diseases. But it's an inflammatory disease of the breast and really to date it hasn't had a lot of treatment.

Most of the literature talks about antibiotics and steroids, and they don't have really good effect. People relapse, and most women go to mastectomy. So as you can imagine, this is a horrendous option for women and for a variety of reasons. And so we found very good clinical benefit from methotrexate. So we show here that, methotrexate use over the course of one to two years leads to resolution in pretty much ninety percent of our patients and complete resolution in eighty percent.

So this is, I think, a disease that rheumatologists are gonna see more and more now, and we have a great medication that we're really comfortable using that leads to resolution of this inflammatory breast condition.

Anna, that's great. Stanford's really lucky to have you. I'm sure they know that. Again, this is Doctor. Rachel Tate coming to you from Rheumatology Winter Clinical Symposium with Doctor.

Anna Pasilova today. And check us out on roomnow.com.

Hello, I'm Ann Stevens from Seattle Children's Hospital and the University of Washington. I'm here at the RWCS meeting in Maui. And I have just recently given a lecture on, neutrophils in autoimmunity. In the last couple of years, there have been some really interesting advances studying the effects of neutrophil nettosis and how this may promote chronic inflammation in the autoimmune diseases that we treat in rheumatology clinics. Nettosis is the process of neutrophil death in which DNA from the nucleus is extruded outside of the cell, and the DNA is associated with all of these granular proteins.

And these proteins we know very well as autoantigens in our diseases such as MPO, PR3, and neutrophil elastase and histones. The neutrophils are starting to come to the surface as a major mechanism of pathogenesis of most of our diseases. So then the question is, what determines whether a patient gets rheumatoid arthritis versus lupus versus vasculitis? We know that neutrophils and netting, this extrusion of DNA with pro inflammatory auto antigens, happens in all of these cases. And what we know is that the associated proteins in a netting neutrophil from a patient with rheumatoid arthritis, those proteins are different.

Those are citrullinated histones, those are citrullinated enolase or vimentin proteins. In lupus, different autoantigens are present, and in vasculitis, different autoantigens. So the presence of these granular proteins are different. What we also know is that we can connect the interferon signature that we know is so important in lupus to neutrophil netting. And that's because the nets are not only our nuclear DNA, but they're composed of mitochondrial DNA.

The mitochondrial DNA has been oxidized by the reactive oxygen species that are produced in an activated neutrophil. This is part of what a neutrophil does. It kills up bacteria by these ROS compounds, and it also oxidizes the mitochondrial DNA. If you take mitochondrial DNA that's been oxidized, add it to a dendritic cell, that dendritic cell is activated to make type one interferons just like in lupus. So this connects findings that were published in 2003 showing that there's a major signature, an mRNA signature in patients with lupus that signifies granulopoiesis and a signature that signifies interferon induced gene expression.

So it connects these granulocytes to the interferon signature. Knowing more about this pathway of mitosis leading to chronic inflammation, leading to breaking of tolerance and autoantibodies to proteins that are in the NETs suggests multiple steps along this pathway at which we can intervene with medications. And the future of this area is focused on drugs that may block nettosis, that may block the reactive oxygen species production, that may block the citrullination of peptides that allows this nettosis process to occur. So we're going to look for these medications coming out in trials in the next few years. Thank you and Aloha.

This is Artie Cavanaugh at RWCS twenty eighteen. Talk today about psoriatic arthritis, there have just been such tremendous developments in psoriatic arthritis. In 2017, there were three approvals for new drugs for the use of psoriatic arthritis, drugs that have been used for other indications, but new to psoriatic arthritis. And that's ixekizumab, tofacitinib, and also abetacept. The more choice we have, the better because we're able to offer our patients a variety of mechanisms of action, hopefully to find the one that works best for them.

Another area of a lot of excitement relates to enthesitis. We've always known about entheses, of course, where tendons and ligaments and joint capsules insert into bone, but we're learning so much more that this is a immunologically active tissue and that it may well relate to tie in some of the diverse aspects that we see in psoriatic arthritis, such as gut inflammation, skin inflammation, and joint inflammation. And of course, the more we learn about the immunopathophysiology, the more we'll able to target dysregulated aspects of the innate and specific immune system and hopefully achieve better clinical results. So an exciting year. Certainly look forward to exciting data coming out this year as well.

Hello. I am Bevra Hahn, and I'm a rheumatologist at UCLA. Today, I'm talking about lupus, and I did a little bit of history going from the time before we had cyclophosphamide or mycophenolate or azathioprine or biologics, to treat lupus and bringing it up to date. So one of the important things that happened in the past was the ban against kidney transplants in lupus patients was lifted in the mid seventies. Before that time, the nephrologists and surgeons weren't allowed to transplant somebody that had lupus because experts knew that the lupus would recur in the transplant kidney.

And in fact, that only happens three percent of the time, and now they're transplanted, as you know, like everybody else. Another thing that happened that improved our care was, a lot of government legislative advances that included the introduction of Medicare and Medicaid and surgery, insurance for emergencies and, the CHIP program for children and the Affordable Care Act or Obamacare, and altogether about one in three Americans are covered by a federal program for their health care, and that's allowed us to really expand the number of people we can treat. And of course, there's been improvement in how we treat patients. There's been the introduction of cyclophosphamide and mycophenolate for people with serious lupus and people with lupus nephritis, although they are not approved by the FDA yet and neither is azathioprine. But we all use them and we know how to use them, and mycophenolate is coming up to the top as the first choice of many people, for patients who have serious life threatening lupus, and that's because it is as effective as cyclophosphamide, but easier to tolerate and it's effective in all races and the same thing can't be said for cyclophosphamide.

And there's recent data that might be a little more effective than azathioprine. So, it's in wide use. And then, of course, belimumab has come in and we know that people with arthritis and skin disease particularly improve on it. About sixty percent of people improve. We now have the subcutaneous form, which is gonna make it so much easier for patients to use.

And looking toward tomorrow, there are a lot of exciting things coming along that look very good in lupus in phase two trials. And one of them is an antibody against the interferon type one receptors. It's called anifrolumab, and it looked very good in a phase two trial. Another one is voclosporin, which is a new calcineurin inhibitor that's supposed to be safer for the kidney. And by the way, tacrolimus plus mycophenolate together looked really good in the Chinese study in terms of increasing the percent of people who get a response to lupus nephritis up to around eighty percent or better, very, very good response rates.

And another new thing we're looking at is ustekinumab, which in recent abstract was shown to be effective in lupus patients who don't have nephritis and better than standard of care. So we should keep our eyes open for all of these new things coming along, and there are many more I don't have time to discuss. But the cap on what I want to talk about is, are we going to have a crisis in physicians who know how to use this? Because there is a big problem with physician burnout. There are two articles in the New England Journal of Medicine about two weeks ago that show that fifty three percent of today's practicing physicians have symptoms of burnout, and half of those will drop out of seeing patients sometime over the next decade.

That means we're gonna lose one out of every four physicians practicing today because of this burnout. The Institute of Medicine has defined it as a crisis. There are many groups who fund health care who realize it's a crisis, and many groups are being formed to try to address the solution to this crisis. If anybody asks you to participate, please help.

Hi. This is Eric Ruderman. I'm a rheumatologist at Northwestern in Chicago, and I'm here at RWCS. I gave an update yesterday on evidence based, information in vasculitis therapy. And one of the things I highlighted, which was really significant in the last year, was the new data on the use of mepolizumab, an anti interleukin-five antibody, in the treatment of EGPA, the disease we used to refer to as Churg Strauss Syndrome.

We've had dramatic improvements in therapy in vasculitis, in GPA, and in giant cell arteritis. And this is the first time we've seen a biologic with tremendous efficacy in EGPA. In patients who are on background therapy with steroids, and in some cases immunosuppressive, there was a much higher rate of remission and a lower rate of relapse in the patients who were treated, with mepolizumab as opposed to placebo. I think this opens up a new opportunity for a new biologic to change the course of therapy. And this disease, just as other biologics like tocilizumab in giant cell arteritis or rituximab in GPA have done before it.

Hi, this is Eric Ruderman. I'm a rheumatologist at Northwestern University in Chicago, and I'm here at, RWCS. I, presented some information this morning on current data in axial spondyloarthritis. A number of new publications and abstracts in the last year on therapy, but one of the key and interesting things to come out in the last year was the importance of fibromyalgia in this disease. As we all know, there's an incidence of twenty to thirty percent of our patients with rheumatoid arthritis or with lupus who have fibromyalgia, and I don't think it's surprising to find that the same percentage of patients who have axial spondyloarthritis also have fibromyalgia, or in other words, pain that doesn't have an inflammatory origin, at least directly.

Interestingly, these patients seem to do less well with biologic therapy, which is not terribly surprising, again, given that their pain is coming from non inflammatory, drivers. What was also shown in the past year, a very nice, analysis of patients with fibromyalgia versus patients with AS or axial spondyloarthritis was that the fibromyalgia patients by and large do not meet criteria for axial spondyloarthritis. So it's not that people with fibromyalgia are being confused, and treated as axial spondylitis that they don't have, but rather that people with axial spondylitis have a relatively, frequent, incidence of fibromyalgia as a sort of co traveler in this disease, if you will, and attention to that aspect of their pain is going to lead to better outcomes with our therapies.

I'm Mark Genovese from Stanford University. I'm here at the RWCS meeting and I was invited to speak on a number of topics including osteoporosis. I think it's important to recognize that osteoporotic fractures both serious and preventable. We also recognize that patients with rheumatic diseases are at an increased risk for developing osteoporosis and bone loss. Identifying those risk factors early and intervening can help prevent those events and the medications that we use for osteoporosis are both safe and effective when used in an appropriate fashion.

Over time I hope to see that we have less osteoporotic events particularly fractures in relationship to our patients with autoimmune diseases and on most patients taking glucocorticoids. Thank you.

Hello, I'm Orin Traum. I'm a clinical professor of medicine at the Keck School of Medicine at the University of Southern California and here at the twenty eighteen Rheumatology Winter Clinical Symposium. I've given a lecture today on telemedicine and telehealth and telerheumatology. This is an expanding field and there are multiple posters at the ACR meeting in San Diego this past November that really focused on how physicians and patients and healthcare systems may utilize this technology. Doctor.

Bevra Hahn just gave a very excellent lecture as the Kahuna here at the RWCS on lupus. Her last slide looked at physician burnout. This may be a way that patients and physicians may be able to interact without physicians having to feel so overwhelmed. The terms telehealth and telemedicine sometimes are interchangeable. The WHO feels that they can be used interchangeably, but in general you're using mobile apps, you're using, electronic health records for patients that are at far distances and this certainly applies in places like Alaska or other states where there are large distances where patients have to leave work, drive to the physician office and then go back.

There's time wasted, there's finances that are lost and it seems to have great relevance especially for patients like that and for the doctors and for people that can't get access to rheumatologists. There seems to be a need. I think this is going to be a great advance in the way that we interact with our patients and something to look for for the future. Thanks for joining me at the RWCS twenty eighteen.

Aloha from RWCS twenty eighteen. My name is Uma Mahadevan. I'm a gastroenterologist at UCSF. This year at RWCS, I covered three different topics. The first topic was how to direct refer a patient for colonoscopy.

Many rheumatologists will want to send a patient to the gastroenterologist due to access issues. Sometimes it's easier just to get them in directly for the procedure they need. But before you send someone in, what are the things you need to think of? In your patient population, do they need to stop their aspirin and NSAIDs? If they're on blood thinners, including warfarin, heparin, or even the newer agents that are antiplatelet agents, do they need to be stopped?

And the answer often is yes. And a lot of that has to do with their risk factors and whether they need bridging therapy. All of this information needs to be shared with the gastroenterologist. If you're taking care of a patient with ankylosing spondylitis, are they safe for conscious sedation or do they need an anesthesiologist present? The more information you put in your referral, the easier it is to get your patient in quickly for the procedure that they need.

The second topic that we covered is small intestinal bacterial overgrowth or SIBO. This is very common in all populations, but particularly as patients age and as they're on various immunosuppressions and proton pump inhibitors. SIBO is an overgrowth of bacteria or dysbiosis leading to bloating, gas, and discomfort. For many patients, this requires a visit to the gastroenterologist, but you can take care of it yourself in many occasions. You don't always have to get testing as it can be inaccurate, but if your patient meets the description of SIBO, you can give them a trial of Rifaximin five fifty milligrams three times a day for ten to fourteen days, and follow that with probiotics to see if their symptoms resolve.

Dietary therapy such as a low FODMAP diet can be helpful as well. Finally, we finished with a review of updates in inflammatory bowel disease. Rheumatology patients and IBD have a lot of overlap. We use many of the same drugs. And in addition to the anti TNF agents, we also have anti integrin agents such as Betelizumab, which has been very effective.

There's been a lot of talk that Betelizumab is gut specific and therefore does not help with rheumatologic or spondyloarthropathy complications of patients with IBD. However, if you treat the underlying bowel disease, in many cases their arthralgias will resolve. Also, tofacitinib will be under consideration by the FDA in March 2018 for approval for ulcerative colitis. So that will be yet another drug that we will share. Thank you and for more information go to roomnow.com.

Aloha. My name is Bernie Rubin. I'm the chief of rheumatology at Henry Ford Hospital in Detroit. I'm here at RWCS two thousand eighteen. We have several fellows who have interesting cases that they have chosen to present.

So I'm gonna talk to Amber Ahmad from the Medical College of Wisconsin. She's a first year fellow about this interesting case of cutaneous polyureitis nodosa. Umber, several of us in rheumatology see polyureitis nodosa, even cutaneous. What's unusual about your case?

Yeah, my patient was actually pretty interesting. She's a 37 year old female who had a cutaneous polyarter nodosa since she was a young child and usually was preceded by strep infection. At this time though the reoccurrence happened when she was 37 and she was initially treated with Cytoxan but didn't really have much of a response with it. When they tried to decrease her dose of prednisone down to less than forty milligrams a day, she saw her had reoccurrence and worsening of her subcutaneous painful lesions. And so she came to us wanting help and trying to figure out what's going to be helpful in regards to these uncomfortable lesions and nodules on her body.

So how long had she been treated before she came to rheumatology?

Yeah, so she did around three cycles of cytotoxin and so she was on the forty milligrams of prednisone. We actually tried to first start her on methotrexate to see if she had any improvement with that. She had minimal improvement with that. And so we had we decided to switch her to Plaquenil from there onwards. And with Plaquenil, didn't tolerate it.

She was having complaints of irritated eyes. And so she tried it. We pretrialed it. Didn't work out. So we went ahead with IVIG, which is not often done.

And actually, there's only nine case reports of it done in the lab.

Really? And so you looked at trying IVIG. And did it work?

Yes, it did. What's really astounding is actually after the first cycle she noticed remarkable improvement of her symptoms and so after the second cycle which is what she was on, actually she was on it last month, she has complete resolution of her symptoms and is down to prednisone about ten milligrams a day.

Wow, that's very interesting. So there's only been a few cases in the literature where IVIG has been used?

Yes, about nine cases total and a few of them are in children as well as the rest of them are in adults. And often, I think of the cases that are in the literature, three of them were involved with children and usually preceded by a strep infection with an elevated ASO. And so, there's very limited cases. And specifically, are the ones involving mainly cutaneous manifestations.

So how many cycles of IVIG has she had?

So far she's had about two cycles of IVIG and her next one is gonna be this month and we're gonna do a total of six cycles. But I guess based on all the cases it really does vary. Some people do it for six months. Some people do it for three months. It just really depends.

But we thought we'd try the six months, see how she does off of it. And if she does great, we'll just keep her on that. But I think right now she's doing pretty good and we're happy with the results.

Very good. Thank you. That's a great case and very interesting. You know, many of us see this kind of a condition and I think the use of IVIG might be something that all the rheumatologists would be interested in looking at in the future.

Yeah, I agree with that. Especially when it makes such a big difference in symptoms of a patient, I think it's a wonderful medication to consider in this specific disease.

Thank you. Great.

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