RWCS Faculty 2 Save

Hi, I'm Alan Gobosky here at RWCS twenty nineteen. I just finished giving a talk on the legal and regulatory aspects of the clinical use of biosimilars in The United States. I was talking about the BPCIA, or Biologics Price Act of 2009, which was the genesis for the development of biosimilars, and the fact that biosimilars were designed to decrease cost and increase access to patients with rheumatoid arthritis and other inflammatory conditions. I was also discussing the regulatory challenges in terms of extrapolation, interchangeability, switching, and more important, nonmedical switching that occurs or would like to occur here in The United States. For more information, go to roomnow.com.

Hi, I'm Alvin Wells. I'm here at the twenty nineteen RWCS in Maui, Hawaii. This week I highlighted a review on several different topics, focused on osteoarthritis and vasculitis. And one of the takeaway messages I'll give to you is that for osteoarthritis the data shows that we should not use hydroxychloroquine, that using anti TNF drugs such as etanercept do not also give you significant clinical benefit. We've also reviewed what the FDA looks for when they are highlighting new therapies for treating the people with osteoarthritis.

Not only improvement in function and pain, but also preventing total knee replacements. In regards to vasculitis, there's new data coming out by using an IO-five blocker, meplizumab, which is very, very effective in people with eosinophilic polygluomatosis. Also showing some data about what do we do for newer drugs in patients who have ankle associated vasculitis. So can we use Rituximab? Can we use Azathioprine or Mycophenolate?

These are very exciting topics and I think they're very relevant to you who are in the daily practice. For more information, I invite you to go to the room now live.

Hi, I'm Ann Stevens from Seattle, Washington here at the Rheumatology Winter Clinical Symposium in Maui. I just gave a talk about the immunology of fibrosis. It's very important for us to understand as rheumatologists what the mechanisms of fibrosis are because there are a bunch of really, really interesting new drug agents that may target these mechanisms. We talked about the induction of fibrosis which is triggered by damage to endothelial and epithelial cells, about the inflammatory response which includes innate and adaptive immunity and then the fibrotic response which is due to activation of myofibroblasts. Fibrosis occurs in a normal healing response but in the case of a chronic fibrotic disease like systemic sclerosis or idiopathic pulmonary fibrosis this process does not turn off properly in part because myofibroblasts not undergo normal apoptosis and dedifferentiation into into normal fibroblasts.

And they continue to produce this extracellular matrix components. We have some new agents that that may be able to interact with different stages of fibrosis including each of those stages I just mentioned. And then some old agents like tocilizumab which interferes with IL-six function which may help to regulate these fibrotic cells. Finally the exciting new frontier of this field is stem cell therapy which being is trialed in localized scleroderma disease and systemic sclerosis. There are a couple of companies now that are developing adipose derived regenerative stem cell therapies that may be the promise for long term treatment and remission of these diseases in the future.

For more information please go to roomnow.com. Thank you.

Hi, this is Doctor. Arti Kavanagh coming to you from RWCS twenty nineteen. A lot of, great lectures and, I was pleased to be part of it and I get to talk on psoriatic arthritis and do the year in review and what a challenge that was an incredible year in psoriatic arthritis. Lot of good new information. Big study was the SEEM study which we've really eagerly awaited.

This is the study of methotrexate, a TNF inhibitor, in this case etanercept, or the combination. We know in rheumatoid arthritis that the TNF inhibitor methotrexate are certainly additive if not synergistic and that's the gold standard of treatment and I think a lot of us and I would say myself included had assumed that we would see in psoriatic arthritis as well certainly for the peripheral arthritis a clinical benefit, but certainly a radiographic benefit. The SEEM results, were very interesting. Therefore, they showed that etanercept and etanercept plus methotrexate were better than methotrexate, but there was really no synergy. So it didn't seem like the methotrexate added anything.

Also, the methotrexate did not do badly. Now in this study there was no placebo, but the rates of response for peripheral arthritis, for skin, for dactylitis, for enthesitis all looked as if methotrexate can be effective. It's actually reasonable studies suggest that methotrexate should remain in our therapeutic armamentarium for psoriatic arthritis. Big year for biologic agents. The TNF inhibitors continue to be the go to biologic agent.

There was a sub analysis of a study of glimep that showed that as in RA you get the x-ray benefit dissociated from clinical response. Even people who didn't have the best clinical response still had x-ray benefits. For the twelve twenty three inhibitor, there's some interesting data showing that it can be effective in enthesitis. We know it's effective in skin. We know it's effective in peripheral arthritis.

Not effective in the spine. And I think we'll hear from Doctor. Ruddemann about the failure of ustekinumab in ankylosing spondylitis. IL-seventeen inhibitors, we have secukinumab and ixkizumab. The new candidate in the block, if you will, is bimekizumab, which blocks IL-17A as those other compounds do, but also IL-17F.

So we'll have to see if there are differences in safety efficacy among those compounds. A lot of data and I think we're continuing to learn from these targeted studies using specific therapies. We're learning about the disease themselves. So really a bedside to bench approach. Very exciting and we look forward to more developments in the year to come.

Hi, I'm Aryeh Fisher. I'm at the Rheumatology Winter Clinical Symposium and I just gave a lecture on the pulmonary manifestations of rheumatic disease. I focused my lecture on autoimmune forms of interstitial lung disease. A couple key points to highlight would be how complex these patients are and a complex intersection between autoimmune diseases and interstitial lung disease, diverse interstitial lung disease patterns, really a need to engage rheumatologists in the evaluation and management of these patients, highlighting different clinical scenarios, autoimmune serologies, CT features, lung biopsy features that may suspect or lead us to believe the patient has an autoimmune form of ILD and recognizing that these patients need thorough evaluation and that we have a lot to learn about how to better manage them. Currently, we use immunosuppressive therapies, but we need more clinical trials and more data to guide how we approach treatment in the care of these patients.

To learn more, take a look at roomnow.com.

Hi, this is Eric Ruderman. I'm here at RWCS twenty nineteen. While here this week, I gave a talk on what's new in axial spondyloarthritis. It was actually a very busy year in a number of areas, but particularly in the number of new clinical trials we saw this year. We saw the first long term trial in non radiographic axial spondyloarthritis with cerdulizumab, comparing cerdulizumab to placebo over an entire year and demonstrating efficacy of cerdulizumab.

We'll see if that persuades the FDA to approve this drug for non radiographic axial spondyloarthritis, the first drug that would be approved for that particular indication. We also saw new trials with an IL-seventeen inhibitor, ixekizumab, in so called radiographic axial spondyloarthritis, or what's basically ankylosing spondylitis, in both patients who were TNF naive and TNF failures, and the drug was effective in both populations patients. And then we saw its two early trials this year in two novel drugs. One was Bimekizumab, an antibody that blocks both IL-17A and IL-17F, which was effective in axial spondyloarthritis in a early population in a phase two trial. We'll see if that pans out in later trials.

And we saw the first data with a JAK inhibitor with filgotinib that was convincingly effective in a phase two trial at ankylosing spondylitis. Those were the trial data. One last thing we saw this year that I thought was very interesting was an abstract from Germany that looked at a mechanism for driving patients with possible axial spondyloarthritis to the rheumatologist's office. They actually used a series of posters on the subway that drove people to a website to see if they had symptoms that might be consistent with axial spondyloarthritis. They then tracked those people down when they went into the rheumatologist and twenty percent of them turned out to have axial spondyloarthritis.

It was a pretty good yield for a direct to consumer advertising program. Look for more information on these and other topics on RheumNow.