Valentine RNL 2025 Review (2.14.2025) Save

It's 02/14/2025. That's right, Valentine's Day. We love you here at RheumNow, and we hear from you that you love us because I'm match made in heaven. I'm Jack Cush with rheumnow.com. This week on the podcast, I'm going to do a review of a few of my favorite things from last weekend where we did RheumNow Live in Dallas.

Great meeting, almost 500 people online and in the room, over 20 faculty, 62% of whom were women faculty. A lot of things about this meeting that were really superb. And I think the big hit of the meeting was someone who wasn't speaking and lecturing, but was our faculty, in fact she was our co host Doctor. Janet Pope from Canada, was our online virtual host. For over 300 people who were online and viewed RheumNow Live virtually, Janet was their super concierge.

She was their mentor, their peer, their reminder. It was just a grand experience for anyone who watched the day and a half meeting online because they had Janet there guiding the way, leading the discussion, making it a really interesting experience for the online community and that's what we want out of this meeting. And really we should want that from all of our meetings. Artie and I, Artie Cavanaugh and I hosted the on-site audience where it was also a great discussion, great sessions. It was on Saturday and Sunday the eighth and ninth of February, a day and a half meeting with sessions, you know, blocks devoted to rheumatoid arthritis, psoriatic arthritis, JAK inhibitors, vasculitis and spondyloarthritis and in between we threw in seven or eight TED like talks and keynote talks that were just fabulous.

So some of my favorites I'll go over for you to let you know what you missed out on. If you had been there in Dallas you could have participated in karaoke on Saturday night which was either embarrassing or fun or painful depending on who was singing. And I'm mainly talking about me. It was brutal. But when I wasn't singing from my dinner I was lecturing and I lectured about flare and RA.

I told the audience flare and RA is a stone in my shoe. It's something I keep thinking about, something that's bothering me and it's bothering me because I think it's a pedestrian problem that we deal with. We deal with flares all the time. But do we really? Do we understand them?

Do we know how often they occur? And we have the same solution for all patients with flares. Tell them to take steroids. Tell them to take a medrol dose back. Some special regimen that you dreamed of.

Artie Cavanaugh calls that, Do you play steroid poker? My steroid regimen is better than your steroid regimen. Do you have people come in for injections of some sort? You know, what are the alternatives other than steroids? The point that I wanted to make in my session is we do a lot of different things.

A lot of this is managed over the phone. We tell a patient to come in or not come in. We tell them bed rest and ice and elevation or come in and take steroids as a shot or whatnot. We add or change analgesics. We give them dose packs or again five, ten, twenty of prednisone in some daily regimen that you dreamed up.

I am an intra articular is good but is it any better? We don't really know. And if you have enough of attacks, do you treat it like it is gout? You had more than two attacks this year. I'm going to change your regimen.

I'm going to maybe add on regular daily steroids or I'm going to add on and change your DMARC. Again, there's no science to this. It's all guesswork and it's a big part of your business. The problem is the following: the definition of flare until recently and the research coming out of Vienna that showed that a flare is defined as an increase in your simple disease activity score SDAI or clinical disease activity score the exceed die of greater than 4.5. 4.7, 4.5, it's basically greater than 4.5.

And that defines a flare. All other flares have been guesswork. The problem is the patient considers a flare differently than the doctor. The doctor, all are concerned about pain but the doctor is more married to the importance of a swollen joint and an elevated, acute phase reactant and his exam or his global impression. The patient on the other hand is more swayed by a lot of psychological factors, distress, fatigue, poor sleep, and whether or not I can go to work or not.

And our definitions differ between the MDs and the patients. The magnitude of the problem is much larger than you think. Many studies have shown depending on whether it was an impetus like I'm going to taper my DMARD or my biologic down or I'm going to try to stop the biologic that's expensive. You know the rates are generally about thirty percent for any kind of tapering and over fifty percent for any kind of stopping. So there is people that you can play games with their drugs and get away with it but the majority are going to have problems.

Would you say that if I asked you what happens with your flares? The majority have problems and then there's even worse problem is that there are downstream consequences to bouts of inflammation that are irreversible or irreconcilable. Forget about the changes in quality of life. There's a real hit to the musculoskeletal system with more radiographic progressions, more erosions, more cardiovascular events. Forget about the fact that work participation, productivity losses, treatment changes, cost of comorbidity management, It's a big problem for which we don't really have a solution.

So number one, don't taper, don't stop, don't endorse that. It's crazy. I know patients are going to want to do it, but it's a bad idea. Secondly, if you measure a metric in practice then you have a way of objectifying that it really is a flare. As I said, an increase in C Dye of 4.5.

It's the same as an increase in whatever it is that you measure including Rapid three. And you can use remote assessment tools to know what you're in fact dealing with. The bad news is analgesics don't work. The bad news is rest and time doesn't work unless you're back in nineteen fifty, sixty, seventy when they would hospitalize patients for flares. And total bed rest, I mean total bed rest, bed pan bed rest does lower acute phase reactants.

It can control disease but nobody really does that. At current day, guidelines are steroids. But why does it have to be steroids? Why wouldn't it be short term use of a short acting, quick acting drug like a JAK inhibitor or colchicine or Anakinra. Think we need to have really drug development in this area.

That would be the way to go. I tell people again a flare is a crisis and a crisis is both danger and opportunity. And the opportunity is one, listen to the patient, they're telling you the problem. It's an opportunity for you to really make substantive changes in their treatment and you know recognizing that these people are falling into the category of difficult to treat RA the more they have these flares. We had a great session on psoriatic arthritis that included great lectures from Artie Cavitt on combination therapy and Ken Gordon on head to head trials but Alexis Agde tackled the issue of whether aggressive treatment for psoriasis will prevent the development of psoriatic arthritis.

I keep reporting these, I've talked about these here on the podcast. The problem is that there's at least 11 studies out there that have made this claim that if you use aggressive therapies, expensive therapies, biologic therapies, those people are less likely to get psoriatic arthritis down the road. And then Alexis took apart the problem. You know who's at increase? Risk.

What are the things that contribute to risk? What are the modifiable risk factors that contribute to risk of progression? And then she went through the problem of the dozen studies and said that the problems exist in that there's problems of coding, there's problems of channeling bias and confounding issues. These are associations and not causations. A lot of them are missing data and misdiagnoses and there are all kinds of other biases and observational biases.

As an epidemiologist she made fun of herself saying that the definition of an epidemiologist is an individual who does precise guesswork based on unreliable data provided by those of questionable knowledge. Well that seems pretty funny and doesn't seem to apply to her but, this is the kind of data that does come out of epidemiologic studies. There was a recent study that we reported on two weeks ago about if you were on a TNF inhibitor, I'm sorry, an IL-seventeen inhibitor versus an IL-twenty three inhibitor versus a TNF and which ones were less likely to, or more likely to protect you from progression to psoriasis. And IL-twenty three in those studies look good but they suffer from the same biases that I just indicated. And in the end, she said, We don't know because the right study hasn't been done.

Again, there's an inference that maybe if you are aggressive in psoriasis you can prevent psoriatic arthritis but until the right study is done you're not going to know. We had a fabulous session on vasculitis. We had Renny Ray from Penn talk about imaging. We had Richard Conway from Dublin talk about treatment of PMR. That was great.

And then we had a great lecture on EGPA by Michael Wexler, a pulmonologist and head of the division there at National Jewish. It was a really eye opening lecture. Was great to hear from pulmonologists. He went over the issue of basically hypereosinophilic states that affect the lung and that would also include, you know, patients with Wegener's and PAN that can often have eosinophilia. There's hyper eosinophil syndrome, drug reactions, eosinophilic pneumonia, neoplasms, parasites, asthma itself.

And of course then there's a small little disease that we tend to see, that used to be called Church Strauss that is now called EGPA. Great pragmatic lecture, went over all the management. He basically said steroids, steroids, steroids. Oh, dude, by the way steroids are dangerous. And then he talked about the many choices that you have that you can find for treating these people and there's a number of things but the drugs that we've relied on, the DMARDs, the azathioprine, the cyclophosphamide, the mycophenolate rituximab generally have not been proven to work and are certainly not FDA approved.

What is FDA approved is the IL-five targeted therapies. One targeting IL-five, the other one targeting the IL-five receptor that is meprolizumab and benralizumab and both of those look really good. New England Journal article from last year, the Mandara trial which we covered here, showed that they were equally effective in steroid sparing and reducing relapse rates and lowering Birmingham Vasculitis Activity Scores, the BVAS Score. Really effective therapies. But what I liked most about his talk was he said he talks to pulmonologists and he talks to rheumatologists.

In the pulmonary world, he says EGPA is basically asthma complicated by vasculitis. In the rheumatology world, it's vasculitis complicated by asthma. And I think there's a message in there. I think the real approach to this disease is to be aggressive, to use the IL-five inhibitors after you start steroids and treat the hypereosinophilic situation so it doesn't develop into a bad vasculitis where then you may need to add on a vasculitis drug like Rituximab. So, here right now at RWCS in Maui and I asked that question of Anisha Dua and she said, yes, there are situations where especially we in rheumatology might have to not just be using anti IL-five and steroid therapy but also vasculitis specific therapies because we might get the wrong spectrum of the disease, the more aggressive spectrum of the disease.

Again, when you look at these people the disease is defined by hypereosinophiliates. Usually, eosinophil counts greater than a thousand or greater than 10% of the peripheral white blood cell count. Thirty percent of these people are going to have an ANCA, usually a P ANCA. Those people are a little bit more inclined to have the classical systemic vasculitis presentations. Right?

So, a really instructive lecture on EGPA. If you're looking for a good EGPA lecture, again Michael Wexler at National Jewish. Again, he believes that this can be treated aggressively, remission is a realistic goal. Steroids are first line but they're not the end of therapy and we do have to worry about when we step down therapy, steroid refractory disease and patients who continue to have flares despite whatever treatment you're doing. We had a great TED Talk, we call them Step Talks, where we talk about fifteen minute talks on science, technology, education and patients.

And Michelle Petrie, mesmerized as expected, and she brought to bear the new rules on steroids in lupus. And she spoke, as you can imagine, about the dangers of steroids in lupus especially if patients are maintained on them chronically as a crutch. She talked about how you can do steroid sparing therapy. She talked about the fact that you can't avoid steroids in patients with glomerulonephritis. The new lupus guidelines say that patients need to be pulsed and given aggressive steroid management as a big key part of their management along with the other second line, third line therapies that we've covered after ACR.

But I liked her last slide that she showed where she talked about what's going on at the lupus clinic at Hopkins. It's the Hopkins lupus cohort which is she's collected thousands of patients. And in her clinic that she runs and you can imagine how she runs it, right? She's the expert. Sixty four percent of her lupus patients are not on prednisone.

Sixty four percent are not on prednisone. That 0.5 to four point five is five percent. Five to seven point four is thirteen percent. So eighteen percent are on less than seven point five percent. And that eighteen percent are on seven point five or more.

Can you match that in your clinic? I know I can in mine. But the point of this lecture and the point of her address is that we should be more aggressive in how we manage lupus so that we don't rely on steroids especially at higher doses, especially at five milligrams or more. Another great literature on the spondyloarthritis section where we had Desiree Vanderhai talking about the disease modification effects of our aggressive therapies in spondyloarthritis. We had Catherine Bakewell do a fabulous lecture on imaging in spondyloarthritis and we had a lecture from a dermatologist, Jennifer Cather, who is with Baylor and Mindful Dermatology in Dallas on Hidradenitis suppurativa.

The question is, what is it? How do we manage it? Who's supposed to manage it? I asked the question of that panel. Doctor.

Vanderheide, Doctor. Bakewell, and Doctor. Cather, who I think really represent quite a spectrum of people that should answer this question. Is hidradenitis suppurativa something that the derm should manage or the room should manage or better put is it part of the spondyloarthritis spectrum? I don't want to put the words in the mouths of my panelists but in general Desire felt probably not.

While it has features, it doesn't mechanistically seem to fit. But then again, there are some things about it that might make you want to consider it. I believe Doctor. Bakewell said, Yeah, I think it might because of the many features that run with Hydroadenitis suppurativa. And Doctor.

Cather was much more certain that it is part of the spectrum. The question is, who should be managing it? Do you manage it? I manage a fair amount of hidradenitis. Turns out a lot of derms don't want to manage hidradenitis.

It's about one to four percent of the population. It's mostly females in the Western Hemisphere. The etiology is driven by the cytokines that could be attacked by the anti cytokine therapies we use including TNF inhibitors and IL-seventeen inhibitors. It has risk factors of obesity, tobacco, mechanical stress and altered microbiome. You get these characteristic scarring lesions, inflammatory lesions that appear in the intertrogensous areas of the body, the axilla, the groin, the buttocks and whatnot.

These lesions tend to be chronic recurrent and recalcitrant and they often smell bad. I didn't know that odor was such a big problem with this because I've never inquired. I've never asked that question. But odor is a big problem and a big bother to these patients as is the appearance and whatnot. Doctor.

Cathery reviewed the approach which included topical and systemic antibiotics including clindamycin solution and doxycycline, the use of anti androgenic therapies like metformin, finasteride and spironolactone. Retinoid therapy, systemic and local. Laser hair removal can help curtail disease or even prevent disease in people who had problems in sinus tracts and whatnot. And then biologics, specifically adalimumab is approved for use in hidradenitis suppurativa and two IL-seventeen inhibitors are approved for hidradenitis suppurativa. One, secukinumab and two, the dual AF inhibitor bimekizumab was recently approved.

She went over some anecdotal data with JAKs that they may be part of the picture in the future. So, one last thing I think I'll talk about is in our JAK inhibitor session. We had fabulous lectures from John Giles about the end of the story with oral surveillance and cardiac issues. Joe Marola talking about TYK2 inhibitors and where they fit in. An incredible presentation by Madeline Feldman from LSU talking about what happens when JAKs go generic and because you may know that tofacitinib is supposed to go generic at the end of twenty twenty five.

And not I mean there are companies lining up to make the generic of tofacitinib. But there's a lot of funny business and monkey business that only Madeline can cover. And if you get a chance to look at that lecture you should look at it. It's really really mind blowing. But the other lecture in this session was from our Chief of Rheumatology at UCLA, Christina Charles Schulman where she talked about a dermatomyositis update including the use of JAK inhibitors in dermatomyositis and she said a number of things that I think were really really surprising.

One that I wrote down was that because ILD occurs in dermatomyositis doesn't mean it's scarring and forever and deadly. These people can have improvement of their ILD over time and with treatment. She showed case examples and some literature data to back that up. Moreover, it also happens with MDA five positive dermatomyositis. A nasty, nasty subset of disease with horrible lung and skin disease.

Although they may not have much in the way of actual myopathic disease and they get calcinosis and they get some cancers. But anyway their lungs can also regress with appropriate and more aggressive treatment. She talked about calcinosis and mainly the treatment of that is first aggressive treatment of the underlying disorder, the dermatomyositis. Second, problematic lesions can be surgically excised. Third, she talked about roles for JAK inhibitors maybe here, citing some data.

So, there were a lot of new things but the whole, know, takeaway on JAK inhibitors was she basically said there's a lot of data, it's all anecdotal and uncontrolled. Almost 150 cases of patients with dermatomyositis successfully treated with either Topacitinib, Baricitinib or Ruxolitinib, the drug that's used for, myelodysplasia. But there is a phase three trial in process with another one Breplocitinib. It's the VALOR trial, it's in progress. The phase two looked very good but we're going to see in the near future JAK inhibitors being approved for use in dermatomyositis.

Wow! I mean, the drugs that we rely on, methotrexate, azathioprine, they're not approved. They're not even well studied if you ask me. You know the drug that is approved is IVIG and she did talk about that to quite some extent. So anyway, it was a really lively meeting, really fabulous presentations.

I hope that you'll come to RheumNow live next year either online or enjoy the wizardry of our online host Doctor. Pope if you want to watch this from home. Thanks and take care of yourself.