Chikungunya Club Meeting (7.24.2026) Save

Hi, everyone. It's 07/24/2026. This is the RheumNow podcast and I'm Jack Cush with RheumNow. A number of, popular things this week, I think the big hit this week was fibromyalgia, we'll talk about that. We had a really stellar Tuesday night rheumatology webinar that I'll talk about briefly and, a few great articles during our gout campaign that we'll also cover in this podcast.

A few news items rather than journal reports, the European Union this week approved Nirandomolaz, its trade name is just CADE from BI, was approved in the EU for use in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis, IPF and Neurodomolast, as you know, was approved in October and December 2025 for those same indications by the FDA for use in The United States. Are you using these drugs? We had a big long campaign on ILD in September where we discussed this in great length. This is an easier drug to use than Nintedinib, and certainly the prevalence of ILD in our patients calls for some of these drugs. Will you be using them?

Will you be partnering with pulmonary to use them? Again, the experts say that we can use them, we don't need to necessarily partner. I think it's a major advance. Lancet Rheumatology has thrown another log on the fire that is Avacopan. Again, they wrote a really good editorial that I appoint you to that it's a full read, it's in Lancet Rheumatology, it points out what are the problems, sort of reviews the recent history on this, if you're not up to date about why avacopan may be in trouble.

Avacopan, now currently owned by Amgen, has been called out by the FDA, also by the EMA in Europe, and also by Japanese regulators, all of them basically calling for the drug to be withdrawn, and it explains why, but it also is a balanced piece and says, you know what, in post marketing experience, there's good data about its efficacy in real world studies. It's been shown to lower steroid use and the issue of hepatotoxicity, may be overstated since most of that seems to have occurred in Japanese populations. So, it's a nice read, I would point you to it, I think it's worth reading. A report on lupus looked at, the risk of MI in lupus patients by looking at it from a standpoint of MI population. So this is a large UK study of MI patients, almost 800,000 of them, and in that study, point one percent of those patients had SLE, seven fifteen.

When compared to the non SLE patients, not surprisingly, the SLE patients were younger and more female, but if you were a lupus and you had an MI, you had a significantly higher risk of all cause mortality, a sixty two percent higher risk within the first thirty days, and even going out to five years, the hazard ratio is still one point eight four, and this jives with other past reports saying that mortality rate in a lupus patient with an MI really goes up, acutely in the post MI, era right afterwards. So, the interesting thing about this data, them having a higher mortality, this is despite the patients being younger and overall having less traditional cardiovascular risk factors and comorbidities. So, again, this underscores that, patriotism that we should really be looking to get our patients off of steroids or as low as steroids as possible and better managing their inflammatory disease in a number of different ways. A few reports on scleroderma this week, U Star, as you know, is a European, large, prospective, study of systemic sclerosis patients. In this sub study, they actually looked at, the efficacy and safety, more than safety and efficacy of JAK inhibitors in scleroderma and they, in their database of like 19,000 patients, think they only had thirty eight on JAK inhibitors and they matched them up with, scleroderma patients who were treated with, either mycophenolate, methotrexate, or rituximab, one hundred and eighty in those groups.

In all these groups, they were relatively matched as far as their profiles and their demographics. One third of all these patients had diffuse cutaneous disease and two thirds had, limited disease. Limited number of adverse events, twenty three adverse events in almost a thousand patient years on JAK inhibitors, and the efficacy of JAK inhibitors was equal to the other drugs, none of them really stood out, and things that you would look to as efficacy, would be things like, their skin fibrosis scores. In fact, it improved a little bit on the JAK inhibitor with a modified Rodnan Skin score dropping almost two points. Patients on JAK inhibitors had improvement in swollen joint counts and, their lung function as measured by FVC remained stable during the period of observation.

Overall, about thirty nine percent stopped the drug, meaning sixty one percent stayed on it, and that was also on par. The one point that I saw that I thought was interesting is, very few of those patients had calcinosis going in and none of them progressed, but there were no new cases of calcinosis in this cohort, and I'm wondering if that might be one of the hidden advantages of JAK inhibitor therapy. We talked in a few years ago about, I think it was EULAR reports showing that tofacitinib looked very good in a somewhat controlled trial of systemic sclerosis. I think this needs to be, investigated more thoroughly. I like this report about malnutrition in scleroderma.

Obviously, GI disease is common in systemic sclerosis, and the measure of malnutrition in those patients is their BMI. And in a cohort of four fifty systemic sclerosis patients followed for over five years, they found that lower BMIs were not uncommon, and they were associated with several findings. One, pseudo obstruction, two, a smaller oral aperture, and three, a higher MedSCR vascular severity score. The BMI was, the mean for the total population was I think 25, 26, generally didn't change but in many of the patients in whom the BMI was lower, it did tend to have a downward trend over time that was not significant. The point of this report might be you should be using BMI as a vital sign in patients with systemic sclerosis.

We often don't pay attention to to weight and BMI, probably should, for a lot of different reasons, especially a condition like this. I don't know about you, but I've always used the patient's weight as a primary outcome variable in patients with heart failure, you know, that were on diuretics and afterload reducers and whatnot, you know, their weight was gigantically important. Why is it not so for scleroderma? Two reports on Still's disease, one looked at, the efficacy of biologics versus traditional DMARDs, biologics being IL-one, IL-six inhibitors, DMARDs being methotrexate, calcineurin inhibitors, and JAK inhibitors, one hundred and twenty six patients, one third from Germany, one third from Shanghai, and biologics had more sustained event free remissions and event free States. Those were highly significant and they were also, more likely to have their steroids discontinued when compared to the patients that were on the oral DMARDs, methotrexatecalcinerone inhibitors.

And again, this is in line with both the ACR and UR guidelines that say first and primarily your treatment approach to systemic JIA is a biologic, an IL-one and IL-six inhibitor. It's more important than steroids, it's more important than methotrexate, and really that needs to be paramount. I got a question from, one of our colleagues, in her country, they can't, they don't have, IL-eighteen inhibitors and the patient wouldn't take anakinra or couldn't, actually couldn't take anakinra and didn't want to take shots, yet it was newly diagnosed systemic JIA in adult. So what are you going to do? I think that in such patients methotrexate, starting with steroids, methotrexate, and then, probably adding a JAK inhibitor.

Now, that's not in the guidelines anywhere, but you don't have any choices if you can't use a cytokine inhibitor as per the guidelines. Another study comes, from China looking at, lung disease. I put this out there, although I kind of have a problem with it. Two zero nine patients with ALSD, adult onset Still's disease, they identify twenty three percent of those people as having lung disease by chest x-ray. Now that's about right, you know, if you look at large, as I have looked at large cohorts of patients, how many are going to have pneumonitis?

It's about twenty percent. They're not really answering the question of this issue of chronic lung disease in Still's patients, but anyway, as identified by x-ray, twenty three percent had AOSD lung disease, and of those patients, sixty nine percent of them were asymptomatic. They noted that the risk factors for lung disease in Still's were pleuritis. That's kind of a duh, isn't it? Is it not?

MAS, with a 2.6 hazard ratio and, disease relapses, again, a twofold or higher risk. They talk about imaging patterns, I don't think this made a lot of sense because they were all over the map on this, exudative pattern, interstitial pattern, suspected pulmonary hypertension, that goes along with the chronic lung issue in Still's. It's not one disorder, it's not even a narrow set of disorders. It's like a little bit of this, a little bit of that, some protein, alveolosis, and, you know, come on, and the studies of, an HLA association have not worked out. I do think this happens.

I've seen a lot of Stills patients, and I can tell you about four or five out of the over one hundred that I've seen that had chronic lung disease, and you wonder, was it related to them getting an IL-one inhibitor or an IL-six inhibitor? But again, it's very uncommon as per EULAR guidelines, you should be looking for this and have a low threshold for doing imaging for that. A meta analysis of 51 studies shows that guess what, we rheumatologists are not that good at vaccination. Influenza vaccination rates, were fifty percent in RA, forty two percent in lupus, forty three in spondylitis, fifty three in PSA. Pneumococcal even worse, thirty seven percent, thirty percent, thirty nine percent, and forty one percent in those same four disorders.

By the way, I may chastise you here, but you're no worse than your internist colleagues who are also not good at doing vaccinations in their non rheumatology patients. So, but clearly there's a greater need in your patients. This is, obviously not as much an issue in older patients and patients with comorbidities who are more likely to actually get vaccination. But this is to serve as a reminder that something, that we really need to pay attention to, and again, you're probably the people who will be driving this. A study of cancer, and can you, how you treat patients with cancer and a rheumatic disorder.

This is like a nine year study, one hundred and forty eight inflammatory arthritis patients, forty three with SPA, thirty five with PSA, and fifty with RA had a prior cancer, followed for almost sixteen months, and nineteen percent had a cancer recurrence. When they did their comparisons, the post cancer exposure to either biologic or targeted synthetic did not increase the progression of cancer or recurrence of cancer after they adjusted for age and comorbidities. And again, this goes along with the guidelines, your patient's got a cancer, especially if it's a solid cancer, treat them as if they don't have the cancer, treat the disease as you would and pay no attention to the cancer. You take care of the arthritis, let the oncologist take care of the cancer. As you know, we have a gout campaign going on the month of July, that's been really exciting.

I think we've seen some really interesting articles, really high read rates on, why do gout flares start at night? Gout in minority populations by Hai Yun Choi, The Kidney and Gout by Professor Johnson who's a nephrologist, and Joshua Baker writing about uric acid is lower. I mean, should it be lower? Yes, it should, and he tells you the evidence for that. If you didn't see this week's Tuesday night rheumatology webinar, it was just stellar.

Lisa Stamp, Ted Mickels, Angelo Gaffo, and Michael Pillinger, a master class on gout management. The title was upgrading and maximizing your use of classic gout drugs. Mainly we talked about urate lowering therapy and colchicine and the pitfalls of prescribing. It's a podcast, it's a video, it's fifty eight minutes long, check it out. Other reports this week on gout, SGLT2 inhibitors, reduces not only the occurrence of gout, but the use of gout meds, a study of twenty six thousand gout patients with diabetes, most of which were older, and most of which had a lot of polypharmacy.

If they were treated with an SGLT2 inhibitors versus DPP4I inhibitor, they had less allopurinol starts, 38% less. They were also, used less steroids, less nonsteroidals, less colchicine, and less diuretics between a fifteen and twenty two percent reduction. And I bring this up because of all the diabetes medicines that are getting play in rheumatology, mainly talking about GLP-one agonists, as the SGLT2 inhibitors are far, far more effective in gout prevention and gout, better outcomes than are the GLP-one agonists in gout, and that's a slam dunk been seen in multiple studies. A UK primary care database study, of almost twenty one years looked at the potential benefit of being on colchicine. So these are gout patients, thirty one thousand who started on colchicine as a new prescription compared to the same number who did not start on colchicine.

They were older at a BMI of thirty, followed for four and a half years, and colchicine had a twelve percent significantly lower, twelve percent lower risk of arthroplasty, I think it was in the five year period. That was overall. If you just looked at patients who had gout and hip or knee OA and went on colchicine, it was a twenty three percent lower risk of future arthroplasty. So, is there something unique about colchicine? Well, it's anti inflammatory and controlling inflammation might lessen the progression of degenerative joint disease.

Again, since this is an observational study, I don't think you can get too much into how did that happen or what the explanation that might be. Two reports this week on allopurinol hypersensitivity, the actual risk of severe allergic reactions, TENS, Stevens Johnson syndrome, severe cutaneous adverse reactions, scars is what they call is zero point four to zero or to two percent. It may be higher, maybe up to ten percent in people with chronic kidney disease. The report that we put up was the testing for B5801 dramatically increases the risk of this, and it's over a 100 fold increased risk, odds ratio of 117 in this one particular report. Another report, from Hopkins looked at sixteen patients who had allopurinol induced severe cutaneous adverse reactions, and showed that it was not just B5801 that in their study gave a 28 fold higher risk of these reactions, but also HLA A3402, which gave almost a 21 fold higher risk.

So, the B5801 explains about two thirds of these bad reactions that occur in The United States, and there are not many of them, to be honest, but if you had testing for the second, class one allele, you now cover about eighty percent of cases. So, we might add that to your list. Again, patients, who are from, you know, the Han Chinese, Southeast Asians, should be tested for B5801, and then African Americans are higher risk in The United States, but not everybody does it and the question is how often will you get burned and in a career, in a lifetime, maybe only once, but when it happens, there's a risk of death. It's kind of ugly. If you've been following our website, we have some quotes and factoids about gout.

I'm gonna put two up here for you here. Being on low dose aspirin, either eighty one or three hundred and twenty five milligrams increases the risk of gout by eighty one percent. Eighty one percent, almost a doubling of risk. However, if you're on allopurinol or urate lowering therapy, you don't have to worry about that. There is no higher risk.

That's important. Again, ULT is protected and you could be on background eighty one milligrams a day, assuming someone, needs to be on that. And then the other fact that we put up, I think, a few days ago was, forty percent of acute acute gout attacks have a normal uric acid, you know that, because we see that. The other forty percent number is that forty percent of acute gout patients and attacks are not tested for uric acid level. Wow.

And I'm going to throw in the other forty percent number that you all know, which is only forty percent of people who go on urate lowering therapy achieve their target of six or less in uric acid, and that's especially so in primary care, but even in rheumatology forty percent, only forty percent. So, that forty percent number is something that should bother all of us who manage gout. A great report, written up by Chiyo Yokusei from, the Mass General Brigham, on evidence based dietary recommendations. It's a nice read. She talks about, you know, yes, we should all be on low purine diets, but the hazard of that is you'll be on an unhealthy diet and you won't no purines means no protein, which means you're gonna get high fructose things and things that are bad for gout.

We do know that you need to be on high pro and gout patients have diabetes and diabetics need to be on high protein diets. But and again, you know, Atkins diets, which is a high protein diet, has been associated with some severe worsening of gout. So there's a little bit of a conundrum there. The diets that are generally recommended are the DASH diet, which was originally developed or best tested for hypertension management. As you know, anti inflammatory and Mediterranean diets work here, and the other question she gets into is shelf shellfish and seafood.

And the point there is that, I used to say, you know, that seafood recommendation doesn't really count cause I it doesn't I have never seen it. And I got I got booed off stage in New England when I brought that up because they see it all the time. Not a lot of shellfish in Dallas, Texas where I live. So, yes, seafood and especially shellfish is a big problem for a lot of patients, but if the patient is to be well controlled on urate lowering therapy, you could reintroduce the use of shellfish without hazard and without risk. And, of course, she makes the important point of dietary counseling for these patients.

Look for a card on my website called Goutstop that you can print out and give to patients, it's got all this information about diet on there that you might want to impart upon them. A great article, this week also by another person from, MGB, Sarah Tedeschi, talking about, new thinking on calcium pyrophosphate deposition disease, which affects eight to ten million Americans. She begins by going over the fact that the classification and nomenclature has changed. We don't really talk about pseudogout anymore, that's the old term. Now, you know, if you look at this great figure she has in the article, it's a big Venn diagram with overlapping circles, the biggest circle being OA patients with CPPD, then there are two, medium sized circles of either acute calcium pyrophosphate arthritis or chronic calcium pyrophosphate arthritis, and then a smaller circle for the Crown Den syndrome, where the calcification is C1, C2.

Again, chondrocalcinosis is still in there for X-ray only evidence. She talks about imaging, that that well, that's CPPD is really a Crystal ID disorder, but that's not always possible and when not possible, imaging might supplant crystal identification with ultrasonography and CT being, having greater sensitivity, than the conventional radiograph and showing chondrocalcinosis. As you know, management is acute steroids or colchicine chronic. There are no FDA approved therapies, but there are trials, there are three trials that are in progress right now, including one with an IL-six inhibitor, but she says there's evidence for, although not well controlled for hydroxychloroquine, methotrexate, IL-one inhibitors, and or IL-six inhibitors in patients I assume with chronic, CPP arthritis. Lastly, fibromyalgia, oh my goodness, I put this up, It's a review article in New England Journal from last week from David Williams and Daniel Claw, where they review the diagnosis and management of fibromyalgia and, my apologies to quoting them and rewriting their article in a more dense, easier to read fashion, but even mine is a little bit long.

Again, fibromyalgia affects up to six percent of The US population. It is a widespread pain disorder, that wherein fatigue and sleep problems, along with memory problems are a gigantic problem. It is a hypersensitivity disorder. It's essentially mediated hyper responsiveness to external sensory stimuli that leads to pain, brain fog, fatigue, mood changes, etcetera. The diagnosis is clinical, that labs and imaging tests, not really, there's no immunologic tests, sorry, and the thoughts that this is a small fiber autonomic neuropathy or it's an autoimmune disease, autoimmune disease is not well substantiated.

Again, we do know it's centrally mediated, we do know there's a hyper responsiveness. They are, rightly so big on treatment of sleep, that's where all the great gains in therapy are coming from and they're strongly in favor of stretching therapies, Tai Chi, Zhi Gang, yoga, and then also cognitive behavioral therapy. So, again, when it comes to treatment, you know, the tenants are education, self care, focusing on sleep, focusing on movement and stretching, and behavioral means, and they're very big about CBT, cognitive behavioral therapy to help both sleep and or pain, but probably better more so for sleep. They do say that the drugs that are out there and approved that you use all the time, analgesics, muscle relaxants, tricyclics, gabapentinoids, and SNRIs, modest effects, if anything, and then when they do work, they work because of their control on sleep. And there again underscores the importance of sleep.

A few new things that I didn't know about, well, I know about the new sublingual cyclobenzaprine that's FDA approved. I was not aware of combination, a study of combination therapy outperforming monotherapy, gabapentinoids at bedtime plus an SNRI during the daytime had sixty eight percent improvement in global pain compared to forty two percent for duloxetine or thirty nine percent for pregabalin versus eighteen percent for placebo. That's significant, and those are six week results. Obviously, NSAIDs and opioids really don't do anything here and should be avoided. They express some enthusiasm, and let me underscore the word some, for low dose naltrexone as an emerging, unrecognized option, but we need studies in that, and that there is good data about transcranial, stimulation TENS, maybe gabapentinoids, and THC.

It's unclear though where those stand at this point. Anyway, watch for our content on, gout this month. It's going to wrap up next week. Next week, our TNR, Tuesday night rheumatology, is going to be on advanced therapies. Herb Barath, Naomi Schlesinger, oh my goodness, a few others I now I'm blanking on, I should have looked them up, but it's a stellar lineup, and we're going to talk about, the uricase drugs, use of cytokine inhibitors, drugs that are coming down, the development pipeline.

I think it's going to be another exciting session that you'll want to tune into. That's it for this week on the podcast, we'll talk next week, take care.