DERM on RheumNow (November 2025) Save

Welcome to the Derm on RheumNow podcast for November 2025. Hi, I'm Jack Cush, executive editor of roomnow.com. You know, RheumNow is a website for rheumatologists by rheumatologists, but we're more than a website. We're an email, we're a podcast. We intend to keep everyone abreast of the news, the journal reports, the regulatory announcements that affect, not just rheumatologists, but all those who actually take care of patients with inflammation, chronic inflammation, auto inflammatory and autoimmune disorders.

This Derm on RheumNow podcast is a collection of the many citations we have that are dermatology focused, and we will focus on, in this podcast, on psoriasis, psoriatic arthritis, lupus, CLE, vasculitis in its many forms, hydradenitis, dermatomyositis, other connective tissue diseases that affect the skin, as well as the drugs that we both use, including biologics and JAKs, their safety, their efficacy, and more. Again, we'll do this once a month. I hope that you enjoy this, hope you tell your colleagues about it. This week we're going to talk about, hydradenitis suppurativa, we're going to talk about dermatomyositis lupus, what looks like lupus, biologic safety, and more. So let's start out by talking about dermatomyositis, specifically MDA-five positive dermatomyositis.

As you know, those MDA-five positive patients can have really bad skin disease, but the thing that's just deadly in these people is the rapidly progressive ILD. This was a retrospective study of thirty nine patients with MDA-five positive dermatomyositis with ILD, and this single center study showed you their experience in using the JAK inhibitor, baricitinib. They had thirty nine patients, thirty one had major improvement that's about eighty percent in Gottron's lesions, the heliotrope rash, dyspnea, the high res CT scores, ferritin levels, LDH, steroid doses lowered, and six month survival was lower in those who did well on baricitinib. So again, the question is: what is the best treatment for these MDA-five positive patients? There are no head to head trials or well designed trials, and most of it is this kind of anecdotalism that's out there.

I do however, I have reported on a number of studies showing the efficacy of JAK inhibitors in patients with not just dermatomyositis, but especially MDA-five disease. Another report this week was sort of another single center study talking about juvenile dermatomyositis, often difficult to treat, and in this one center from JAMA Dermatology, they reported on their experience with 28 patients with JDM, who over the years, they went to a first line regimen that included pulse steroids for three or four days, followed by mycophenolate. And again, they reported really, really good results. I do treat kids with rheumatic problems. I have treated dermatomyositis in the past.

I've usually used methotrexate and the standard drugs that we often use in polymyositis dermatomyositis. My favorite drug in polymyositis dermatomyositis is leflunomide. It works great! But here's one that looks at mycophenolate with pulse steroids, and then they also showed that patients got on less daily lower doses of steroids over time. I like this report about lupus that's not really lupus.

Specifically, these are 19 patients from a cohort of patients with either myelodysplastic syndrome or chronic myelomonocytic leukemia. They reported on those people that showed up or were misdiagnosed with lupus. So they found in that large cohort, over a thousand patients, nineteen who were diagnosed with lupus and five who were diagnosed with chronic lupus erythematosus, or CLE. What was different about these patients, and by the way, the skin biopsies were not that of lupus. They had all kinds of inflammatory changes, but not specific to lupus, and when they did further analyses, these were thought to be clonal inflammatory process in keeping with their malignancy.

But these patients were different, and what was different about them was that they were older. The average age was 65. There were more male than female: fifteen males, nine females. They had very little renal disease ten percent. A minority with articular disease thirty six percent, and they were infrequently double stranded DNA positive.

So, again, these people could present what looks like lupus or maybe misdiagnosed with lupus, or CLE, chronic cutaneous lupus, but in fact they had an underlying hematologic malignancy that was in place. So, again, they did it this way. They found the malignancy patients and identified the subset of lupus like disease. You may be doing it the other way. You have someone with lupus that's not quite lupus or oddly lupus, maybe you should be thinking about myelodysplasia or leukemia.

A MarcusScan claims data analysis looked at the safety of patients treated with adalimumab, and specifically in the study they're comparing those that were treated with four, hydradenitis suppurativa sixteen fifty patients, or psoriasis almost eight thousand seven hundred patients. And again, this was between 2017 and 2020. The outcome was looking for serious infectious events, SIEs, or hospitalization from a serious infection. And they found that that was much higher with Hidradenitis suppurativa, about fifty percent higher when compared to lupus. And this was especially so for the serious infections of sepsis and genitourinary hospitalisable infections.

Again, fifty percent higher in HS. I always teach that RA is a standard in a pre biologic area, the rate of serious infectious events was nine per one hundred patient years. It turns out that worse than RA and then in the biologics, when they're applied to RA patients, it's between two and six per one hundred patient years. It's not any higher than it was in the pre biologic era, suggesting better control of inflammation gets you a lower risk of of infection. But if you look at how biologics TNF inhibitors especially are used across the board, right, GI disorders, Crohn's and ulcerative colitis, have rates that are actually higher than RA.

But psoriasis has rates that are lower. But turns out that it looks like hidradenitis has a slightly higher risk of serious infections, and I don't think that's a surprise to you, because you see more of these patients than do the rheumatologists. Another safety study looked at the safety of IL-seventeen A inhibitors, and this is a French study of thirty four thousand patients on an IL-seventeen agent or a TNF inhibitor, and they looked at MACE as an outcome: major adverse cardiac events. Three eighty one overall in this cohort of thirty four thousand patients, but overall the use of IL-seventeen inhibitors did not impose a greater risk of cardiac events compared to TNF inhibitors. So the odds ratio was one point two five, but the confidence intervals overlapped one: zero point seven five all the way up to two point zero eight, suggesting that you're safe if you're aware I know that often this comes up, know, psoriasis patients especially have a lot of comorbidity, lot of cardiovascular risk, a lot of obesity, all kinds of things wrong, and you worry about, cardiac events in here, and if the drugs I'm using are contributing to that, this data from a very large French cohort would say, no, that's not the case.

Another interesting study was from JAMA Dermatology about the genetic risks of what they called SCARS severe cutaneous adverse reactions to allopurinol. And they did a match cohort study with a large number of patients, and what was interesting about this study, it was done in The United States. So we know that HLA B5801 is associated with a higher risk of severe allopurinol skin reactions, TENS, Stevens Johnson Syndrome, and but that's data largely drawn from non North American populations, especially in Asians, right? So if you're putting an Asian on an allopurinol, wouldn't be unwise to do some genetic testing for HLA B5801. But this was a US population.

We do know that B5801 is higher in Asians, it's higher in African Americans. And in this study they found, yes, B5801 was associated in North America, which was not very many Asians, mostly African Americans and Caucasians, was associated with a fifty eight sorry, a 28 higher risk of severe allopurinol skin reactions. Oh wait, there's more! HLA A-three 402 also associated with an increased risk of these same reactions, and there it was a twenty fold increased risk. However, these alleles themselves did not account for 100% of these reactions.

More than a third did not have these real alleles, so it's still a complex, idiopathic genesis that we don't quite understand. But I think it wouldn't be unwise still to test for HLA class one alleles B5801 or A3402. I would do it in African Americans and in Asians. I don't know if I would do it in every, you know, Caucasian that goes on allopurinol. I don't think that's going be a very high yield.

Lastly, information about lupus. You know, in September on RheumNow we did a whole month dedicated to interstitial lung disease, and you know, it happens very frequently with autoimmune disease, especially scleroderma, especially dermatomyositis, especially rheumatoid arthritis. How often does it happen in lupus? It's not very common. A Western Australia study of eighteen fifty four lupus patients median age 40 years found ILD in only three point eight percent of lupus patients, although that was still twenty six times more common than non lupus patients.

Risk factors for ILD in was being older, smoking, and having a background of serositis. Yes, like all other ILD patients, whether scleroderma, RA, dermatomyositis, or lupus, it's always associated with a significantly increased mortality risk. In this lupus cohort, a 50 fold 52 fold increased risk of mortality. That's big. So yeah, if you find your lupus patients that you're managing their skin disease and their autoimmune disease and they're having symptoms, work them up, send them to pulmonary, send them in the room, that's something we've to jump on.

Two more reports: Michelle Petrie, the world's leader in lupus from the Hopkins lupus cohort, has been advocating for strong monitoring of vitamin D levels in lupus. Vitamin D is not just important in bone, it's got a lot of immune effects, and she just published a retrospective study of their cohort showing that vitamin D levels below 20 compared to those that were in the normal 30 to 39 range had a doubling of mortality risk and a tripling of their major cardiovascular event risk when they were followed up for six years. Following chronic lupus, check their vitamin D. Vitamin D is important here, and if you follow me on RheumNow, you'd know I'm kind of against all this brouhaha about vitamin D, because it's associated with everything, is it not? And show me the studies that show that giving vitamin D fixes something?

Those studies are scant. Right? We do know it's beneficial in bone, we do know it's beneficial in immune function. I take vitamin D every day, I have my patients take it as well, and I do measure it. Lastly, at ACR twenty twenty five, held in October in Chicago, a lot on content you can go to our website and see it but the ACR did publish non renal lupus guidelines looking at different organ involvements other than the kidney, and they did address mucocutaneous disease.

Had three recommendations that were strongly evidence based: one, that everybody should be on hydroxychloroquine at the right dose, weight based dosing. Number two, if you go on steroids, the goal should be to be on five milligrams or less of prednisone within six months. And the third kind of like duh goal is that if they don't respond to your immunosuppressive, change immunosuppressives. But then they have a lot of other recommendations that are expert opinion. Let me run down these for you in your discipline.

So, for acute LE, SCLE, and chronic cutaneous LE, mild disease gets they recommend adding quinacrine, and then, if you're not doing well, switching from hydroxychloroquine to chloroquine. So, antimalarial therapy: hydroxychloroquine, then quiniquine, and then maybe chloroquine if you must. If they have moderate to severe disease, they're probably on an antimalarial, plus you can add in any one of these: mycophenolate, ifrolumab works great in lupus skin disease, by the way and belimumab. If they have refractory lupus skin disease, they have lenalidomide I guess it's the better, safer version of thalidomide and our lupus experts in dermatology in our area end up using a fair amount of these drugs. They have bullous LE and other acute LE manifestations, mild disease gets dapsone severe disease gets azathioprine, methotrexate, mycophenolate or an anti CD20 monoclonal, which is rituximab not approved for lupus, but a new one just approved for lupus is obedentuzumab, a new anti CD20, and that might be very effective in bullous LE.

Chilblains LE, calcium channel blockers, PDE5 inhibitors and, pitoxiflin, and then leukocyte classic vasculitis, they recommend colchicine and dapsone. All of that is expert opinion, but that's the best we have, is it not? I'll close with a quote from my favorite podcaster and guru and marketing and entrepreneur, Seth Godin. His blog is called seth'sblog.com. I would subscribe to it.

He has a great podcast called Akimbo. He's got tons of episodes for you to listen to. This quote says, it takes the title is 900,000 versus nine. It takes about nine hundred thousand minutes to become a board certified dermatologist. At that point, you'd be very skilled and very well informed.

However, it takes less than nine minutes to make your patient feel seen, understood and reassured. If you skip the nine minutes you wasted the nine hundred thousand. Sethsblog.com Tune in next month for Derm on Rheum. Take care!