DERM on RheumNow PODCAST (March 2026) Save

Welcome to the Derm on Rheum podcast for March 2026. I'm Dr. Jack Cush, executive editor of RheumNow.com. This podcast is a monthly podcast dedicated to dermatologists and skin-focused health care professionals where we discuss the intersection between rheumatology and dermatology. To do this, we curate the news and research and regulatory advances on a number of disorders relevant to you, including psoriasis, psoriatic arthritis, lupus, vasculitis, hidradenitis, other connective tissue disease. We also discover and discuss the many drug similarities we have — biologics, JAK inhibitors, and other therapeutics that are really central to dermatology. The focus is practical use, real world efficacy, knowing the side effects, knowing the advances. We hope that you can follow this news on RheumNow.com. You can go there, sign up for either the daily email that we send to everyone, which has sort of five news items every day, or a weekly email, or even a topic email.

This week on the podcast: many FDA regulatory decisions on psoriatic disease and lupus, a reminder about eosinophilic fasciitis, and also should you worry about fibromyalgia.

At the top of the list is the FDA approval of an oral IL-23 inhibitor, icotrokinra, for plaque psoriasis. It was approved just recently this month for use in moderate to severe plaque psoriasis in adults but also in children age 12 and over who are at least 40 kg in weight. To be eligible you need to be a candidate for systemic therapy or phototherapy. There's a new package insert that you can consult and basically it tells you the drug looks pretty safe. It starts working at four weeks. It seems to have maximal responses by 16 weeks as far as PASI 90 responses. The starting dose and usual daily dose is 200 milligrams orally given every day and given 30 minutes before food. Looks like you need an empty stomach to get full absorption.

Approval is based on four ICONIC trials — these phase 3 trials showed efficacy and safety in over 2,500 adults and adolescents with either active plaque psoriasis, but also there were sub-studies on scalp psoriasis and genital psoriasis, and there were also two studies against other drugs that you use, including deucravacitinib and ustekinumab. The trials basically showed that nearly 70% of people have almost complete clearing of their skin and at least 55% achieve a PASI 90 by week 16. Major advance for you. We're waiting to see what it's going to do in psoriatic arthritis, where there are trials going on right now.

FDA also active in pediatric disease by approving secukinumab for kids over the age of 12 with moderate to severe hidradenitis suppurativa. As you know, secukinumab is already approved for adults with hidradenitis. The FDA has also accepted the supplemental BLA — biologics license application — for tildrakizumab, the IL-23 inhibitor, for use in psoriatic arthritis. Of course, it's approved already for use in psoriasis as an IL-23 inhibitor. A supplemental BLA biologic license application means they want to amend their indication list and add this to the list based on the data, and they're developing that data.

Also approved this month was deucravacitinib, the TYK2 inhibitor, for use in psoriatic arthritis. Currently available in psoriasis, now it's available for psoriatic arthritis. This happened on March the 6th. The indication is adults with active PsA based on the results of two phase 3 POETYK PSA-1 and PSA-2 trials showing efficacy and safety. I think this is a nice addition. TYK2 inhibitors will sort of round out the oral options for patients with psoriatic arthritis.

The other big news, at least for us rheumatologists, was UCB announcing in a press release the topline results of their B-BOLD study. UCB makes bimekizumab, the dual IL-17 inhibitor of 17A and F. This was a head-to-head trial of bimekizumab against the IL-23 inhibitor risankizumab — 553 patients — showing with a primary endpoint of an ACR50, which is a pretty good response, sort of like your PASI 90, at week 16 they had favorable results of the bimekizumab IL-17 against IL-23. The patients had to be either biologic naive at entry or they could have been exposed to one, but a max of one TNF inhibitor. We don't have the details and data, but we don't have head-to-head trials like you do in dermatology. You guys I think are smarter and more aggressive in seeing who's the top dog, what's your go-to drug when your first option may not work as well.

In rheumatology we have very few — can count them on one hand — the number of head-to-head trials, and certainly very few in psoriatic disease. And this sort of is a retrospective network analysis using the Trinetx — I don't know if you're familiar with the Trinetx network — this is a linkage of many EMRs and they do studies that involve hundreds of thousands of patients, and they do propensity matching and maybe they give us data that
you can't get otherwise. But this is sort of simulated data, not real data. It's not a real clinical trial. It's not even a real registry. They're just finding out what's out there and then trying to correct for it with propensity matching.

Well, anyway, in this study of 123,000 adult psoriatic arthritis patients who are matched against non-PsA controls, also 123,000, they showed what you already know — that psoriatic disease is associated with a significantly higher cardiovascular morbidity and mortality. MACE events are 74% higher. Mortality is a doubling of events. Heart failure almost a doubling of events. MI 71% higher. CVA 49% higher. And this was all in psoriatic arthritis patients, not psoriasis, where maybe the inflammation burden might be even higher.

The other thing that was important about this analysis was that when they compared patients treated with biologic DMARDs versus conventional oral DMARDs like methotrexate, or I guess apremilast, that biologics significantly reduced both MACE events and mortality events somewhere between 5 and 10%. And that was a significant reduction when you consider it's hundreds of thousands of patients. But is it real? Again, sometimes when you can't do the real trial, you do the best you can with either meta-analyses, or registries, or even this sort of, you know, trietics EHR kind of study. But in fact, these are not grade A evidence. These are like grade C evidence. And at best these are data that are supportive of a hypothesis upon which you should design a larger trial.

I know you don't talk a lot about or don't even want to think about fibromyalgia. We see a lot of it in rheumatology. I put up a report this week that said amongst the psoriatic arthritis patients, fibromyalgia is seen according to systematic reviews 18% of the time. There's a range of, you know, 10 to 60%. But the sort of the median seems to be 18%. And you know what? You're going to see that in psoriasis as well. Why is this important? Well, if the psoriatic patient also has fibromyalgia, they have higher disease activity scores related to the fibromyalgia more so than inflammation. If you have fibromyalgia, there's worse disease outcomes. There's poorer response to systemic therapies. They're unable to achieve your superlative disease activity states, and it's just a bad contributor. Fibromyalgia you would identify as someone who has a lot of complaints, widespread pain and problems with sleep. You can refer them to a rheumatologist for further documentation of the diagnosis and how to treat that, because it's going to screw up your clinical results in practice and what you're trying to do to control their psoriasis.

The JAMA this week — or this month — put out a patient education page on eosinophilic fasciitis. I think it's a nice resource that you can have and hand out to your patients. This is rare, you know. I haven't seen an EF patient in about 5 years, but it's in the differential diagnosis of skin thickening as you know. It starts out with both swelling and redness in the limbs, arms and legs, that later that swelling or edema becomes thickening of skin and, you know, leathery skin, but it's got that peau d'orange, that stippled orange-peel-like appearance. And the other distinguishing feature of this is they do not have Raynaud's, and it really doesn't involve the fingers or toes like scleroderma and scleroderma variants will. Obviously the diagnosis is often made by you and we send them to you for a full thickness skin biopsy.

A number of reports on lupus reveal. As last month or last podcast we talked about the SC TULIP trial, which was subcutaneous anifrolumab being used in lupus, and in skin lupus it seemed to work very well. This is another study, a real world study called the REVEAL study, of 236 lupus patients who initiated anifrolumab. Half the patients had musculoskeletal complaints but two-thirds had mucocutaneous disease. Going in they had a SLEDAI score of seven — that's sort of moderate disease activity. By 6 months 26% achieved remission. Two-thirds had low disease activity state called an LLDAS. And this seems to have a rapid onset of action. Why is this important? Because anifrolumab seems to be great in cutaneous lupus, may also be great in cutaneous dermatomyositis, and it's a type I interferon inhibitor given as an infusion.

As you remember last month we told you about the FDA issuing a complete response letter, CRL, to AstraZeneca, the manufacturer of anifrolumab. And all that means is it says halt, and they were slowing down the BLA application for approval of anifrolumab, also called Saphnelo, for use as a subcutaneous administration in lupus. Interesting that the FDA has done that, while the EMA in Europe has already approved it. But further news on this complete response letter, which doesn't
mean complete response, it means hold on, we're going to reanalyze your data. It actually was issued to the company back in October of 25, wasn't announced until February, and the FDA was citing critical quality data, especially data on safety from that SC TULIP trial. Nonetheless, they do expect a decision on this BLA, an extended indication, sometime in the first half of 2026.

Another last key study that's relevant to you is a New England Journal published on obinutuzumab in active non-renal lupus in the New England Journal this past month. This was a study of 303 lupus patients who did not have nephritis, and many of them had active skin and musculoskeletal disease. The endpoint in this trial was an SRI-4 response, that includes the SLE index and other measures. Obinutuzumab, the intravenous anti-CD20 B-cell depleter — I'm sorry, not IL-20, the intravenous anti-CD20 B-cell depleter — showed an efficacy of 77%, placebo response rate of 54%, a 23% delta or treatment effect difference that was highly significant. Both the primary and secondary endpoints all favored obinutuzumab. That included reduction of steroid dose, sustained SRI-4 responses, SRI-6 responses, and also flare rates. So again, this is another option in the management of non-renal lupus, which could include problematic skin disease relevant to what we all do.

That's it for this week on the Derm on Rheum podcast. Please give us a good review. Please sign up at RheumNow.com to receive our news either weekly or daily. Or you can sign up for the psoriatic news that would come to you once a week, and/or the lupus news that would also come to you once a week. Go to RheumNow.com and sign up. Take care. We'll talk next.