DERM on RheumNow PODCAST (May 2026) Save

Welcome to the Derm on RheumNow podcast for May 2026. Hi, I'm Dr. Jack Cush, executive editor of RheumNow.com. RheumNow is a website for rheumatologists by rheumatologists, but you know, we discuss so many dermatologic issues. We share a lot of the same patients, a lot of the same drugs, the same regulatory and safety concerns, and that is the crux of what we cover in this podcast for you and your dermatology colleagues. This month we're going to discuss a lot of information on psoriatic disease lab testing, some new drugs, and a head-to-head trial in rheumatology — and you guys are used to head-to-head trials. We don't usually get enough of them.

So let's begin with a study I like about telangiectasia counts in scleroderma. This is a retrospective international study where they collected data on a large cohort of patients with systemic sclerosis and they let the patients and the doctors both do telangiectasia counts looking at the face, forearms and hands, and then they correlated MD and patient results. They were kind of moderate but it did show that this is a worthwhile measure. I don't know about you but most rheumatologists do a modified Rodnan skin score in patients with either limited or diffuse systemic sclerosis — scoring 0 to 3 skin tightness in 18 areas starting in the fingers ending up in the toes, and then we follow that serially over time. Why not do telangiectasia counts? Easy to spot, easy to count. It's the face, hands and arms. The categories are zero, 1 to 6, 7 to 15, greater than 15 — not good. But the point is that high telangiectasia counts are correlated with a higher risk of pulmonary artery hypertension and a higher risk of digital ulceration. So it's got some predictive value. It's cheap. Why not do it?

I found a nice report in JAMA Dermatology about a parvovirus B19 infection. It's worth taking a look at because it's got some really neat pictures — not that you guys need pictures as we do in rheumatology. 40-year-old male with two days of an asymptomatic rash, fever of 39. Arthralgias, rash initially on the cheeks but later kind of widespread in the inguinal area, flanks, axilla. The white count was 2, CRP was 1.24 milligrams per deciliter. Diagnosis was made by PCR for parvovirus B19. And it just is a nice example of a disorder that you may see more than we do, but I like the pictures. I like the presentation. It's got the joints, it's got the skin, it's the rheum-derm package. Is it not?

So, when you're seeing your patients, how often are you doing the tests that we do? Do you do sed rates and CRPs? Do you do batteries or panels? I wouldn't recommend batteries and panels — you're fishing for p-values, you're fishing for insight and it usually gives you results you've got to deal with. But I have a few studies here that say maybe it's worth doing some labs with some intention.

For instance, should you be doing B27 in patients with psoriatic disease? This particular study — how big was it? It was a large 333 patients in CASPAR, that's a psoriatic arthritis registry, and they looked at the utility of B27 testing in a psoriatic arthritis registry. I don't know that it would do as well in a plain psoriasis without arthritis cohort. But in this study 12% of patients were B27 positive. And you know when we think about the subsets of PsA, we often talk about 15% or so being B27 positive with maybe a higher risk of axial disease. B27 in the population is associated with not just axial spondyloarthritis and ankylosing spondylitis but also with uveitis, sometimes with valve disease, sometimes with enthesitis. So in this study the B27 positive people had an earlier onset of disease, they had more axial involvement — double the amount of axial involvement — more enthesitis.

The other interesting thing here was that being B27 positive in this study was associated with higher FIB-4 scores, which as you know is a marker for hepatic fibrosis. Our studies have shown it's worth doing the FIB-4, and what you know is a calculator — you can put this on your phone. I think the numbers are the patient's age, the AST, the ALT, and the platelet count, and it'll tell you the risk of hepatic fibrosis. You know, this is kind of an issue for you guys and psoriasis, and it's an easy calculation. You could have your staff do it and enter it into the chart, maybe follow it serially.

Turns out that B27 had no association in the study between the sexes, the presence of dactylitis, uveitis — which was surprising — or drug responses.

Another study of PsA looked at the utility of rheumatoid factor. So again, this is PsA — if you're worried about arthritis, do a rheumatoid factor. In this study, rheumatoid factor was found in 16% of PsA patients. By the way, rheumatoid factor is kind of non-specific. CCP or ACPA
antibodies very specific for lupus and that's about the right same number when you do ACA testing in PsA. They're about 15–16% positive. Anyway, it turns out that about 5% of these were present at baseline when they're first seen. If they were rheumatoid factor positive they were less likely to achieve MDA — minimal disease activity — with about a 47% reduction even with aggressive therapy, and they're also more likely to discontinue their biologic DMARD, two to three times more likely, suggesting that those people are going to be more difficult. Now we do know that in rheumatoid factor and anti-CCP positive seropositives, psoriatics are going to have a higher risk of polyarticular RA-like disease with the potential for erosions. Is it RA? Is it PsA? Is it overlap? Who cares? Treat them aggressively. We're doing that already.

Another lab test which I kind of always discarded as being unimportant — and that's RNP antibodies. When you order RNP antibodies, you get Sm and RNP. Sm is the one that's specific. Sm is the one in lupus that has an association with lupus nephritis and risk of poor outcomes. RNP associated with MCTD and overlap. So anyway, a registry of almost 600 lupus patients found that 30% were RNP positive. And guess what? RNP positive versus RNP negative — RNP is associated with more disease activity, higher SLEDAI scores. When you were RNP positive you were also more likely to use higher doses of steroids, and they had more renal, more skin, more serologic activity and were less likely to achieve LLDAS — that's the low disease activity state for lupus — or lupus remission. And if you were RNP positive, you were 18 times more likely to also be Sm positive. So pay attention to RNP. It really does have value.

The last two reports are about drugs. MedPage Today had a nice report — I think it was about toll-like receptor inhibitors in cutaneous lupus. And you know, the only toll-like receptor drug that we have right now is hydroxychloroquine; presumably that's one of the mechanisms by which hydroxychloroquine works. There's a drug in development that's in phase three — enpatoran — it's a small molecule oral TLR 7 and 8 inhibitor, and they report on the results of the WILLOW trial, a phase 2 study where enpatoran was found to be superior to placebo in relieving skin manifestations. This was presented — lead author was Eric Morand from Australia — a double-blind controlled study. They reported on the first part of the study where adults with cutaneous lupus with little or no systemic disease, I think it was 100 patients, were analyzed. They used different doses of enpatoran and the bottom line was the CLASI score was better in a dose-dependent manner. So this is a new therapy — just like, you know, they're investigating TYK2 inhibitors; deucravacitinib, which is approved for skin psoriasis and psoriatic arthritis, has some positive results in phase three and they're going forward to pursue that for lupus. You may be seeing this other oral small molecule inhibitor, the TLR 7/8 inhibitor enpatoran, and there are others behind it that are in drug development.

There was a good report from two colleagues of mine in rheumatology from the Baltimore area, Shivani Garg and Don Thomas, both very interested in lupus, talking about what's the dose of hydroxychloroquine, and their title was "5 mg per kilogram is just the starting point." We know the American Academy of Ophthalmology says that dosing of hydroxychloroquine should be less than 5 mg per kilogram based on actual body weight. But they say it's the starting point and that really your dosing needs to be based on drug levels. Better to get morning levels after they take their dose at night. The absorption of hydroxychloroquine varies tremendously with only some relatedness to renal clearance. So usually these folks are doing doses of 400 to 600 a day and following the blood levels, aiming at a blood level of 750 to 1150 nanograms per mL. When people are not doing well, it's usually because they're less than 750 — that's either they're not taking the drug or they're not absorbing the drug. Levels above 1150 are not associated with more toxicity; as much as there's no added efficacy, why go there?

Okay, you're going to have to — and that's where most rheumatologists are going now — monitoring hydroxychloroquine levels. Maybe you want to do that as well.

I think we talked before about the preliminary results of the BOLD study. This is exciting in rheumatology because it's one of the few head-to-head studies of bimekizumab versus risankizumab in active PsA patients. 553 patients, a double-blind randomized placebo- and active-controlled trial. They reported the 16-week outcomes. They're going to present this data in about a week at the EULAR meetings in London that I'm going to be at. At week 16, this was again a blinded trial — the ACR50, that's a high benchmark for joint outcomes — 49% for
bimekizumab, the dual IL-17 inhibitor, versus 38% for risankizumab, which is significant. The secondary endpoints were not significant but also favored the IL-17 drug, including the minimal disease activity 49% versus 39%, the PASI 100 was 53% versus 46%. And then a simultaneous ACR50 plus a PASI 100 was 33% versus 24%. And that was P equals 0.08. Not quite significant, but these are significant results and do inform you know which drug we may want to be using. IL-17 dual inhibitor versus IL-23. We know that these are two very powerful drugs in skin psoriasis. We're encouraged by these results in psoriatic arthritis.

That's it for this Derm on RheumNow podcast. Tell your colleagues. Next week we're going to be in London at the EULAR meeting with a ton of reports. Sign up at RheumNow.com. Watch us on Twitter. Get our daily news. Sign up for the weekly quiz where you can learn that way, or wait for the end of June when I do the June Derm on RheumNow podcast. Take care. Be good.