DERM on RheumNow PODCAST (October 2026) Save

Every day, every month, RheumNow publishes news and information on JAK inhibitors, IL-17s, IL-23s, lupus, myositis, scleroderma all the stuff that could change your practice of dermatology. I'm Jack Cush, executive editor of roomnow.com and this is a podcast for you: Derm on RheumNow. This week the podcast will scratch the surface and find new drugs for dermatographism, hidradenitis, lupus, discoid lupus, and psoriatic arthritis. Guess what? Probiotics lose out to placebo and loose lips sink ships?

No. Big hips, meaning obesity, sinks psoriatic biologic success. So, let's begin with some news from the FDA. I began, the month of October telling everyone that the FDA was reviewing Sun Pharma's BLA application to have their IL-twenty three inhibitor that you use, Tildrekizumab, and have it now approved for psoriatic arthritis. A decision was due by the end of the month, and guess what?

Just yesterday the FDA did approve, ILUMYA, Tildrekizumab, an IL-twenty three inhibitor, for use in active psoriatic arthritis. This extends its indication beyond moderate to severe plaque psoriasis, and the indication is going to be based on two very large phase three trials INSPIRE one and two with over 800 patients in a fifty two week set of studies. That's good news for those of us who like the IL-23s, it's getting to be a busy therapeutic area. The FDA has also been active, they approved Rembrutinib, a BTK inhibitor called Reps ido. This is made by Novartis.

It's the first drug approved for adults with dermatographism not controlled by H1 antihistamines. Unbeknownst to me that Reimbrutinib was already approved for chronic spontaneous urticaria, so now it's going to be indicated for dermatographism. Novartis made note this week that the European Commission has approved secukinumab, the IL-seventeen inhibitor, for use in polymyalgia rheumatica. Not something that you treat a lot of, it's older white people with aches and pains in the shoulders and hips, but it's an IL-seventeen inhibitor now with expanding use and I think that's going to change a lot of things. IL-seventeen inhibitors have been actively researched and did well in GCA and then failed in GCA and now they look like they're doing good in PMR, these are related conditions.

Anyway, this is the first IL-17A inhibitor approved for polymyeles rheumatica in the world, but especially in The EU. Merck also made announcements about its anti TL1A, It's called Talisocobart, a phase two double blind randomized placebo controlled trial with severe hydradenitis suppurativa, the week 16. High SCR 50 responses seventy two percent, sixty four percent and fifty two percent on high dose, mid dose, low dose versus thirty five percent placebo. It looks like this anti TL1A is going to be on the path for approval for hydradenitis suppurativa and it's being made by Merck. It's not yet approved, but that might could happen.

Biogen gave updated news this week about its litofilimab study, the amethyst study, a phase twothree trial. Previously they reported the week 24 results, now the week fifty two results are out. This is a phase twothree trial. It's not a gigantic trial, but what's unique about it is that it is in CLE, chronic lupus erythematosus patients not otherwise well treated. Ninety three patients and the outcomes were great.

You know, skin in twenty seven percent, that's a CLA IGA, investigator global assessment of zero to one, and a twenty nine percent class E 70 response also being seen at week fifty two. That looks very good and I think we're going down the pathway now of lupus drugs getting approved for skin indications. Instead of going after a global lupus indication or lupus nephritis indication, a number of companies, there are three in fact, that are developing their drugs for the indication of chronic CLE, chronic LE. Anifrolumab is another one that's already approved for lupus, but that's going after a CLE indication, and I think the Toll like receptor targeting drugs are going after the same. News this past month from EADV showed that a new drug that targets plasmacytoid dendritic cells this is an anti ILT7 called Daxdilimab.

Daxdilimab it was shown to be effective in discoid lupus, a phase two trial in seventy two patients with refractory DLE, and it was daxilimab versus placebo, and they showed significant classy A responses compared to placebo as early as week four with greater than fifty percent classy A responses that later on rose to sixty two percent versus twenty four percent in placebo. That's really good news, we're going to like looking at that kind of data in the practice of rheumatology. But we're to co manage those patients with DLE and CLE with you. So it's going to affect both of us. An Italian retrospective study looked at five sixty two patients with plaque psoriasis on biologics, and a third of their patients were obese, thirty four percent.

They showed something that you know well, I don't think rheumatologists know as well, is that obesity clearly impairs responses to biologics. But the important thing about this trial was it impaired primary responses, not secondary non response. So, primary non response means you give them the drug and they don't ever respond to it. Secondary non response is you give them the drug, they respond, but then they lose response. Again, obesity impairs primary or basically drives primary non response.

If you had obesity, primary drug failure was seen seventeen percent versus six percent if you didn't have obesity. That's almost a threefold higher risk. And for every five kilogram per meter squared increase in BMI, there was a thirty seven percent higher risk of non response. Turns out that there was a lower risk of biologic failure if you were on an IL-seventeen inhibitor or an IL-twenty three inhibitor, suggesting that weight and obesity is less important when you're using an IL-seventeen or an IL-twenty three, and it's about fifty percent less. And that's kind of...

I think that's important. Again, other important part was obesity did not affect secondary failures or failures due to drug toxicity. We've talked before about the problem of drug survival in psoriatic disease, both in skin and joint disease. That patients who start on a new, expensive, novel therapy, whether it's a JAK inhibitor or a biologic, you know, fifty percent or less are still taking the drug at two years. And that's a new study coming out of the British Society of Rheumatology.

They have a registry of psoriatic arthritis patients showing that demographics and disease severity will affect outcomes. At twelve months these patients did pretty good: twenty four percent minimal disease activity, twenty four percent ACR 50 response those are high level responses for arthritis in psoriatic arthritis. However, with a median of thirty one months of follow-up, more than one third almost forty percent of patients were off the drug. Discontinuations were higher with PDE4 inhibitors, apremilast, and patients with poor baseline disease activity and poor, worse, patient reported outcomes, survey data if you will. So again, this is disappointing, And I don't know if it's because psoriatic disease is so much harder to treat than for instance rheumatoid arthritis, or is it that we have so many treatment options in psoriatic disease that people are meaning patients and or clinicians, are quick to bail out to move on to the next best great therapy that you might have at your disposal.

Think about it, it's up to us to figure that out. I have reported in the past about probiotics maybe being effective in inflammatory arthritis. Here's a single center study of sixty six moderately active psoriatic arthritis patients with a PAST of greater than 3.2 that showed when you gave them probiotic versus placebo for twelve weeks no benefit. In fact the placebo outperformed the probiotic sixty five percent to forty three percent looking at a PASS DAS less than three response. Moreover, they looked at other things where that might have been affected by a probiotic that might predict or correlate with outcome, and that included gut permeability markers and stool microbiome profiles.

Not great news. But yet our patients like probiotics, do they not? You know, again, if it doesn't hurt, and it doesn't cost a lot, I'm all for it. I to use a probiotic called PB8. PB8's got about 14,000,000,000 drugs, five different strains beyond lactobacillus.

It can be at room temperature or refrigerated, and it's really quite affordable. I used to get it at Sprouts and Whole Foods. I think you have to get it online now if you can't find it at those places. Methotrexate in scleroderma. You know, I've looked at the data coming out of UT Southwestern about the efficacy of methotrexate, which is really, quite impressive, especially with limited disease or focal localized disease.

This is a study of ninety two patients with early, less than two years of systemic sclerosis, who were treated with methotrexate. Almost eighty percent of them had diffuse systemic cirrhosis. At three months, thirty four percent had a... Of the diffuse patients had a greater than twenty five percent reduction in skin severity as measured by modified Rodnan Skin score. This increased, going out to six months up to sixty two percent improved modified Rodnan Skin score.

So I think that that's really very encouraging. Should this be background therapy? Again, we often don't know what to do, what the best therapy is. To me it's my first drug and then I'm usually going to add on top and usually get quite experimental. Glucocorticoids had no effect on skin outcomes, and even they did see the disease progression in the patients who were on monotherapy who discontinued it.

Seventy five percent of those people had worsening of their skin disease. Again, it's not a double blind, randomized, or even controlled clinical trial. It's an observational data set that's basically hypothesis generating, but encouraging for those of us who are looking for guidance. Earlier this month I put out a report on IVIG and scleroderma, and another author wrote about IVIG and scleroderma. He wrote that there's good evidence that it may seem to work but there are no control trials.

So that's kind of disappointing. The meta analysis showed 11 studies, three sixty three patients, IVIG safe, significant improvement in modified Rodnan Skin score, also in GI manifestations, very significant. And not surprisingly, if they had inflammatory myositis, which is a small subset of systemic sclerosis patients, that the CK levels went down and their myositis also improved because that's also an unproven off label use of methotrexate in patients with inflammatory myositis, whether they have scleroderma or not. My last report is on TB. I've got a bone to pick with leaders in dermatology about the guidelines that say that when you're using a biologic, especially a TNF inhibitor, you need to do annual testing for TB.

Wrong! Talk to all the experts, true experts on TB, and they'll say: Nope. Once you've proven it to be a non issue, no risk, you only do repeat testing when risk changes. So if you've got a patient named Skippy or Susie from Connecticut where the risk of TB is somewhere between one in five cases per hundred thousand, You know, prove that they don't have a TB risk or latent TB, give them biologic, don't worry about it. Of course you know this is mainly a risk associated with TNF inhibitors.

Although the guidelines say you have to do TB testing for pretty much all the biologics, it's really a TNF risk. TNF is needed to form granulomas and curtail the spread of the TB bug once it's inside the body, and once you inhibit TNF, boy, the granulomas break down, the bug spreads, and you get reactivation. Well, here's a study about TB burden in Latin America, which is substantially higher than the risk in The United States. As I said, risk in The United States, Western Europe, Canada, Australia, England, etc. Is really low, less than five cases per hundred thousand.

But in Panlar, the Latin American countries, you know, it's more like fifty to a hundred per hundred thousand. And then give them a TNF inhibitor, it goes up two to tenfold, two to ninefold. So in their review of five ninety imid patients, that includes some of your patients, some of my patients, half of whom were on steroids, a risk factor for TB. Forty four percent were on a biologic, the vast majority of those being TNF, which is the main driver. Twenty nine percent on JAKs and twenty seven percent on DMARDs, conventional DMARDs.

The bad news was that only seventy three percent were screened for TB. That means twenty seven percent weren't screened. And you have to be screened for TB if you're from TB land, like Latin America, and if you're going to go on an aggressive therapy like a biologic or TNF inhibitor. Anyway, those who did get screening, they found fourteen percent who had LTBI That's high. That's much higher than we might see here, but it's an endemic area.

A subset of those four thirty who had the screening done, only ninety nine percent ninety nine of them had repeat screening. That would be in conforming to NPF guidelines for annual TB screening. I don't recommend it, but in a high risk population I do. But in a high risk population or a population that's low risk that has new exposure, I do recommend repeat testing. Anyway, when they did repeat testing twelve months later, they found five new TB cases.

And that's explainable in a lot of different ways. One, that well they're in a high risk population, it's endemic, they were re exposed. But these were LTBI, they were not active cases. The more likely thing is that they were first tested and they missed a few who were anergic. Anergic because they had inflammatory disease and so you didn't get a positive TB test, right?

But then when you can correct their inflammation with a TNF inhibitor for instance, now their energy goes away and you get their true responses and you now find this really small number as they did five new cases for latent TB. Overall in this cohort there were only two cases of active TB found. I think it's an instructive study that tells us about the dynamics of TB risk, especially amongst our patients, especially amongst our patients in, high risk areas. Think about it. So that's the view from the rheumatology side of the aisle.

If you need a second opinion, you know where to find us at roomnow.com. We'll see you next month for this podcast Derm on RheumNow. Take care.