DERM on RheumNow (June 2026) Save

Welcome to the Derm on RheumNow podcast for June 26. I'm Jack Cush, executive editor of rheumnow.com. This podcast is for dermatologists about dermatology issues that we cover on rheumnow.com. We've got a lot of overlap between us. We do a lot of consulting and sharing of patients, hence, my sharing information with you.

Tell your colleagues in dermatology, especially your NPs and PAs about this podcast. It's a great way to stay abreast of what's important and what's new in dermatology and biologics and drug safety, etcetera. I think the big news this month that you may not be aware of is that the FDA has approved a generic version of tofacitinib. Breckenridge Pharmaceuticals is the manufacturer, they make the pills in Spain. They were approved for both the five and ten milligram dose of tofacitinib, not the extended eleven milligram dose, for use in both adults and children with the same disorders for which, tofacitinib is currently approved.

It's available now at a pharmacy near you. Will you use it? What will be the savings? Will it expand the use of JAK inhibitors? My goodness.

Use of JAK inhibitors in dermatology is just gargantuan compared to what we're doing in rheumatology. You've got so many indications approved and soon to be approved, it would be important to stay abreast of the availability of generic tofacitinib. By the way, tofacitinib has been generic and available in Southeast Asia, India, Pakistan, a lot of countries, for a few years now, and they are the pills there are dirt cheap, really cheap. Will they be cheap here like methotrexate cheap? Not likely.

But what if it was? What if it was as cheap as any other immunosuppressant or DMARDs? Would you not use it? If it was a lot cheaper than the trade drug, would you not use it? Again, we'll find out, over time what this is gonna mean to your practice.

A population based study looked at the risk of psoriasis based on pollution. Here, we're looking specifically at particulate matter, looking at the size of the, of the pollutants PM 2.5 and PM 10, and shows that in a population based study, at least a nineteen percent increased risk of psoriasis. And this was both with, short term exposure, the people who seem to be at greater risk were those who live in urban areas, not surprisingly, younger people, lower socioeconomic group people, ever smokers, and those who had allergies seem to have higher risk of developing. So just like in rheumatology, many of our disorders, not just rheumatoid arthritis, have shown that, pollution, particulate matter, smoking, environmental triggers are triggers to immune activation. I assume in someone who's predisposed genetically, but waiting for that exposure that sets off the key and lock that turns on the immune response that goes wrong and becomes an autoimmune and inflammatory disorder.

Will this become part of therapy in the future? It's possible. It's people are working in in environmental medicine are working at this. I like this report about the risk of TB when you take an IL twenty three inhibitor. As you know, when you use any biologic, especially IL-twenty three, IL-twenty three twelve twenty three, the ustekinumab drugs, now a ton of biosimilars, when ustekinumab.

The IL-seventeen inhibitors, all four and soon to be five of those, all three of the IL twenty three inhibitors, they all have the, package insert recommendation that you should test for TB, prior to use of the drug. Oh, by the way, when you're talking to a guy who and you can talk to the podcast. That's okay. No one's gonna worry too much. You're talking to a guy who knows a lot about TB.

I work with the world's best TB people on committees and on the FDA. There's no guideline that says that other than NPF guidelines, which I don't agree with, that says that you need to do annual TB testing. No. No. And, of course, that was a bad idea when you were doing TST PPDs because you would induce immunogenicity.

But even if you're doing IGRA assays, right, TB spot, QuantiFERON, it's still not indicated. You do it once, and you're done. If it's positive, you respond to it. When you're done, you only do it when risk changes, meaning they go to, Calcutta and do medical relief work in, you know, with lower socioeconomic, groups and in, risky populations. You take a trip to India and visit Taj Mahal with your camera?

No. You don't get tested or treated after that. You do get tested after coming back from exposure or a high risk situation. Anyway, let me get to the report. I just went off on a rant.

Sorry about that. This is a report of 34 studies, in all different IL twenty three inhibitors showing no risk. Basically, there were 34 studies in psoriasis showing no new new new new cases of TB. And you know if it happened, it would get reported. Right?

That's almost a a selection bias. This is a selection bias in favor of knowing the real the real safety, but no new cases. One case out of 34 studies, thousands of patients with one reactivation of TB. We call that LTBI or latent TB infection. In eight studies with psoriatic arthritis, no new cases, no reactivation cases.

So does that mean you don't need to do TB testing? No. The package insert says you gotta do it. But it should tell you what you do when TB is on the table. I've taught from my many learnings, teachings, and writings that, the risk of TB and opportunistic infection, it's the same, is really highest in people receiving TNF inhibitors.

You need TNF to make a granuloma and to sustain a granuloma. You inhibit TNF, granulomas break down, those bugs get out and spread. Right? Is it just TNF? Yes.

It's TNF, TNF, TNF, TNF, a little bit of gamma interferon, and maybe alpha interferon. And I think alpha interferon is a significant risk. Right? So when you have a TB situation, or opportunistic in in situation and you're wondering, what drug can I use? Don't use a TNF inhibitor.

Everything else is okay, including the 17 inhibitors, twenty three inhibitors. This study addresses the 23 inhibitors. Okay? B we just got back from the ACR not the ACR, the UR meeting in London, the first week of June. Great meeting, a number of important, presentations, a lot of them on psoriatic arthritis.

We talked about the Together PSA study. Ixekizumab, coupled with a GLP-one, has a significant benefit over the IL-seventeen inhibitor alone, that was covered. The B BOLD study, I think I mentioned it in the last podcast. The full data was presented as a late breaker by Joe Marola. He's one of yours, a dermatologist from Harvard and now Southwestern.

He's also a rheumatologist. Who's gonna claim him? I know Joe Marola. I want him on my team. He presented the data of this, I think, important landmark study in rheumatology.

You got tons of head to head trials in dermatology. We have none or very few. This is a head to head of bimekizumab against rizenkizumab in patients with psoriatic arthritis. I think it was thirty, forty percent of them had previously received a TNF inhibitor. And it's important, five fifty three patients randomized to receive either drug.

The primary endpoint was an ACR 20, a combined joint endpoint I'm sorry, ACR 50, a high level joint endpoint at week 16. Significant benefit of bimekizumab over, the IL twenty three drug, ACR fifty of forty nine percent versus thirty eight percent. That's p equals 0.0058. The advantage was maintained out to week 24. Interestingly, other outcomes, skin outcomes and secondary joint outcomes, there might have been a numeric advantage for, bimekizumab, but it was not significant.

This included minimal disease activity, PASI one hundreds, DAPSA, and a few others. So why? There are theories, but we now await the paper. This is a an important study that now you can point to your your room colleagues and say, might wanna look at that head to head b bold study, bimekizumab versus rizenkizumab. The other big study that will affect practice is the RA bridge and RA branch.

Why am I talking about RA? Oh my god. You know, he's a rheumatologist, can't help himself. This is a large scale FDA mandated study of baricitinib and the risk of venous thromboembolic events, VTEs. Let me give you a prelude and tell me that I'm wrong or tell me that I'm right.

Most of my good friends who are medical dermatologists, after the release of the oral surveillance study done with tofacitinib that then ended up changing the package inserts for all JAK inhibitors saying that you must use a JAK inhibitor after a TNF inhibitor because of this increase high or because of a higher number of cardiovascular and malignancy and serious infectious events in the JAK inhibitor compared to TNF inhibitor. And that's been out there, and it's changed practice. It had a tremendous effect on dermatology use of JAK inhibitors. It had a modest effect on rheumatology use. Why?

Well, we use a lot maybe a lot more JAK inhibitors, but we looked at many of the reports that came after that, that looked at the analyses to show who exactly was at risk. The entry criteria for oral surveillance was over age 50 or 55 with a cardiovascular risk factor, right? But it turns out that people who had the highest risk of all those three bad things, cardiovascular events, MACE events, malignancies, lymphoma and lung cancer especially, also some skin cancer, and then, serious infectious events, hospitalisable infections. The people who got those bad outcomes were 65 with a prior history of MI or cardiovascular event who were smokers. So now apply that to all your patients that use a JAK in.

How many of them are 65 smokers with a prior MI? Yeah. It's a small number of your pop population. Your 37 year old with atopic dermatitis, no problem. Your, you know, your 29 year old, you know, very attractive lawyer who's lost all her hair from alopecia universalis can go on a JAK.

You know? Do you have to try a TNF inhibitor before the JAK if the TNF inhibitor is indicated for that disorder? Yes. I think you should just to be in compliance with the package insert. But for alopecia areata, alopecia universalis, TNF numbers are not indicated.

I'd go right to JAK's. Why wouldn't you? So RA bridge branch is a and remember, oral surveillance was what? Four thousand five hundred patients followed four years, double blind, randomized, placebo controlled trial of tofacitinib versus two different TNF inhibitors. Same design for the RA bridge and RA branch study.

Three thousand five hundred patients followed for almost four years. The primary endpoint achieving a certain number of VTE events, either pulmonary emboli or DVTs. They stopped the study prematurely because they, weren't gonna change the results. And they showed unequivocally that baricitinib at both doses, two milligrams a day and four milligrams a day, significantly increased the VTE events. Thirty six hundred patients followed for up to six years, eleven thousand patient years of follow-up.

Again, the entry criteria was having one prior VTE. Have you had a prior VTE, more likely to get it in the future, that's why they include those. Or age 60 BMI greater than thirty or if you were age 50 to 59 when you're overweight with a BMI greater than twenty five. And again, this had a it was a non inferiority study with an upper limit of non inferiority 1.8. This exceeded that, which means that the JAK inhibitor was not non inferior, meaning there were more events, significantly more events.

And again, the incidence rate was, the hazard ratio was 1.6, exceeded the upper limit, of confidence level at 2.6, and that was true for only VTEs. It did not show an increased risk of MACE. It did not show an increased risk of cancer or opportunistic infections. And where it didn't show these risks, there was no difference between the low dose and the high dose. There was a marginally but significant increased risk of serious infections.

So this is follow-up data to oral surveillance that should give you either confidence, or if you're chicken and whittle and you're worried about this, you're more worried about using these drugs. You know, send them to the rheumatologist or don't use those drugs at all. When I've asked rheumatologists their interpretation of the study, does it give them more confidence or not? I am getting a split message. And I consider myself an expert on this because I've been on the FDA advisory committees and when they submitted the atofacitinib, I study these issues all the time.

I have less worry based on this data. But my colleagues are split. Some say less worry, some say, well, you know, and they waffle, you know, and they still are worried. You have to decide for yourself, but know that RA Branch and RA Bridge are out there. My last report, no.

Two more reports. Probiotics in psoriatic arthritis. You know, we see goofy things on diet and whatnot. I'm a big believer, not in probiotics, but a low gluten, low no carbohydrate diet as being tremendously effective in psoriasis. We did an uncontrolled study.

We didn't publish it and asked me some time about it. But, this study, it's called the MEDISPA study, examined the effects of probiotic therapy on sixty six PSI patients with moderate activity receiving placebo or a probiotic with just lactobacillus and bifidobacterium. Twelve week study, the primary outcome was, either lowering of the disease activity or achieving remission with a PASS less than 3.2. The placebo was better than the probiotic, sixty five percent versus forty three percent. So you might say to your patients, doesn't look like probiotics do anything.

I would say this isn't the study that would have done. You know, to have an effective probiotic, you need to have five or more strains, fourteen, fifteen billion, CFUs or bugs in there. They don't have to be live. That doesn't have to be refrigerated, whatever. I'm still okay with probiotics, but this study proved that it didn't work.

Another interesting study, on CLA CLE looked at a stepwise approach to treating CLE. This came from professor Whitman, at at EULAR, and he really showed to me, something that was important that I don't pay enough attention to. Smoking is a bad, bad player in rheumatoid arthritis and many inflammatory arthropathies. We know smoking is a bad player in autoimmune disease. In his presentation, he showed smoking reduces the efficacy of antimalarial drugs, significantly reduces the efficacy.

So if your patient's on antimalarial and they're not doing well, number one, do a hydroxychloroquine level. You can get that now to see if they're taking the drug. And then ask them if they're smoking. But if they're a smoker, it also worsens skin activity, and not only the severity of skin, but also the development of organ damage beyond the skin. So these are important lessons coming out of EULAR that I hope that you'll find useful for your practice.

That's it for this week. Tell your colleagues about the Derm on RheumNow podcast. Take care.