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Rheum Scholarship (8.21.2026)

Aug 21, 2026 11:22 am
Dr. Cush reviews the news and journal articles from this past week on RheumNow.com; talking about lumbar belts, scholarships and misdiagnosis.
Transcription
Hi, everyone. Welcome to the RheumNow podcast. I'm Jack Cush with rheumnow.com. It is 08/21/2026. This week on the podcast, back braces, scholarships, and misdiagnoses.

Of course, this is what you would expect from a rheumatology podcast. This week, let's begin with a report on the prevalence of autoimmune disease. This new data come it's about six months old. I just came across it, thought I should share it. It's based on EHR, diagnoses of autoimmune diseases, comes from six, large US health health care systems and their EHR, data, and they estimate that in The United States there is about fifteen more than fifteen million Americans who have autoimmune diseases.

And, you know, depends on what you include in that disease. I think their number was somewhere around 20 different diagnoses. This amounts to about four point six percent of The US population. It's about twice the rate in women as it is in men. That number of fifteen million is having at least one autoimmune diagnosis, and not surprisingly, thirty four percent of that overall number have two or more autoimmune diseases.

The sex ratio is one point seven to one, women to men. Good numbers to keep in your hat. A review of fatty liver disease, steatotic liver disease, you know, they changed this from NAFLD to MASLD, metabolic dysfunction associated steatotic liver disease, and we're gonna have to go with that. That's somebody else's definition. It's not our domain.

But this is a study of what happens in psoriasis. A hundred and one patients psoriasis, a hundred twenty seven with PSA, and a hundred and two controls at this center. They did, elastography everyone, and they found a fairly high amount of this liver disease in psoriatic patients in general compared to controls. Controls nine percent. Psoriatic arthritis thirty two percent.

Psoriasis forty eight percent. Why is psoriasis more than psoriatic arthritis? I thought it might be the other way around. But these were significant compared to controls. They also showed by FibroScan, or elastography, that the numbers were elevated in PSO 6.01, PSA 5.1, versus controls 4.9.

A trend there. I think the really dangerous number is above seven, is almost confirmed liver fibrosis. So these people are at risk. They have these abnormal findings. You should worry about this.

I saw an interesting report this week on JAMA about non rigid lumbar belts for nonspecific low back pain. I think you've seen them. They're black. You know, they're wide. They wear them around their waist.

They got Velcro fasteners. You wonder, are they looking for time off from work? Are they trying to remind themselves not to, you know, hurt their back or lift badly and whatnot? I often think these bracings, especially the, you know, these Velcro, ones that people can buy, they're not necessarily issued by a clinic or a doctor, I often think they're reminders more so than effective. But in this study, a French study of one hundred and sixty eight patients with nonspecific low back pain, they either got these non rigid lumbar belts or nothing, and the belt had better twelve week outcomes as far as lower pain scores and less need for typical back pain medication.

I thought that was worth sharing. An Italian study looked at scleroderma patients, and that subset of people who have scleroderma but don't have the typical scleroderma pattern are nail fold capillaroscopy. So in this study they do nail fold video capillaroscopy. It's a higher quality of imaging. They have a lot of patients in this Italian spring registry or cohort of systemic sclerosis patients, sixteen eighty nine patients, and they found that five point three percent, although they have a confirmed diagnosis of systemic sclerosis, do not have that pattern.

You know the pattern I'm talking about. There's dropout, there's dilated loops, right, and and may with or without hemorrhages, and this portends a more confirms a diagnosis, and maybe portends a more serious subset. Well, again, they only found a minority, five point three percent of their almost seventeen hundred patients. And when they class when they looked at them clinically, they had mild disease. They had less vascular compromise as evidenced by less pitting scars, thirty three versus forty eight percent.

Less telangiectasis, fifty two percent versus seventy four percent, less calcinosis, three percent versus twelve percent. And overall, higher DLCO scores at twelve months, twenty four months, and I think in five years as well. So, again, this is surprising that this subset exists. It's good to know that if they don't have those findings, they may have milder disease, but it's also good to know, or bad to know, that if they do have that scleroderma pattern on nail fold canopuloscopy, it's going to be a rough go for those people. They're going to have more vascular complications.

They're going to have more lung disease. It's not a good thing. Should you be doing nail fold capillaroscopy on all your patients with scleroderma? Yes, you should. Now, again, one of these devices that does it really well are expensive, but you don't need to use those devices.

I use a a 10, plastic child's microscope I bought from The Container Store. You can buy them on on Amazon with a 10 x lens, and it works fabulous. I use a little KY jelly. I'm in there. I can see everything.

You do three or four fingers on both hands. You can do it periodically over time. You can correlate that with your modified Rottman skin score. Yes, you should be doing these things in practice on a regular basis. Another study this week looked at CAR T cell therapy in systemic sclerosis.

They found this was a literature review they found twenty nine reports trials of CAR T cells. Twenty seven of the twenty nine were using a CD19 CAR T cell therapy. The other two targeted CD20 or BCMA. Twenty of the twenty nine were autologous. Only two of the 29 had a comparison arm.

One was had a rituximab comparison arm. And all the studies included or most of the studies included patients with limited systemic sclerosis or CREST. Why are CREST patients or limited getting CAR T cell therapy? I don't know. I mean, this is not cheap.

This is not safe. This, this is aggressive therapy. There's a lot of holes here. And the largest series is the one that was originally reported by, doctor Shet and Erlangen, where he had six patients with diff diffuse cutaneous systemic sclerosis, and they got better. They had better skin.

They had better lung outcomes. The bottom line is it's too early to be talking about this. We need data. We need bigger trials and longer trials and randomized control trials. And then we can postulate on the utility of this new intervention, at least in systemic sclerosis.

Polymyalgia rheumatica is something that's been in the news this year. The question is, when should you use the IL six inhibitor in PMR? And so in this analysis, it was a retrospective analysis of Medicare data, and they looked at PMR patients who were steroid treated but had not either a biologic or targeted synthetic. And then they entered them if they went on either IL-six or conventional DMARD. At one year, they looked at the outcomes, and the outcomes being steroid use and hospitalization for infection.

So they showed that the IL-six inhibitors were way better than conventional DMARDs, presumably a steroid sparing or treatment of refractory PMR. Excuse me. But they had significantly better numbers as far as glucocorticoid discontinuation, twenty eight percent higher with the IL-six inhibitor, and twenty eight percent higher numbers as far as those achieving one or two milligrams of steroid per day. But they did have a doubling of the infection rate with biologics, and the rate with the conventional DMAR remember, these are PMR and they're also on steroids was five point seven hospitalized infections per one 100 patient years, conventional DMARDs, versus twelve point two, a doubling. By the way, that's what you see in the clinical trials.

A doubling of SIE rates, and it goes from one on placebo to two on a biologic, with or without a background of methotrexate. And these are sicker patients. Right? They're they're being treated for a different disease. They have steroids in play.

I I I think that this speaks in favor, certainly, of an IL-six inhibitor. And it's interesting because the EULAR guidelines from that were just published said that when you get a steroid spare in PMR, you should use an IL-six inhibitor. Oh, and by the way, you can use methotrexate. The data is lousy on methotrexate. We've talked about that.

But the reason it made it into the UR guidelines is because not all countries, not all jurisdictions have access to biologics or all drugs, and maybe the best they can do is methotrexate. I would use the IL-six inhibitor if I needed to. Number of my PMR patients that are on IL-six, definitely less than five percent. I might very well be underutilizing that, given the fact that we can't get people off steroids with PMR. The big news, I think, this week was the revelation that the EMA, and the European Commission finalized the withdrawal of Tavneos from clinical availability in the European market.

You know, they've been working on this for several months. They noted the same inconsistencies with the reporting on the ADVOCATE trial for that was a registration trial for avacopan, citing that the pivotal trial was incorrect and misleading, and taking note of the vanishing bile duct syndrome. They had their legally binding order issued on August 4 confirming the recommendations from the CHMP and that they withdraw the drug. Now this has not yet happened in The United States. It might happen in The United States, but there's a lot still in play.

Amgen, the maker of avacopan, has asked for a public hearing, citing the real world evidence that looks good for avacopan. So the fate of this is still up in the air in The United States. Another report this week about cancer risk with targeted therapies in axial spondyloarthritis. This is a French claim a French claims insurance claims study of fifty six thousand SPA patients, of whom twelve hundred developed a cancer. A thousand solid tumors, a hundred and sixteen hematologic malignancies.

These are patients who are exposed to either TNF inhibitors, IL-seventeen inhibitors, the ustekinumab twelve-twenty three inhibitor, exclusive IL-twenty three inhibitors, and JAK inhibitors. And they showed that being exposed for more than six months compared to less than six months actually had lower, significantly lower rates of cancer. Zero point eight six, that was and with confidence intervals all under one, fourteen percent lower risk. But this was mainly driven by a lowering of risk for hematologic malignancies, lymphoma leukemia, mainly where it was a thirty five percent lower risk. It wasn't significant, although it wasn't higher, for solid malignancies, solid tumors like breast and lung and colon, and that sort of But the bottom line is these drugs are not associated with cancer in patients with axial spondyloarthritis.

Came across a press release congratulating AbbVie for their 2026 scholarship program. They granted 34 scholarships to students who have inflammatory diseases. They've been doing this program for ten years. They've awarded over $6,000,000 to over 350 students with the diseases that you and I treated. This is all just in The United States and all of these are scholarships for higher education.

I put in the link. You can see the current recipients. You can see what the program has done. These are and by the way, if you have a patient, a student of yours who is in need of funding for their education, they issue up to $20,000 per year. And if you get it the first time, it's renewable for another three years or a total of four years.

Hence, the $6,000,000 investment by AbbVie for patients with inflammatory arthritis and inflammatory diseases. Congratulations to them for not just doing it, but even publicizing it. I think that other companies are doing a lot of patient centered, and benefiting programs that we may not know about, and they I think they should be more boastful of what they do. Because as part of their mission, and every company I've ever dealt with say it's all about the patients. Well, is further evidence beyond what they do in drug development.

A few reports on lupus looked at pregnancy. This was a systematic review of the use of biologics and targeted therapies in lupus nephritis patients during pregnancy, a study that spanned from 2,000 to twenty twenty five. And overall, the safe drugs included hydroxychloroquine and azathioprine. These are cornerstone drugs, always used, safe to use, no downside. Acceptable data exists for tacrolimus, and also for aspirin as a preventative measure for preeclampsia.

The big reminder here is the drug that you're not allowed to use, that you'll lose your house, your family, and career is if you use mycophenolate in a pregnant woman. It is our most teratogenic drug. You worry about cytotoxin. You worry about methotrexate. You worry about leflinamide.

Nothing compares to mycophenolate. It's way worse. Don't do it. Avoid it. They said that belimumab has a pregnancy registry, and that's encouraging, but there isn't like a final report on that, but it still is encouraging if a patient needs belimumab and is pregnant, I probably would do it.

But they were pretty explicit in saying, not ready for prime time with newer drugs like voclosporin, anifrolumab, and the newly approved obinutuzumab, meaning there's just not enough data to support that. And as we talked about in the past, there's not enough data to allow for JAK inhibitor use in pregnancy, because it just hasn't been well studied yet. I like these reports. I think that they're instructive and helpful for us in seeing patients in clinic. A nice review also appeared on being aware of what the rashes of lupus, and especially dermatomyositis, which are typically red and or violaceous in white, will not appear as such in people of color, people with darker skin, where erythema may often look brown or dark, deep purple, where Gottrin papules are mistaken for dry skin.

Same thing for the heliotrope rash. It's mistaken for dry skin. The problem with this is that people of color often experience delays in diagnosis for dermatomyositis and lupus. And this has been really well written about with anti MDA-five monoclonal antibodies, where the rash is often not appreciated. And it's an atypical, difficult rash as well.

So, again, something to talk about with your consulting dermatologist. A French study of ninety RA patients with one hundred pregnancies showed that RA patients had more preterm births, a doubling of the risk, more small for gestational age. Small for gestational age was more common, fourfold more common, in nulliparous women. And the preterm birth was associated with higher maternal age and glucocorticoid use of greater than ten mg a day. These are a pregnant ninety women with one hundred pregnancies.

Forty six percent were on steroids, thirty nine percent were on biologics. So, again, this, I think, is encouraging data. Two more reports. The misdiagnosis of Still's disease. I like this report.

It was just a report on six patients with pediatric systemic JIA, and basically said that even though pay even though you may slap a diagnosis of Still's disease on them, that you should realize it's an exclusionary diagnosis. There is no pathognomonic, test or confirmatory test. You need to meet criteria. But meeting classification criteria for Still's disease in the adult or the kid, is not it's just a start. It's not a final diagnosis.

Time will tell whether it's a final diagnosis. You should worry about the diagnosis when there is a non response to typical cytokine inhibitors and high dose steroids. The red flags when Still's is not the right diagnosis based on this six patient report was onset of age before two, a positive family history of a febrile illness, an atypical rash like panniculitis, or non evanescent rashes persistent organomegaly, persistent cytopenias, coronary artery problems, interstitial lung disease, and recurrent abdominal pain. So in their cohort, what were the diagnoses? One was familial HLH.

The other one was FAPA syndrome, also called Marshall syndrome, which there is no genetic test. Another, Takayasus, another Mevolani Kinase Syndrome or the hyper IgD syndrome. By genetic testing, one was found to have an NLRP twelve variant that is associated with auto inflammatory disease. And then there was a patient with inflammatory myofibroblastic tumor, something I'm not familiar with, but obviously it can look like Still's disease. And I've seen I see since I get a lot of Still's consults, and most of them don't have Still's disease, I think the diagnosis is often made wrongly.

And you need to think about these alternative diagnoses, because it does happen. There was a press release this week about an encouraging phase twothree experience with the neonatal Fc receptor targeted therapy, efgartigimod, efgartigimod, or EFG. This is available and FDA approved in The United States for generalized myasthenia gravis and CDIP, chronic inflammatory demyelinating polyneuropathy. In Japan it is approved for immune thrombocytopenia. They put out the data of their ALKEVIA study, a multi center phase two, phase three.

They had eighty nine patients in a phase two trial, and then a phase three study of one hundred and seventy five patients. In the Alkevia two studies, they actually included a total of two sixty four patients who either had dermatomyositis, polymyositis, or immune mediated necrotizing myositis. The good news was that these studies showed a positive fifty two week primary endpoint with improvement in the total improvement score, the TIS. The TIS was significantly better at week fifty two for the immune mediated necrotizing myositis and the dermatomyositis patients. It's highly significant, with clinical responses being seen at week four and rising to week fifty two and being sustained.

They did not show significance for polymyositis and no data on efficacy or otherwise was shared. They mentioned that muscle and skin improved in these patients on efgartigimod, efgartigimod. But they didn't show any CLASI or CDASI data, which is the Victoria Worth tool to measure cutaneous dermatomyositis responses. The TIS responses looks at CPK, functional measures, MD global, and another measure that's pretty much muscle dominant. And it's it's a it's a validated tool.

But again, there was no skin measure here. So we we we await full release of the data. Hopefully, maybe we'll see that at ACR in November in Florida. I think that'll be very exciting. I wanna point you to a tribute to one of my mentors, the amazing legendary quiet giant of a rheumat rheumatologist teacher and researcher, Thomas Metzger from the University of Pittsburgh.

I met Tom when I was a resident doing my, internal medicine residency in New York. He invited me to go to Pittsburgh to do research on his Still's disease dataset. We we published then the largest report on Still's disease. I did that as I entered my fellowship. We published on 21 patients.

I went and actually looked at, I think, 23 patients. Two patients proved ultimately to not have Still's disease. Another lesson from today's report. 21 was the report. I think it's one of the best reports.

Of course, I would say that because I did it. During my time there, I wrote it up. During my time there, I woke up in the middle of the night and wrote down Cush criteria for Still's disease, which still stand up today. Five major, five minor criteria, get 10 points, you got the diagnosis. But Tom was amazing.

What was amazing was I was this unknown person that wanted to work on something he was interested in. He invited me. He put me up at his house with his family. Who does that? Who are these rheumatologists that would do something like this?

I was blown away by that, and, I've been forever grateful. And his passing is a really hard thing for anyone who's ever met Tom Metzger. I invite you to read the tribute. I've got about twenty, twenty five comments from worldwide leaders and people that he trained. It's it's amazing, how much effect he had, in his very large world, and he did so in such a truly exemplary manner.

I encourage you to read his tribute. I'm still tearful about his passing, but glad to know that he taught me so much about what a rheumatologist should be, can be, how to go about your business. You know? He was all about doing it the right way. Again, he is the model.

He is the model for what is great about rheumatology. He is the inspiration as to why I love rheumatology, and I'm sure you have someone in your life life who did this for you. You probably should tell them how influential they were in your life and your career. Take care of yourself. We'll talk next week.

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