Rheum Scholarship (8.21.2026) Save

Hi everyone, welcome to the RheumNow podcast. I'm Jack Cush with RheumNow.com. It is August 21st, 2026. This week on the podcast, back braces, scholarships, and misdiagnosis. Hm. Of course, this is what you would expect from a rheumatology podcast.

This week, um, let's begin with a report on the prevalence of autoimmune disease. Uh, this uh new data — it's about six months old, I just came across it, thought I should share it [snorts] — uh it's based on EHR diagnoses of autoimmune diseases, comes from six um large US health care systems and their EHR um data, and they estimate that in the United States there's about 15, more than 15 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 4.6% of the US population. It's about twice the rate in women as it is in men. Um, that number of 15 million is having at least one autoimmune diagnosis. And not surprisingly, 34% of that overall number have two or more autoimmune diseases. The uh sex ratio uh is 1.7 to 1, uh women to men. Uh, good numbers to keep in your hat.

Uh, a review of uh fatty liver disease, steatotic liver disease. You know, they changed this from NAFLD to MASLD, metabolic dysfunction associated steatotic liver disease. Um, and we're going to 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. 101 patients psoriasis, 127 with PsA and 102 controls at this center. They did uh elastography on everyone and they found a fairly high amount of this um liver disease in psoriatic patients in general compared to controls. Controls 9%. Psoriatic arthritis 32%. Psoriasis 48%. Why is psoriasis more than psoriatic arthritis? I would have 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 numbers above 7 is almost confirmed uh liver fibrosis. So these people are at risk. They have these abnormal uh findings, you should worry about this.

Um, I saw an interesting report this week in JAMA about non-rigid lumbar belts for non-specific 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, uh, uh, these, uh, Velcro, um, ones that people can buy, um, they're not necessarily issued by a clinic or a doctor. Uh, I often think that reminder is more so than effective. But in this uh study, uh a French study of 168 patients with non-specific low back pain, they either got these non-rigid lumbar belts or nothing. Um, and the belt had better 12-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 uh and that subset of people who have scleroderma but don't have the typical scleroderma pattern on 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, 1,689 patients. And they found that 5.3%, 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 may with or without hemorrhages. And this portends — more confirms a diagnosis and maybe portends a more serious um subset. Well, again, they only found a minority, 5.3% of their almost 1,700 patients. And when they looked at them clinically, they had mild disease. They had less vascular uh compromise as evidenced by less pitting scars, 33 versus 48%, less telangiectasias 52% versus 74%, less calcinosis 3% versus 12%. And overall higher DLCO scores at 12 months, 24 months, and I think at 5 years as well. So again, this is um — mean, 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 capillaroscopy, it's going to be a rough go for those people. They're going to have more um vascular complications. They're going to have more lung disease. Uh, 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 uh plastic child's microscope I bought from the Container Store. You can buy them on Amazon with a
10x 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 Rodnan 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 29 reports of trials of CAR T cell. 27 of the 29 were using a CD19 CAR T cell therapy. The other two targeted CD20 or BCMA. 20 of the 29 were autologous. Only two of the 29 had a comparison arm. One 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 is aggressive therapy. There's a lot of holes here and the largest series is the one that was originally reported by Dr. Schett in Erlangen where he had six patients with 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 controlled trials and then we can postulate on the utility of this new intervention at least in systemic sclerosis.

Polymyalgia rheumatica — something that's been in the news this year. The question is when should you use the IL-6 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 yet received either a biologic or targeted synthetic, and then they entered them if they went on either IL-6 or a conventional DMARD. At one year they looked at the outcomes, the outcomes being steroid use and hospitalization for infection. So they showed that the IL-6 inhibitors were way better than conventional DMARDs, presumably as steroid sparing or treatment of refractory PMR, excuse me, but they had significantly better numbers as far as glucocorticoid discontinuation. 28% higher with the IL-6 inhibitor and 28% 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 the biologics, and the rate with the conventional DMARD — remember these are PMR and they're also on steroids — was 5.7 hospitalized infections per 100 patient years conventional DMARD versus 12.2. A doubling. And by the way, that's what you see in the clinical trials — a doubling of serious infection event rates, and it goes from one on placebo to two on biologic with or without a background of methotrexate. And these are sicker patients, right — they're being treated for a different disease, they have steroids in play. I think that this speaks in favor certainly of an IL-6 inhibitor, and it's interesting because the EULAR guidelines that were just published said that when you need a steroid sparer in PMR that you should use an IL-6 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 EULAR 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-6 inhibitor if I needed to. The number of my PMR patients that are on IL-6 — definitely less than 5%. 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 — that was the registration trial for avacopan — citing that the pivotal trial data was incorrect and misleading, and taking note of the vanishing bile duct syndrome. They had their legally binding order issued on August 4th 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 claims — a French insurance claims study of 56,000 SpA patients, of whom 1,200 developed a cancer, a thousand solid tumors, 116 hematologic malignancies. These are patients who were exposed to either TNF inhibitors — 17
inhibitors, the IL-17AB, IL-12/23 inhibitors, um, exclusive IL-23 inhibitors, and JAK inhibitors. And they showed that um uh being exposed for more than 6 months compared to less than 6 months actually had lower, significantly lower rates of cancer. 86% — that was — and with uh confidence intervals all under one, uh 14% lower risk. But this was mainly driven by a lowering of risk for hematologic malignancies, lymphoma, leukemia, mainly lymphoma, where it was a 35% lower risk. It wasn't significant, although it — it wasn't higher for solid malignancy, solid tumors like breast and lung and colon and that sort of thing. But the bottom line is these drugs are not associated with cancer in patients with axial spondyloarthritis.

Came across a press release uh congratulating AbbVie for their 2026 uh scholarship program. They granted 34 scholarships to students who have inflammatory diseases. Um they've been doing this program for 10 years. They awarded over $6 million to over 350 students with the diseases that you and I treat. 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, um they issue up to $20,000 per year and uh if you get it the first time, it's renewable for another 3 years, or a total of four years. Hence the $6 million 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 um 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, every company I've ever dealt with says it's all about the patients. Well, this is further evidence um beyond what they do in drug development.

A few reports on lupus looked at uh pregnancy. This was a systematic review of uh uh the use of biologics and targeted therapies in lupus nephritis patients during pregnancy. A study that spanned from 2000 to 2025. And overall the safe drugs included hydroxychloroquine and azathioprine. These are cornerstone drugs, always used, safe to use, no downside. Um acceptable data exists for tacrolimus and also for aspirin um uh as a preventative measure for preeclampsia. Um the big reminder here is the drug that you're not allowed to use — that you'll lose your house, your family, and your career um — is if you use mycophenolate in a pregnant woman. It is our most teratogenic drug. You worry about cytoxan, you worry about methotrexate, you worry about leflunomide — nothing compares to mycophenolate. It's way worse. Don't do it. Avoid it. Um 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 um not ready for prime time with newer drugs like um voclosporin and 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 uh in seeing patients in clinic. Uh a nice review also appeared on um being aware of what the rashes of lupus and especially dermatomyositis — which are typically red and/or violaceous in whites — will not appear as such in people of color. People with darker skin where erythema may often look brown or dark deep purple, where Gottron's papules are mistaken for dry skin. And 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. Um and this has been really well written about with anti-MDA5 monoclonal antibodies where the rash um is often not appreciated. Uh and it's an atypical, difficult rash as well. So again uh something to talk about with your consulting dermatologist.

A French study of uh 90 RA patients with 100 pregnancies um showed that RA patients had more pre-term births — uh a doubling of the risk — more uh small for gestational age. Uh small for gestational age was more common, four-fold more common in nulliparous women. Uh and the preterm births were associated uh with higher maternal age and glucocorticoid use of greater than 10 milligrams a day. These uh RA pregnant — 90 women with 100 pregnancies — uh 46% were on steroids, 39% were on biologics. So again this I think is encouraging data.

Um two more reports. The misdiagnosis of Still's disease. I like this report. It was just a report on six patients with uh pediatric systemic JIA and basically said that even though — 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 an adult or a 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's a nonresponse 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 — meaning a static rash — 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 PFAPA syndrome, also called Marshall syndrome, for which there is no genetic test. Another was Takayasu's, another was Mevalonate Kinase syndrome, or the hyper-IgD syndrome. By genetic testing, one was found to have an NLRP12 variant that is associated with autoinflammatory 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 2/3 experience with the neonatal Fc receptor targeted therapy efgartigimod, or EFG. This is available and FDA approved in the United States for generalized myasthenia gravis and CIDP — chronic inflammatory demyelinating polyneuropathy. In Japan, it is approved for immune thrombocytopenia. They put out the data of their ALKEMIA study, a multicenter phase 2/phase 3. They had 89 patients in a phase 2 trial and then a phase 3 study of 175 patients. In the ALKEMIA 2 studies, they actually included a total of 264 patients who either had dermatomyositis, polymyositis, or immune-mediated necrotizing myositis.

The good news was that these studies showed a positive 52-week primary endpoint with improvement in the Total Improvement Score, the TIS. The TIS was significantly better at week 52 for the immune-mediated necrotizing myositis and the dermatomyositis patients — highly significant — with clinical responses being seen at week four and rising to week 52 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, but they didn't show any CLASI or CDASI data, which is the validated tool to measure cutaneous dermatomyositis responses. The TIS response looks at CPK, functional measures, MD global, and another measure — it's pretty much muscle dominant. It's a validated tool, but again there was no skin measure here. So 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 want to point you to a tribute to one of my mentors — the amazing, legendary, quiet giant of a rheumatologist, teacher, and researcher Thomas Medsger 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 data set. 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 Medsger. I invite you to read the tribute. I've got about 20–25 comments from worldwide leaders and people that he trained. 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 who did this for you. You probably should tell them how influential they were in your life and your career. Take care of yourself.