2026 Resolutions (1.9.2026) Save

Happy New Year. It's 01/09/2026, and this is the RheumNow podcast. Hi. I'm Jack Cush, executive editor of roomnow.com. It's 2026.

It's gonna be a better year. It's gonna be a better podcast. I'll give you my resolutions at the end of this. That means you gotta stick around for a bit. So this week on the podcast, we're gonna talk about bendability and its use in clinic.

A better way to treat RA that involves getting outside of yourself or outside. And a novel advance in GLP-one agonists. You know GLP-one agonists are called the incretins. I thought incretins were little men who jumped out of spaceships and were stealing my flip flops, but that's another story. So the first report is on preeclampsia and its association with antiphospholipid antibodies.

Thought this was interesting. A hundred women with severe preeclampsia were compared to forty controls, just pregnant women without preeclampsia, and they assessed patients for antiphospholipid antibodies. They found them much more more frequently in those with preeclampsia, thirty four percent versus ten percent. That's a four and a half fold increased risk for APL positivity with severe preeclampsia. The preeclampsia occurred both early and late in pregnancy, so it did have predictive value.

It might be something you might want to look at if you have preeclampsia in a patient, or conversely a patient who has antiphospholipid antibodies could be at risk for preeclampsia going forward. Johnson and Johnson announced some top line results of a phase 2b JASSMIN study, which assessed the efficacy and safety of nipocalimab in lupus patients. NIPO is an FcRn blocker that has been shown in other studies to reduce autoantibody production and B cell activity. It's been shown to have efficacy in Sjogren's and maybe in RA quasi results in RA. This study was in lupus where it met its primary endpoint at week twenty four, which is a significant reduction in the SRI4 response versus those on placebo.

No new safety signals, no granular data. This is going to be presented later on at another meeting. These are top line results. Another study appeared this week about CAR T cells. You know, there's a lot of CAR T cell drugs in development.

I think there's at least 40 companies doing about 80 studies right now on CAR T cell therapy in autoimmune diseases. Yeah. And we're talking about this like it's the next coming of, you know, savior in rheumatology, but really we've got very little data. And we're about three to five years away from getting good data that we can hang our hat on. Right now we have these small reports, and here's a report called the CASL study.

It's a phase one-2A CAR T cell trial of twenty four patients with refractory lupus, scleroderma and myositis. And it's like ten nine what is it? It's let me look at the numbers here. Nine with lupus ten with lupus, nine with scleroderma, and five with myositis. Again, they were treatment refractory, and they're getting this autologous CD19 CAR T cell therapy called MB CAR T19.1.

Its primary goal of the study, being a phase one early two study, was safety. And they had no cytokine response syndromes, no CRS grade two or higher, no ICANS safety concerns at week twenty four, and that was all good. More importantly, they did assess efficacy outcomes and twenty two out of the twenty four patients met a predetermined efficacy response. So in lupus, nine out of ten met doris remission, with lupus. Nine out of nine scleroderma had no progression of scleroderma and four out of five had a major or moderate response to myositis outcomes.

The bottom line is that all these patients did go off of glucocorticoids and were off of immunosuppressants for the first six months. If you look at the graph that we showed you in the tweet on that, that complete response is really at six months, but that responses are lost over time, variably. But again, they only had a, you know, probably a one time treatment. So again, another bit of early encouraging data, but I would tell you to be skeptical still because we don't have really great data, really controlled data. Arthritis Care and Research had a nice report on generalized joint hypermobility syndrome.

It was a meta analysis and systematic review of 46 studies and 23,000 patients. They looked at the utility of the Bayton criteria in making the diagnosis of hypermobility syndrome. Using the usual Bayton criteria, it was about two percent in the populations that were studied. It was more prevalent in younger adults, about five percent in young adults between 18 and 25. And we know hypermobility is sort of a pediatric rheumatology problem, more so an adult rheumatology problem.

But young adults can have this too. Young adult patients presenting with what looks like what you think might be axial spondyloarthritis, early disease, or non radiographic axial spondyloarthritis, or fibromyalgia, you should probably be doing the Bayton score on these people. And you know what that is. There's five maneuvers. It's the fourth finger that goes back more than 90 degrees.

It's your thumb flexed to the vulvar surface of the forearm. It's a hyper extension of the elbows, hyper extension of the knees, and being able to bend over and put your palms on the floor. That's nine points. The criteria for hypermobility is six points out of nine, but what they showed was that that the number of points necessary to make the diagnosis change according to the age. So six points is right for young people 18 to 25, but they propose five points or more if you're 26 to 65.

And then if you're over 65, it's four points that you need to make the diagnosis. I don't know that I agree with that, but they did the research, at least the meta analysis. It's something that should be considered. And I would tell you that if you're like me, you probably don't test enough for hypermobility syndrome in patients who have ill defined complaints and no evidence of synovitis or bony hypertrophy. I like this report this week: a large population based study showed the connection between obesity and low back pain, and we know there's a connection, but I like the numbers here.

And the study found that for weight gain, you have a 7% increase in low back pain for every one unit of BMI that you increase or every 10 pounds. That's very instructive. 10 pounds of weight, you know, or 30 pounds of weight gain by your patient, they now have a twenty one percent higher risk of chronic low back pain. I like that. A VA study looked at RA, and RA patients with calcium pyrophosphate deposition disease, CPPD.

This is older men at the VA, their average age around 65. They found sixty four patients, or amongst their RA population, two point three percent who had codes, ICD-nine, ICD-ten codes for both RA and CPPD. The ones who had CPPD were older, they had more comorbidity more spinal disease, diabetes, but less ACMA positivity. And if they were seropositive RAs with CPPD, they were less likely to achieve low disease activity, and use more prednisone, and use more biologic or targeted synthetics. They were also more likely to have death and total joint replacement.

But the takeaway on this article was, if you have RA and CPPD, maybe you should be rethinking your diagnosis of RA, especially if they're seronegative. Think about it. I think it's good advice. I like this report that appeared recently in J. Rheum.

It's from Adelaide University in Australia, talking about green space exposure reducing the risk of RA. What is green space? You know, isn't that a band? Maybe I'm getting that confused. But we do know there's plenty of evidence out there about toxic exposures and increasing the risk of RA.

It starts with diet and obesity. It's obvious with smoking. It's obviously being, you know, near pollution and, you know, hydrocarbons and, you know, solvents and whatnot. Tons of studies showing an increased risk of RA. That's substantial.

Right? You could very well say, and we should have this whole specialty of environmental rheumatology that we should be making ourselves knowledgeable in, because it's all about lifestyle, is it not? But anyway, this full read article in, J Room shows and it's the lead author author is Stanhope, shows that exposure to to green space, that's gardens, fields, being outdoors, being around greenery, being away from the toxic exposures has, in three studies, been shown to have a protective effect against developing RA. So, could you not prevent RA by going green? This again underscores the importance of lifestyle in both the assessment of our patients and the counseling of our patients.

A UK group did an interesting study of almost eighteen fifty RA patients who were starting on a biologic or targeted synthetic. They found that thirty percent or so were on steroids at the beginning of therapy, and they followed them over a year and then even beyond. And they saw that two thirds of patients were still on steroids, and largely didn't change or wean their dose. What's going on? Why are you using expensive, very potent drugs?

The main reason is to get control of the disease. Secondary reason is to get them the heck off of steroids. But we don't do that. And this is a call for, you know, that we probably need to pay more attention to this. I think the article was meant to point out that we're not vigilant in basically limiting or weaning steroids, but that maybe we should be doing better, or maybe that the therapies that we're using aren't as complete as we think that they are.

Japan has more experience with this phenomenon of methotrexate associated lymphoma, lymphoproliferative disorders. This report I put up this week, thirty eight RA patients who developed a methotrexate related, meaning they got methotrexate and they developed an associated LPD myeloproliferative disorder, and of the thirty eight, twenty two spontaneously regressed when they stopped methotrexate, but sixteen were non spontaneous regressors. Of that fifteen sixteen, a third of them died five. If you were a non regressor, meaning that it was gonna continue, the lymphoproliferative disorder, you were more likely to have high LDH levels at the start of therapy and at diagnosis. They were more likely to have lower lymphocyte recovery after you stop methotrexate, And clearly, they had a higher mortality risk.

You know what? I think this is really interesting, but I've never seen this. And I've treated as many people with methotrexate as you have. And I think I'm looking just like you are. I have I have some of my colleagues here in The US, I do know, have seen a case or two of this.

But I've never seen it, but it's still something to be notable of since you are the world's experts in methotrexate, are you not? Speaking of methotrexate, here's a study that I don't know what to do with. You know, there's a lot of not a lot, there's a few a handful of studies about methotrexate and its use in polymyalgia rheumatica, PMR. Either refractory disease or in new onset disease. And I'm going to show you one, and by the way, I'm on the fence, I don't believe that it really works based on the data I've seen.

I've seen more recent studies where it just really doesn't seem to work. This is a relatively small study, 58 patients, but it was a randomized controlled trial. These are new PMRs with less than eight weeks of steroids. And they were then either given twenty five milligrams per week of methotrexate or placebo, and they had a weaning protocol for the steroids over twenty four weeks. At week fifty two, the endpoint being glucocorticoid free remission, seen in eighty percent that were on methotrexate, only forty percent on placebo.

Yes, this is significant at point zero zero four two. Do I believe it? Well, I got to because they published it. Seems like their methodology is fine. They're faulted for a relatively small study.

Alright? I need to see big studies, 200 plus, well designed trial, maintenance of blind, right? And at least a twenty four week, if not fifty two week, endpoint. So, again, take with that what you will, but I wanted you to be aware of it. Another really important study was published this week about metformin, using a novel co twin study of twelve hundred and sixty one pairs of people, half of whom were treated with metformin because they had diabetes.

They're also that half was also had higher, I guess, glucose levels, A1C levels, higher BMIs. The other half did not. The other twin did not. So basically, what they showed was even though the metformin people did have higher BMI's and diabetes, whatever, being on metformin they had less incident osteoarthritis in the periphery. That means hand, knee and hip osteoarthritis with a forty percent reduction at ten years.

The over at ten years the rate was six point seven percent in the treated twins on metformin versus nine point seven percent in the non treated twin as far as osteoarthritis. And again, the non treated twin did not have the higher BMI. Okay? But the treated twin had a lower incidence of OA. I think that's a really well done and important study.

Nordic Registry study of nonsteroidals. We don't get to talk about nonsteroidals. It was basically the first twenty years of my career in rheumatology from 'eighty four to 2004, when I started doing biologic trials. Did I a lot of nonsteroidal trials, and we used a lot of nonsteroidals back then back then. So this is three Nordic countries, about 750,000 patients, and they found that, these are OA patients, and they found that non steroidal use was being used by up to forty percent under 60.

About fifty to fifty eight percent started the non steroidal before the OA was officially diagnosed. Overall, nonsteroidal use increased annually, up until about age 55, and then it seems to decline, probably reflecting our concern about nonsteroidal use in the elderly. But what they point out in this study is, one, that nonsteroidals are being used, especially in younger OA patients, and that OA patients in general have a substantial risk of GI complications, especially if on nonsteroidals, reinforcing the fact that OA and nonsteroidals are your invitation to aggressively question the patient about GI symptomatology and complications. We reported, Wednesday, Thursday, about the Lilly, phase three together PSA trial. This, again, top line results, press release, no formal data formal data to be presented at a meeting upcoming in 2026.

This is a PSA trial, two seventy one patients, who either received the IL-seventeen inhibitor ixekizumab, or the other group got and these are active PSAs, right? Who are also obese. So one group got ixekizumab, the other group got ixekizumab plus tirzepatide Zepbound, the combination of the GLP-one along with the IL-seventeen inhibitor. And guess what? At week thirty six, the combination was better in the outcomes.

And they chose as an outcome, a combined outcome, of an ACR50 high bar plus at least 10% weight loss from the weight loss drug. So that combined outcome was achieved in 32 on combination therapy versus zero point eight percent on ICSI alone. More importantly forget about the weight loss part, what happens when you use the GLP-one in patients with psoriatic arthritis? Does it affect the ACR-fifty responses? And guess what?

ACR-50s were better with the combo. Thirty four percent ACR 50 on combo versus twenty percent on ixekizumab alone. Now, again, there was weight loss involved, I don't have the actual numbers to know how much, but that opens the door for the possibility that maybe these GLP-one incretin therapies have some effect on inflammation and immunology more so than just weight loss. It could be that if they lost a substantial amount of weight, would also do better as far as their ACR 50. So, I thought that that was important.

I want to point you to a really nice article on reproductive health in the lupus clinic. It's written by nurse practitioner, June Chew, from the NIH. It's a really nice article, in keeping with our APP program from last month and this month, you'll be seeing a lot of news and information about nurse practitioners and physician assistants. I want to end with two things. Let's end with a Ask Cush Anything question.

This is from Doctor. Lauren Johnson.

Hi Doctor. Cush, my name is Lauren Johnson. I'm a rheumatologist in Spokane, Washington. I have a question regarding ECD4 testing in lupus. My patient is a 50 year old woman who was diagnosed with lupus in California based on an advice panel showing a positive ECD4 at 52, the upper limit being 15.

She also has a high titer IgG beta-two glycoprotein-one of 149, a persistently low C4 level ranging from 10 to 23, and in 2017 she had an ANA of one to six forty, but since then she's had a negative ANA by IFA. ANA subsets have been consistently negative, including a FAR double stranded DNA test, and my initial evaluation with her did not show any signs of clinical lupus. Hematology evaluated her and did not think she had APS. Neurology is also treating her with IVIG therapy for GAD positive autoimmune encephalitis, but this diagnosis has also been questioned. She had anaphylaxis to hydroxychloroquine, and unfortunately, she had sepsis due to CellCept in 2017, and she's been off of all therapy since that time.

My question is, in this ANA negative patient without other clear signs of lupus, would you rely on EC4D testing as a diagnostic tool, and if so, you trial immunosuppression? Thank you.

Hi, Doctor. Thanks, Lauren. That's a really, hard question and a hard case, and I'm glad you're managing it. As a skilled rheumatologist, they need guidance on this. No, I would not use immunosuppressive therapy on this patient because this patient doesn't have lupus.

This patient doesn't meet old criteria and new criteria for lupus. This patient has autoimmune features. Right? And you see plenty of ANA positive consults that you're not gonna put on therapy. You don't necessarily have to meet criteria to go on hydroxychloroquine or something else.

But at the same time, those criteria are instructive in making decisions, hard decisions like this. So number one, never treat a lab test. Number two, hang your hat on hard and fast clinical findings that are truly indicative of the disease you wish to treat, or the disease the patient is concerned about. You know, this patient is an in betweener. You know, she doesn't fit neatly into any box.

She clearly has autoimmune disease, evidenced by the ECD4, the positive advice panel, beta-two glycoprotein antibodies, the low C4 levels, the intermittent ANAs, and being diagnosed with, you know, GAD5 autoimmune encephalitis. But, you ask, should she be treated? Well, if she's getting IVIG or gamma globulin therapy, that's probably more potent than anything that you would do to try to control autoimmune disease. Although, they probably don't know what they're treating, and you wouldn't know what you're treating. Let someone else play with the gamma globulin.

And I look at this as a positive test consult, whether it's a, you know, an at risk person with arthralgia who has a positive CCP, or it's someone with autoantibodies being considered with MCTD or or lupus, you know, I only treat what I see. And and I think that she develops serositis, give her a drug for serositis, and say, maybe this is lupus. But, again, she doesn't meet criteria, and the best you can do I'd say I'd say because of the autoimmune features, she may be at risk. But the good news here is, one, she hasn't progressed despite having these symptoms for how long? That's good news.

If she's gonna have an aggressive autoimmune disease, don't you think it would have reared its ugly head by now? Two, that she's already on treatment, and that you, as an experienced, you know, autoimmune specialist, are gonna follow her for what she has. Until then, she gets symptomatic management, without stepping into immunosuppressants, biologics, and expensive therapies. Again, we wanna, thank Lauren for what I thought was a really interesting case. Remember, February is RheumNow live in Dallas.

We hope you're gonna be there. Registration's filling up. I think we have, you know, maybe 40 seats left for in the room. We hope that you'll go to rheumnow.live and register. It's gonna be a great meeting.

I was talking to two of the, or talking to doctor Mike McClung, who's, like, the world's greatest on osteoporosis. And he's gonna do a fabulous talk, the keynote speech on Saturday afternoon on fifty years of osteoporosis. You don't wanna miss it. He's too good to miss. On Sunday, we have this great session called staying ahead of spondyloarthritis.

Dennis Padubney, who's like a world leader in spondyloarthritis, is gonna talk about diagnosing axial disease. Then we have Jessica Walsh and Catherine Bakewell who are gonna be on stage together talking about treatment and complications of spondyloarthritis, and that's gonna be a really fabulous session. And then right after that, there's gonna be these two talks on myositis by Rohit Agarwal from Pittsburgh. He's the man on myositis, talking about asymptomatic elevation of CK and what to do about it, and then an update on the myositis autoantibodies and how they should be used. We hope to see you in Dallas.

Go to rheumnow. Live to register. Oh, what about my New Year's resolutions? Here we go. Number one, RheumNow in 2026 is gonna have more authors, more invited off authors doing more invited commentaries and perspectives.

Two, RheumNow is going to have a Spanish version of its website available to those of you, who like Spanish over the English. Number three, we're gonna be covering more meetings. We're sending more of our faculty who are so good at covering ACR and, and ULAR and RheumNow Live. We're gonna be sending them to all the other meetings and ask them to write reports and do tweeting from the meeting. Follow us on social media where you'll either either on LinkedIn or Twitter, you'll see a lot.

And the last thing is we're gonna be fully invested in artificial intelligence on RheumNow. We're already using it for a number of different things, especially for quizzes and surveys. We find it really useful. And and I think oh my god. He's gonna use AI, and AI is gonna take over.

No. It's not. You know, at RheumNow, we are the authority. We are the experts. We provide the perspectives on the information articles and news reports that we find.

But we're gonna now use AI to expand the data and the info that we receive, and how we present that to you. And AI is also really good at organizing information into more presentable, more digestible forms. AI will not be writing our articles. Don't worry, our authors and I will be, and we'll be fully transparent about when we do use AI. But those are our resolutions for 2026.

Maybe you should ask yourself if RheumNow is using AI, why aren't I? Let's talk about it. We got 2026 ahead to do that.