RheumNow Live Preview (1.30.2026) Save
Transcription
Hi everyone. This is the RheumNow podcast. It's January 30th, 2026 and I'm Jack Cush with RheumNow.com. Actually, RheumNow.live. That's right. Our meeting's coming up in one week. We hope you'll be there. I'm going to give you top five reasons why you should come to RheumNow Live. Number five, it's next week, but it's cold and it's far, but you can be there online. Register now. Number two, no, number four. If you register, you'll get full access to everything, including the handouts, the downloads, the lectures, the pictures, the pre-learns, whatever. Number three, something you didn't expect, live entertainment, Saturday night, Colin Boyd. He's great. One of Arty's favorites, one of my favorites. Number four, I was looking at all the talks and I liked this set of talks by Rohit Aggarwal from Philadelphia. He's doing a step talk, actually two of them, and they're like TED talks. One on myositis antibodies testing and the other one on asymptomatic CK. Not a lot of slides. This is wisdom from the guru of myositis from the University of Pittsburgh. I'm liking this.
And the last one is registration gives you, and I think it's the number one reason, access and download to more than 400 review questions from this year's meeting 2026, from the 2025 and the 2024 meeting. It's a lot of questions. It's really good. So certainly enough reasons.
When I look over the program, there's a few things that really jump out at me, and that's when we begin on Saturday morning. We've got a session, we call them pods, on RA, and Elena Myasoedova is talking about mortality in RA. And you know, why there's a trend downward that looks good, but still there's bad news, why we sort of stalled, why your DMARD therapies are the first most important thing you can do to reduce mortality risk in RA, but it's still not enough and there's more you got to do.
Second on the agenda is Kristen Deane from Colorado. This is the center where all the great research is being done on the earliest biology that starts RA, pre-clinical RA, at-risk disease, and this mucosal hypothesis theory that they're working on, and she's one of the main investigators. You think you need to know this because it is this interface, I think, with the environment through the mucosa, inhaled, GI, that we're going to find 10 years from now is where we're going to focus prevention of disease. And that's just my idea.
Next down the program is from a friend from HSS, Susan Goodman. You may not know Susan Goodman, but she's done the ACR task force and all the great work on how we should manage our patients perioperatively. And it happens and sometimes we don't quite know what to do with their therapies, what the surgeons are saying. She's written the guidelines. She's the guru. She's the source. She'll be on stage.
Bob Terkeltaub is maybe the world's greatest authority in gout and he'll be giving two gout talks, one on gout pearls and the other one on the rich history of gout. You don't want to miss this.
Next, you know, Arty and I, we're New Yorkers, but we moved to Texas and we like, you know, sort of this Texas music scene. And in the '90s, we actually got into, we discovered the Dixie Chicks. Well, we don't have the Dixie Chicks showing up. We got the spondyloarthritis chicks showing up. And that may be sexist, but I'm telling you, these two gals together, Katherine Bakewell and Jessica Walsh, two friends, two academics from Utah, are going to be on stage and they're giving, you know, their talks on spondyloarthritis, but you know, it's going to be much more. They're doing a tandem side by side thing, and it's not just going to be highly informative, it's going to be entertaining, because they are really, really good.
Two more. Matt Baker from Stanford is going to talk about all the hot stuff going on in Sjögren's. You know, the drought is over on therapy. We've got therapies coming in and maybe you don't know about them. This includes Nipocalimab, Telitacicept, Ianalumab — that was actually presented, a few of these were presented, including the NEPTUNE 1 and 2 trials presented as positive phase three trials at ACR. This is good news for Sjögren's.
And then lastly, on the last day, Michael Putman, who's been managing our pre-learns for this meeting, and if you haven't seen Michael's pre-learns, you're really missing out. And he's going to give an address on relapses of PMR and GCA. Is it all about steroids or is it all not about the steroids? Michael's going to tell us.
All right, so this week on the podcast, we got a number of things that are worth reviewing. The Journal of Rheumatology has an interesting report about remission in RA and lupus. This is a single center study from Dresden, Germany, led by Michael Aringer, and I like this study because it put some hard numbers on some real world
patients. So they're looking at 100 RA and 100 lupus patients from their center. And they use standard measures for remission — SLEDAI and SLEI. And what do you think they found in lupus? 100 lupus patients, 392 visits. I was shocked by this. 88% achieved either remission or low disease activity state in lupus. Was it as good in RA? It was better in RA. 91% of almost 400 RA visits in 100 patients. No difference between RA and lupus as far as how often they're achieving remission, but they did actually have some more remissions in lupus than RA because we accepted remission and LDA as the outcome measure there — that 88, 91% — but there were more remissions in lupus: 79% versus 69% in RA. And I find that really surprising, but this is the real world. This is probably what you're seeing.
Other good news this week comes from two different sources. The Lupus Foundation of America announced that the US government House of Representatives has approved $27 million for lupus funding in 2026. In 2025, the whole thing was a new administration, all these cutbacks, research is being screwed. Well, it looks like a lot of that money is coming back. And that money is going to be available from the CDC, the Department of Defense, and other agencies. At the CDC, funding increased by 40%. At OMB by 33%, and $415 million has been put into the NIH budget for lupus. So this is really good news, especially if you're a lupus researcher.
Also this week, there was a stakeholders meeting called the Lupus Accelerating Breakthroughs Consortium, and they looked at skin lupus and outcomes. I think it was sort of a documenting paper where, as a consortium of lupus leaders, the meeting and the paper has all the stakeholders, including representatives of the FDA. And they say that the CLASI measure should be the recommended measure. That's the Cutaneous Lupus Erythematosus Disease Area and Severity Index — I think it was established by Victoria Werth at the University of Pennsylvania. She's got a version of it for dermatomyositis. So CLASI should be the primary endpoint in clinical trials that can be used to get drugs approved in lupus.
My beef in lupus is that it's really hard to prove a drug works in lupus with the current measures. Although the SRI-4 seems to have furthered things in the last 10 years, it's still hard to get a general lupus indication. If I'm developing a drug, I'm going after a single indication. And why not go after CLE — lupus skin disease — and why not use the CLASI as your primary endpoint? The FDA is going to accept it now, and we have consensus and guidelines and experts on this. This should really further lupus research and drug development.
JAMA published this week an interesting general paper about deprescribing. Yes, deprescribing — you know, this is really important, and I brought this up during ACR because the ACR updated its JIA guidelines. It's the systemic JIA guidelines that was presented by Susan Shenoi. An important part of their update to JIA treatment guidelines — as you can imagine, this drug, not that drug, whatever — was the component of deprescribing and down-ratcheting therapy as we are adding on therapy. And that's really never been discussed, and this leads to the problem of patient confusion through polypharmacy and safety issues, does it not.
So this JAMA paper basically shows if you employ two different interventions using an EHR — your electronic health record — in a study of 1,146 patients, most of them being older (mean age 74), they were able to either reduce the number of drugs being used — deprescribing — by either 6.12% or 10.4%. And the overall approach to using the EHR as a reminder to deprescribe can lead to 40% more success in deprescribing. It is something we should talk about, something we should think about.
Again, I tell my patients, especially the ones I'm seeing that have that long laundry list and they're confused about their drugs — I tell them and I write down: if another doctor is going to give you two more drugs, you've got to say, "Oh, good, thank you, but Dr. Cush said if you're going to give me two, you've got to take two away." So it's got to be zero-sum management, or even again, deprescribing. The simpler the regimen, the more the compliance. The more the compliance, the better the outcomes.
Speaking of outcomes, there is the STRONG-STAR Consortium, started out of I think Fort Hood, Texas and the military base there. They published a report in Arthritis Care and Research about a longitudinal study of 1,761 military service members and their assessment before and after they were deployed. They found that the prevalence in males and females pre-deployment was about 2%. But post-deployment — meaning after they went to wherever they went — fibromyalgia meeting criteria went up to 8% in males and 11% in women.
A significant change. Underlying all this was PTSD. It turned out that if you had PTSD before you were deployed, you had a three-fold higher risk of fibromyalgia after deployment. And then similarly if you have PTSD before and after, it went up from 21 to 23% in males and 18 to 26% in females, suggesting a slightly bigger effect in females. Pain being a bigger effect in females.
I again — this STRONG STAR Consortium has published in the past about military service and the risk of fibromyalgia, and it's an underlying feature in that Gulf War syndrome, a lot of which was fibromyalgia-like disease. I think this is what underlies the post-COVID syndrome. And so, again, I applaud them for their efforts.
Another interesting effort — and again this is a stone in my shoe, this is a bug that I keep going back to — is the use of ADHD drugs in our patients. You know, they're good for ADHD, are they not? That's why they developed them. They're FDA approved. And there are four of them that are out there on the market. But in our patients, it leads to worse sleep. Worse sleep leads to fibromyalgia. Fibromyalgia and ADHD drugs leads to, you know, them seeing you thinking they've got multicentric reticulohistiocytosis or whatever they're worried about.
So, a Lancet study of a European EHR network called DARWIN showed a shocking statistic that in five major countries in Europe, all the biggies, the use of ADHD drugs more than doubled between 2010 and 2023. In some places it went up fivefold. In the UK it went up 20-fold in females, 15-fold in males. What?
Again, look at the drugs when they show up in your office. I try to deprescribe ADHD drugs. I know their utility in severe ADHD, especially in children. I think they tend to be overused in adults, in America at least.
Seminars in Arthritis and Rheumatism looked at the cardiovascular risk in idiopathic inflammatory myopathy patients — myositis patients — and in this sort of multi-country international expert dataset that was a retrospective chart review of 336 IIM patients. They found that over a third of them had a moderate to high risk for cardiovascular disease, and of those people only a third of them were actually receiving a statin. So even though there's a risk, maybe we're not paying attention to how it should be managed.
It turns out that, not surprisingly, cardiovascular risk is 20 to 80% higher in people who have dyslipidemia or people taking steroids. But would you have guessed that necrotizing myopathy gives you a 4.6-fold higher risk of cardiovascular events? That's kind of gigantic. What is it about them? And it's not just the steroids, because that's sort of factored in in the analysis, I believe. So something to consider in your IIM patients.
A Turkish study from the Turkish League Against Rheumatism — TAR — studied PSO and PSA patients looking at periodontal disease. Now we know periodontal disease is a risk factor in rheumatoid arthritis; a lot has been written about that. I don't think I've seen this in psoriasis and psoriatic arthritis. Anyway, they found periodontitis in PSA more than PSO — 47 versus 31% — almost significant at p=0.058. But it was significantly associated with disease activity and with enthesitis as measured by the MASES measure. So again, something to look at in your PSA patients and PSO patients. Do they have periodontal disease? You should be addressing it because it's complicating things and may be driving things.
You know, we all make mistakes, even me. And I like that when the listener or reader writes me an email saying, you know, you kind of screwed up on that one. I appreciate that and I usually will put it out there in case it gets seen again so that I don't mislead people.
But I found a really interesting publication this week called "Retractions in Rheumatology." And it's really interesting — these investigators looked at the retractions in rheumatology between 1989 and 2024 and found 381 rheumatology articles that were retracted officially. Two-thirds of them come from Southeast Asia; about half of the cases come from China. Reasons for retraction were mainly what they call scientific misconduct — about three-quarters of the cases — data fabrication, bad and fake peer reviews, duplication of previously published data, authorship deceit; there's a whole bunch of things that go on. 15% data errors, 8% other reasons.
But the important part is that this was pretty uncommon back between 2000 and 2009 — only 18 reports were found in that 9-year period. In a three-year period, 2021–2023, it was 207. So why is it increasing? Is it worrisome? Is this deceitful rheumatologic research and practices, or is it the fact that over
time we have the internet and more eyeballs? You know certainly more eyeballs are a big contributor but both there are there and the author's recommendation was uh early on in a rheumatologist career they need strong heavy exposure to research especially methodology and ethics and I think that that would go a long way um in the education of better rheumatologists in the future.
Um, you know, I'm interested in uh serology, rheumatoid factor, CCP. Um, I'm going to be giving a — I gave that lecture at RheumNow Live last year. I'm going to be lecturing on that at RWCS in a few weeks.
Um, the Mayo Clinic did an interesting report. Um uh and this, you know, is Cynthia Crowson, Elena Myasoedova, you know, uh John Davis, all the great, you know, researchers at the Mayo um did a retrospective population study from Olmsted County on RF and CCP in 1,300 plus incident RAs. So the question is who was RF positive? Who was CCP positive? Who was double positive? What does it all mean? Well, they lay it out.
Um, at diagnosis, only 37% were dual positive for RF and CCP. Only 13% were CCP positive at diagnosis only at diagnosis and only 12%. What again they had 38% who were seronegative. So when you add all those combinations of positivity up, you know, it was again that 60% number we often quote and 30% being seronegative. But I didn't know that so few were double positive um or even single positive.
Ultimately being double positive um resulted in a higher risk of erosive disease and future flares. Um 31% were going to have erosions future flares in double positives versus I guess single or zero negatives with 69% versus 59%. Only rheumatoid factor positivity um related to mortality risk. So we do know that CCP has a really really strong um a really much more so an RA erosive risk and CCP probably has a greater risk of developing RA than does RF. Um and there are certainly other autoantibodies in play that we don't often measure but rheumatoid factor has a higher mortality risk and I find that um interesting.
Um if you like this subject um you should look at um I have a few videos up right now called advanced practice rheumatology. I did it as a part of our um a campaign in December and in January. I got one up on the evaluation of the rheumatic patient, methotrexate um difficult to treat RA. These are short roughly 10 12 minute videos. Um I got one up on RF and CCP and I throw in a little sed rate and CRP for you. Um you might want to look at that especially if you're uh an APP looking to um strengthen your knowledge base.
Again, 2026 RheumNow Live — great me great rheumatologists go to great meetings like this. I hope you'll join Arty Kavanaugh and I and a powerhouse faculty on February 7th and 8th in Dallas. Um you can register at RheumNow.live. Take care of yourselves. We'll talk next week.
And the last one is registration gives you, and I think it's the number one reason, access and download to more than 400 review questions from this year's meeting 2026, from the 2025 and the 2024 meeting. It's a lot of questions. It's really good. So certainly enough reasons.
When I look over the program, there's a few things that really jump out at me, and that's when we begin on Saturday morning. We've got a session, we call them pods, on RA, and Elena Myasoedova is talking about mortality in RA. And you know, why there's a trend downward that looks good, but still there's bad news, why we sort of stalled, why your DMARD therapies are the first most important thing you can do to reduce mortality risk in RA, but it's still not enough and there's more you got to do.
Second on the agenda is Kristen Deane from Colorado. This is the center where all the great research is being done on the earliest biology that starts RA, pre-clinical RA, at-risk disease, and this mucosal hypothesis theory that they're working on, and she's one of the main investigators. You think you need to know this because it is this interface, I think, with the environment through the mucosa, inhaled, GI, that we're going to find 10 years from now is where we're going to focus prevention of disease. And that's just my idea.
Next down the program is from a friend from HSS, Susan Goodman. You may not know Susan Goodman, but she's done the ACR task force and all the great work on how we should manage our patients perioperatively. And it happens and sometimes we don't quite know what to do with their therapies, what the surgeons are saying. She's written the guidelines. She's the guru. She's the source. She'll be on stage.
Bob Terkeltaub is maybe the world's greatest authority in gout and he'll be giving two gout talks, one on gout pearls and the other one on the rich history of gout. You don't want to miss this.
Next, you know, Arty and I, we're New Yorkers, but we moved to Texas and we like, you know, sort of this Texas music scene. And in the '90s, we actually got into, we discovered the Dixie Chicks. Well, we don't have the Dixie Chicks showing up. We got the spondyloarthritis chicks showing up. And that may be sexist, but I'm telling you, these two gals together, Katherine Bakewell and Jessica Walsh, two friends, two academics from Utah, are going to be on stage and they're giving, you know, their talks on spondyloarthritis, but you know, it's going to be much more. They're doing a tandem side by side thing, and it's not just going to be highly informative, it's going to be entertaining, because they are really, really good.
Two more. Matt Baker from Stanford is going to talk about all the hot stuff going on in Sjögren's. You know, the drought is over on therapy. We've got therapies coming in and maybe you don't know about them. This includes Nipocalimab, Telitacicept, Ianalumab — that was actually presented, a few of these were presented, including the NEPTUNE 1 and 2 trials presented as positive phase three trials at ACR. This is good news for Sjögren's.
And then lastly, on the last day, Michael Putman, who's been managing our pre-learns for this meeting, and if you haven't seen Michael's pre-learns, you're really missing out. And he's going to give an address on relapses of PMR and GCA. Is it all about steroids or is it all not about the steroids? Michael's going to tell us.
All right, so this week on the podcast, we got a number of things that are worth reviewing. The Journal of Rheumatology has an interesting report about remission in RA and lupus. This is a single center study from Dresden, Germany, led by Michael Aringer, and I like this study because it put some hard numbers on some real world
patients. So they're looking at 100 RA and 100 lupus patients from their center. And they use standard measures for remission — SLEDAI and SLEI. And what do you think they found in lupus? 100 lupus patients, 392 visits. I was shocked by this. 88% achieved either remission or low disease activity state in lupus. Was it as good in RA? It was better in RA. 91% of almost 400 RA visits in 100 patients. No difference between RA and lupus as far as how often they're achieving remission, but they did actually have some more remissions in lupus than RA because we accepted remission and LDA as the outcome measure there — that 88, 91% — but there were more remissions in lupus: 79% versus 69% in RA. And I find that really surprising, but this is the real world. This is probably what you're seeing.
Other good news this week comes from two different sources. The Lupus Foundation of America announced that the US government House of Representatives has approved $27 million for lupus funding in 2026. In 2025, the whole thing was a new administration, all these cutbacks, research is being screwed. Well, it looks like a lot of that money is coming back. And that money is going to be available from the CDC, the Department of Defense, and other agencies. At the CDC, funding increased by 40%. At OMB by 33%, and $415 million has been put into the NIH budget for lupus. So this is really good news, especially if you're a lupus researcher.
Also this week, there was a stakeholders meeting called the Lupus Accelerating Breakthroughs Consortium, and they looked at skin lupus and outcomes. I think it was sort of a documenting paper where, as a consortium of lupus leaders, the meeting and the paper has all the stakeholders, including representatives of the FDA. And they say that the CLASI measure should be the recommended measure. That's the Cutaneous Lupus Erythematosus Disease Area and Severity Index — I think it was established by Victoria Werth at the University of Pennsylvania. She's got a version of it for dermatomyositis. So CLASI should be the primary endpoint in clinical trials that can be used to get drugs approved in lupus.
My beef in lupus is that it's really hard to prove a drug works in lupus with the current measures. Although the SRI-4 seems to have furthered things in the last 10 years, it's still hard to get a general lupus indication. If I'm developing a drug, I'm going after a single indication. And why not go after CLE — lupus skin disease — and why not use the CLASI as your primary endpoint? The FDA is going to accept it now, and we have consensus and guidelines and experts on this. This should really further lupus research and drug development.
JAMA published this week an interesting general paper about deprescribing. Yes, deprescribing — you know, this is really important, and I brought this up during ACR because the ACR updated its JIA guidelines. It's the systemic JIA guidelines that was presented by Susan Shenoi. An important part of their update to JIA treatment guidelines — as you can imagine, this drug, not that drug, whatever — was the component of deprescribing and down-ratcheting therapy as we are adding on therapy. And that's really never been discussed, and this leads to the problem of patient confusion through polypharmacy and safety issues, does it not.
So this JAMA paper basically shows if you employ two different interventions using an EHR — your electronic health record — in a study of 1,146 patients, most of them being older (mean age 74), they were able to either reduce the number of drugs being used — deprescribing — by either 6.12% or 10.4%. And the overall approach to using the EHR as a reminder to deprescribe can lead to 40% more success in deprescribing. It is something we should talk about, something we should think about.
Again, I tell my patients, especially the ones I'm seeing that have that long laundry list and they're confused about their drugs — I tell them and I write down: if another doctor is going to give you two more drugs, you've got to say, "Oh, good, thank you, but Dr. Cush said if you're going to give me two, you've got to take two away." So it's got to be zero-sum management, or even again, deprescribing. The simpler the regimen, the more the compliance. The more the compliance, the better the outcomes.
Speaking of outcomes, there is the STRONG-STAR Consortium, started out of I think Fort Hood, Texas and the military base there. They published a report in Arthritis Care and Research about a longitudinal study of 1,761 military service members and their assessment before and after they were deployed. They found that the prevalence in males and females pre-deployment was about 2%. But post-deployment — meaning after they went to wherever they went — fibromyalgia meeting criteria went up to 8% in males and 11% in women.
A significant change. Underlying all this was PTSD. It turned out that if you had PTSD before you were deployed, you had a three-fold higher risk of fibromyalgia after deployment. And then similarly if you have PTSD before and after, it went up from 21 to 23% in males and 18 to 26% in females, suggesting a slightly bigger effect in females. Pain being a bigger effect in females.
I again — this STRONG STAR Consortium has published in the past about military service and the risk of fibromyalgia, and it's an underlying feature in that Gulf War syndrome, a lot of which was fibromyalgia-like disease. I think this is what underlies the post-COVID syndrome. And so, again, I applaud them for their efforts.
Another interesting effort — and again this is a stone in my shoe, this is a bug that I keep going back to — is the use of ADHD drugs in our patients. You know, they're good for ADHD, are they not? That's why they developed them. They're FDA approved. And there are four of them that are out there on the market. But in our patients, it leads to worse sleep. Worse sleep leads to fibromyalgia. Fibromyalgia and ADHD drugs leads to, you know, them seeing you thinking they've got multicentric reticulohistiocytosis or whatever they're worried about.
So, a Lancet study of a European EHR network called DARWIN showed a shocking statistic that in five major countries in Europe, all the biggies, the use of ADHD drugs more than doubled between 2010 and 2023. In some places it went up fivefold. In the UK it went up 20-fold in females, 15-fold in males. What?
Again, look at the drugs when they show up in your office. I try to deprescribe ADHD drugs. I know their utility in severe ADHD, especially in children. I think they tend to be overused in adults, in America at least.
Seminars in Arthritis and Rheumatism looked at the cardiovascular risk in idiopathic inflammatory myopathy patients — myositis patients — and in this sort of multi-country international expert dataset that was a retrospective chart review of 336 IIM patients. They found that over a third of them had a moderate to high risk for cardiovascular disease, and of those people only a third of them were actually receiving a statin. So even though there's a risk, maybe we're not paying attention to how it should be managed.
It turns out that, not surprisingly, cardiovascular risk is 20 to 80% higher in people who have dyslipidemia or people taking steroids. But would you have guessed that necrotizing myopathy gives you a 4.6-fold higher risk of cardiovascular events? That's kind of gigantic. What is it about them? And it's not just the steroids, because that's sort of factored in in the analysis, I believe. So something to consider in your IIM patients.
A Turkish study from the Turkish League Against Rheumatism — TAR — studied PSO and PSA patients looking at periodontal disease. Now we know periodontal disease is a risk factor in rheumatoid arthritis; a lot has been written about that. I don't think I've seen this in psoriasis and psoriatic arthritis. Anyway, they found periodontitis in PSA more than PSO — 47 versus 31% — almost significant at p=0.058. But it was significantly associated with disease activity and with enthesitis as measured by the MASES measure. So again, something to look at in your PSA patients and PSO patients. Do they have periodontal disease? You should be addressing it because it's complicating things and may be driving things.
You know, we all make mistakes, even me. And I like that when the listener or reader writes me an email saying, you know, you kind of screwed up on that one. I appreciate that and I usually will put it out there in case it gets seen again so that I don't mislead people.
But I found a really interesting publication this week called "Retractions in Rheumatology." And it's really interesting — these investigators looked at the retractions in rheumatology between 1989 and 2024 and found 381 rheumatology articles that were retracted officially. Two-thirds of them come from Southeast Asia; about half of the cases come from China. Reasons for retraction were mainly what they call scientific misconduct — about three-quarters of the cases — data fabrication, bad and fake peer reviews, duplication of previously published data, authorship deceit; there's a whole bunch of things that go on. 15% data errors, 8% other reasons.
But the important part is that this was pretty uncommon back between 2000 and 2009 — only 18 reports were found in that 9-year period. In a three-year period, 2021–2023, it was 207. So why is it increasing? Is it worrisome? Is this deceitful rheumatologic research and practices, or is it the fact that over
time we have the internet and more eyeballs? You know certainly more eyeballs are a big contributor but both there are there and the author's recommendation was uh early on in a rheumatologist career they need strong heavy exposure to research especially methodology and ethics and I think that that would go a long way um in the education of better rheumatologists in the future.
Um, you know, I'm interested in uh serology, rheumatoid factor, CCP. Um, I'm going to be giving a — I gave that lecture at RheumNow Live last year. I'm going to be lecturing on that at RWCS in a few weeks.
Um, the Mayo Clinic did an interesting report. Um uh and this, you know, is Cynthia Crowson, Elena Myasoedova, you know, uh John Davis, all the great, you know, researchers at the Mayo um did a retrospective population study from Olmsted County on RF and CCP in 1,300 plus incident RAs. So the question is who was RF positive? Who was CCP positive? Who was double positive? What does it all mean? Well, they lay it out.
Um, at diagnosis, only 37% were dual positive for RF and CCP. Only 13% were CCP positive at diagnosis only at diagnosis and only 12%. What again they had 38% who were seronegative. So when you add all those combinations of positivity up, you know, it was again that 60% number we often quote and 30% being seronegative. But I didn't know that so few were double positive um or even single positive.
Ultimately being double positive um resulted in a higher risk of erosive disease and future flares. Um 31% were going to have erosions future flares in double positives versus I guess single or zero negatives with 69% versus 59%. Only rheumatoid factor positivity um related to mortality risk. So we do know that CCP has a really really strong um a really much more so an RA erosive risk and CCP probably has a greater risk of developing RA than does RF. Um and there are certainly other autoantibodies in play that we don't often measure but rheumatoid factor has a higher mortality risk and I find that um interesting.
Um if you like this subject um you should look at um I have a few videos up right now called advanced practice rheumatology. I did it as a part of our um a campaign in December and in January. I got one up on the evaluation of the rheumatic patient, methotrexate um difficult to treat RA. These are short roughly 10 12 minute videos. Um I got one up on RF and CCP and I throw in a little sed rate and CRP for you. Um you might want to look at that especially if you're uh an APP looking to um strengthen your knowledge base.
Again, 2026 RheumNow Live — great me great rheumatologists go to great meetings like this. I hope you'll join Arty Kavanaugh and I and a powerhouse faculty on February 7th and 8th in Dallas. Um you can register at RheumNow.live. Take care of yourselves. We'll talk next week.
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