Follow the Money (4.23.2026) Save
Follow the Money (4.23.2026)
Transcription
It's April 23rd, 2026. This is the RheumNow podcast. Hi, I'm Dr. Jack Cush, executive editor of RheumNow.com. This week, the podcast is all about follow the money. Maybe that'll be apparent by the end of the podcast.
Last ACR, I got excited about an abstract that showed rheumatoid factor had predictive value in EGPA. I thought it was surprising. I wouldn't have expected it. It was interesting. I hope you remember it. That's why my lead story today is on citrullinated histone 3 in patients with ANCA-associated vasculitis.
So the story here — it's a small study. It's 65 patients with either MPA or GPA and they looked at biomarkers and reported on citrullinated histone 3. And that comes about in the formation of neutrophil extracellular traps, which we know is a bad player in autoimmune disease. It's driven by alpha interferon and a number of other signals. It's a main amplifier and they looked at this as a possible marker of neutrophil activation.
So they studied it in 65 patients with MPA and GPA and showed that citrullinated histone 3 had a significant correlation with both the BVAS and the risk of end-stage renal disease. BVAS, the Birmingham Vasculitis Activity Score, had a correlation coefficient of 0.39, almost 0.4. You know, not fabulous, but significant and good enough, saying that there's probably something there. And the risk of end-stage kidney disease was about 18% higher in the presence of this specific histone.
And again I like it because it's a citrullinated product that has a relationship then to CCP. And that rheumatoid factor EGPA thing makes me think we should be doing rheumatoid factor and CCP and ANA testing in patients with GPA and MPA. I think it tells us that there's a lot going on, that there's heightened immunologic activity and it could be a potentially useful marker. Right now you have to order a CCP or a rheumatoid factor to get maybe the same value. I don't believe that this is commercially available as a lab test for your patients.
A study of perioperative risk when you're using biologics and DMARDs was undertaken through a TriNetX study. As you know, TriNetX is a network of many many many electronic health records where you can do studies that you wouldn't normally be able to do. They link up all the clinical data. They then try to normalize it by doing propensity matching. Some of these TriNetX studies are very very good. Some of them are, you know, I think a stretch.
This one reiterates a point that was made by Dr. Susan Goodman of HSS at RheumNow Live, where she talked about should you continue therapy — biologics, DMARDs — in patients undergoing surgery. The ACR guidelines say yes. This TriNetX study looked at almost 8,000 patients on DMARDs and 2,600 of those people were on biologic DMARDs, and they looked at these RA patients who are undergoing elective hand surgery and what the influence of being on the drug — meaning continuing it or not continuing it.
One-third of the patients under study were continuing their biologic DMARD during hand surgery. And they showed no significant difference as far as key outcomes that the surgeons worry about, that being wound healing and soft tissue infections. Wound healing was the same in both groups — 1.4% — soft tissue infections was either 2 or 1.5%, not significantly different.
You should continue patients on DMARDs and biologics who are undergoing surgery, and to stop it is a bit goofy, especially since these drugs have long half-lives. To really be off the drug would put the patient at risk for flare and inflammation, which is far worse for surgical risk than being on these drugs. Inflammation drives infection risk, not biologics, not DMARDs.
The FDA accepted Genentech's application to extend its indication on ocrelizumab — which as you know is an anti-CD20 monoclonal antibody — recently, what, eight, nine months ago? No, back in September I believe it was approved for lupus nephritis. Now, because they've done the phase three ALLEGORY study showing that ocrelizumab significantly reduces disease activity as measured by general lupus measures of disease activity, that is going to be now their extended indication. They've submitted it, it's not yet approved, but it looks good based on this data, and we should look forward to that in the future.
As you may know, INCEPTION is an ankylosing spondylitis, or axial spondyloarthritis, cohort study. In this specific study that we reported, 631 patients who had ankylosing spondylitis — sorry, axial spondyloarthritis — did not have hypertension, were started on non-steroidals and compared to axSpA patients with no hypertension who did not take non-steroidals, following them over 10 years, and found no significant increase in the risk of incident hypertension. So in early axSpA, non-steroidals with 10-year follow-up don't seem to cause hypertension. They had a total of 88
cases out of 631. And again it was not significant. I bring it up because I don't think many of our fellows or younger rheumatologists are using non-steroidals. I think you've been taught that they're dangerous or they really don't work or whatever, but honestly, what do you have to treat pain, especially early on, especially before you start them on other more aggressive therapies for axSpA? I still use non-steroidals except for when I can't use them and shouldn't use them and there are contraindications, right? Age is a relative contraindication but obviously no hematologic, cardiac, and GI reasons would be to avoid non-steroidals as adjunctive therapy in all your patients, not just axial spondylitis.
So one of the issues I think that we worry about in axSpA is x-ray progression. We really don't have great studies on that because unlike RA and PsA where you could see x-ray progression in as little as 16 weeks and certainly within one or two years, x-ray progression and the methodology used to prove that in axSpA is slow, slow — you need really two, five, ten year studies. So I like this study that looked at x-ray progression over time in a large cohort of 3,400 AS patients, 75% male, 84% B27 positive, and they looked at the influence of comorbidity. We know comorbidity and other disorders is a bad player for disease severity, and such was shown here — patients who had greater than two comorbidities had a much higher rate of x-ray progression. Also the comorbidities specifically of psoriasis and uveitis were associated with more x-ray progression in AS patients.
Again, the question is, this data — most other people including primary care do not. Who's managing the comorbidity? You should be managing the comorbidity, at least starting the management and ensuring proper management if you're not going to take it on wholeheartedly going forward. It is a big, big issue throughout all the disorders that we treat with inflammatory arthritis.
A big concern — and I learned from Christina Charles-Scaman at RheumNow Live two years ago when she lectured on dermatomyositis — is that ILD is a bad player throughout the connective tissue disease and autoimmune disease spectrum. PsA — well, it's rare in PsA, right — in RA, in lupus, and especially in systemic sclerosis. I mean, the outcomes are really bad, and that's why we devoted a whole month to interstitial lung disease back in September on RheumNow. But Christina showed me that dermatomyositis patients with ILD do really, really well, and you just have to treat them and you can turn around their — it can respond.
So I like this study coming out of China, which is a target emulation trial of MDA5-positive dermatomyositis with ILD. Dermatomyositis — bad. MDA5-positive — even worse. As you know, MDA5 has bad skin disease and bad progressive lung disease as part of the autoantibody association. So what they did was they studied 106 patients who were taking upadacitinib and 328 who were taking tofacitinib and looked at their outcomes, especially the devastating outcome — one being six-month risk of being transplant-free. It's a fairly short follow-up but the numbers in the outcomes were good: 72% and 67% for upadacitinib and tofacitinib respectively. And that shows you, one, that dermatomyositis can respond. Two, it likes to respond to JAK inhibition, and there's a lot of evidence of that, not just this study, but this study sort of supports the pre-existing evidence.
And all this is encouraging because we are now on the verge of the FDA approving a JAK inhibitor. I think it's brepocitinib that we talked about last week — the New England Journal paper in dermatomyositis. Looks very good. And we can expect — I think, I hope — that it'll get approved by the FDA within the next six months.
So in this study, upadacitinib was non-inferior to tofacitinib, meaning they're about the same in MDA5-positive dermatomyositis with ILD.
Other poor outcomes that we worry about — antiphospholipid patients — a lot of things can go wrong there. But thrombocytopenia: we always talk about the triad — recurrent fetal loss, thrombotic events, and thrombocytopenia. I've got to say I haven't seen a lot of that in association with APS. So this was a retrospective study of 432 patients with APS and looked at the influence of thrombocytopenia. Any thrombocytopenia was seen in 142, or 33% — a third. That seems — maybe I'm not looking hard enough, or maybe I'm not looking longitudinally at those patients. But 13% had severe thrombocytopenia, meaning a platelet count of less than 50,000. Who did that happen in? It happened in the APS patients who were classified as having ITP or CAPS — catastrophic antiphospholipid syndrome. And when it was present, it was associated with significantly higher mortality rates.
When this happens, I think it's time to call in the cavalry, the hematologist, and to get aggressive on the management.
of these patients. And there are good new guidelines on that, are there not? That you could look up and help to guide you as well.
Uh, I know rheumatologists and physicians in general over time have been often bothered by direct-to-consumer advertising on television. You know, it is a thing in the United States. It's not in Canada, although American TV goes over the border and that is infuriating, I guess, to some. And the thing is a recent report shows that yes, again DTC is up this year compared to last year. If you look at the top 10 pharma companies on ad spending, that DTC was up to almost $3 billion, up from 2.1 billion last year — $3 billion in 2025, 2.1 in 2024. The total amount spent on DTC from the pharmaceutical industry — I think I saw that it was 35 or 39 billion in 2025. It's a lot, right?
But here's the kicker: the top three spenders in DTC are your drugs. Number one, Skyrizi, 440 million. Number two, Tremfya, 431 million. And number three, Rinvoq, 376 million. You know this because you watch TV. Why do they let this happen? Is it a good thing or a bad thing? I've actually followed this information. I've got a good lecture on this topic. And you know it infuriates physicians because patients come in and ask inappropriately about should I be on Tremfya when I have osteoarthritis, right? Obviously that makes no sense and that means you have to now devote time to this. But the FDA, who has studied this in many ways, including back to when they approved this over 20 years ago, has shown that because of DTC, patients will now discuss with their physicians either drugs or diseases that they would not have normally discussed. And there's very strong evidence for that. And that's why DTC is a part of your medical life.
What may not be a part of your medical life is rare diseases — autoinflammatory diseases like hyper-IgD syndrome, which is due to a genetic defect in mevalonate kinase. It's an MVK deficiency or defect. It's rare. It's autosomal recessive. It's an autoinflammatory disorder where, because of this gene defect, there's exaggerated innate immunity, activation of the inflammasome, that leads to lots and lots of IL-1 beta and probably IL-18 and IL-6 and other things, but mainly IL-1 beta. And they present — in its milder forms, actually, you know there are severe forms of mevalonate kinase deficiency that give a lot of developmental problems and whatnot — but the hyper-IgD syndrome, the periodic febrile syndrome, usually presents in kids as a febrile disorder. It can present in adults and there are actually a number of reports, and this particular report that we put up was a discussion of an adult and the syndrome.
Again, how do these people present? It's usually periodic fever, but it's not like Still's disease or Schnitzler syndrome, which is daily fever — daily quotidian fevers, right, especially in Still's. Here they get fever — they call it a periodic febrile syndrome because they get 3 to 7 days of fever that recur every several weeks, sometimes two times a month. But there's no predictability, no true periodicity.
But what is important diagnostically is two things. One, that the fever bouts are recurrent and they last 3 to 7 days — and that's in contrast to Still's, which is every day; contrast to TRAPS, which is 2 weeks of fever, 10 days to 14 days, right — so 3 to 7 days. And the other big red flag is that they don't meet criteria for Still's. And how do you know? Well, you get someone who you think has Still's, you go to StillsNow.com, you look at the Still's disease diagnosis calculator, you check the boxes on the symptoms, and it'll tell you whether you meet Yamaguchi, Cush, or ILAR criteria for Still's disease — and that's for kids or adults. And if you don't, you're now stuck mislabeling this patient, and that's your invitation to do genetic testing for an autoinflammatory monogenic disorder, which would include MVK deficiency, right.
Again, they present with fever, although not as high as the others — like 101, 102 — just for a few days and up to a week. They have GI symptoms, oral ulcers, myalgia, arthralgia, and they can get serositis. Again, it looks a lot like the other autoinflammatory patients that you've seen. Consider doing the genetic testing.
Uh, consider using monotherapy or combination therapy in RA. You want to get me riled up? Tell me how important monotherapy is in RA and I'm going to tell you — really, the disease I spent my whole life studying and battling and trying to treat — you think is going to be treated by one drug with one mechanism of action? What are you, out of your mind? And I truly believe that to be true. Nonetheless, here's a network meta-analysis report of 31 studies looking at 13 different conventional synthetic DMARDs — traditional oral DMARDs — asking the question: does monotherapy work, using as an outcome does it benefit or —
x-ray progression scores when done annually, and the answer is yes — leflunomide, sulfasalazine, and gold were better than placebo and equal to methotrexate. Congratulations — methotrexate, sulfasalazine, leflunomide, and gold that nobody uses anymore does work as monotherapy. The big fault in this study is why are they looking at monotherapy alone and not comparing it to combination?
I did, after looking at this and reporting this, and you know combination therapy — methotrexate with any combination — Jim O'Dell and the RAIN network proved that methotrexate plus any biologic, tons of studies have proven that combination is the way to go. Hence, and I do this and I'm just thinking about this now, I see a brand new RA, I usually start them on methotrexate and then I order labs and I bring them back. Um, maybe that's good for the very first visit just to make sure everything's good, and then at your second visit, 4 weeks later, why are you not putting them on combination therapy?
I've written about the fact that everybody with RA should also be on hydroxychloroquine. I don't care what you're on, it has the same benefits in RA as it has in lupus. Or instead of adding hydroxychloroquine to methotrexate, use a triple DMARD therapy of the RAIN network, or put them on methotrexate and a biologic. You can always withdraw therapy later on. But why not be aggressive right from the outset? Again, combination works better than mono. Congratulations. Mono does work. But that's 1980s thinking in RA management, is it not?
There was a report this last week from JAMA Network Open about a large cohort of giant cell arteritis patients who were treated with aspirin. So this is a retrospective French study of 14,500 patients over age 50 newly diagnosed with GCA, and a portion of the group got aspirin in low dose and the others did not, and they looked at cardiovascular outcomes — MACE, major adverse cardiovascular events — at one year and at three years. The patients treated with low-dose aspirin had better outcomes, 14% or 22% less — better cardiovascular and all-caused mortality outcomes. That's impressive.
Why would you not then put everyone on aspirin? Well, that's the flip side to the study that showed there was a significant increase in bleeding from the GI tract. And that was only seen in the first year, not in the 3 years. In sub-analyses they showed that the biggest protective effect for the low-dose aspirin group was for MACE in women, where there was a 22% benefit, and also in GCA patients who also had diabetes.
So do you use aspirin or not? I would, unless there was a contraindication to it — and you know the contraindications — and age could be one; age plus GI plus renal plus, obviously you're not going to be putting them on aspirin. But aspirin does have some protective effect, and you know 12 to 20% is nothing to discard — 14, excuse me, to 22% is nothing to discard as being an insignificant benefit. I'd walk a mile for that.
Um, so the big downer of the week was rheumatology salaries. Medscape came up with its annual report on physician salaries, congratulating us physicians — I'm patting myself on the back 'cause I'm one of those — with a roughly 3% increase in salaries overall, with eight specialties earning more than $500,000 per year. Who are these people? And we know they're not rheumatologists who haven't invested in Bitcoin.
So, um, yeah, the bad news is a survey of almost 6,000 physicians, only 1% of whom, by the way, were rheumatologists, showed [snorts] that rheumatology ranked in the bottom four of overall annual salaries in the United States. That was $284,000 according to this Medscape survey. Um, Doximity did a similar survey showing that it was about the same, maybe about $20,000–$30,000 less. But the other bad news from Doximity and other reports is that the lowest paid are pediatric rheumatologists. I'm sorry, they're the second lowest paid. I think it was — I can't remember who it was — I think it might have been physiatry that might have been the second lowest paid. Um, and that's sad. Their average salary was $231,000 per year.
So, you know, should we cry? Should we invest in Bitcoin? No. Again, you got the best job ever. Rheumatologists are happy for a lot of reasons. One is the quality of the interaction. Two is the intellectual stimulation. Three is that you're well paid. Four [snorts] is that you love your job. If you want more money, there's a lot of ways to make more money. Get your own website, start your own blog and your own podcast. Good luck — maybe you'll make some more money. But there's a lot of other things, and a lot of rheumatologists do have side gigs to augment their income. And by the way, that's a nationwide salary. If you look at that Medscape article, salaries differ significantly throughout the country. They're highest actually on the West Coast. Um, and there are other things in there that
tell you about how you can do better. One of the biggest problems is — first off, the other thing they said is rheumatologists expect their salary to be the same this year as it was last year. I mean, we're not — there were several specialties, I think there were eight of them, that had significantly more than 5% increase in salary expectations for next year. Rheumatology is not one. We're expecting the same next year as we got this year, as we got last year. And last year it was again $284,000.
But they, you know, they made some points in there, including that most physicians are not very good at negotiating salary. You should think about that if you want to increase your salary. Anyway, hope you enjoyed this podcast. I did. We'll talk next week. Take care.
Last ACR, I got excited about an abstract that showed rheumatoid factor had predictive value in EGPA. I thought it was surprising. I wouldn't have expected it. It was interesting. I hope you remember it. That's why my lead story today is on citrullinated histone 3 in patients with ANCA-associated vasculitis.
So the story here — it's a small study. It's 65 patients with either MPA or GPA and they looked at biomarkers and reported on citrullinated histone 3. And that comes about in the formation of neutrophil extracellular traps, which we know is a bad player in autoimmune disease. It's driven by alpha interferon and a number of other signals. It's a main amplifier and they looked at this as a possible marker of neutrophil activation.
So they studied it in 65 patients with MPA and GPA and showed that citrullinated histone 3 had a significant correlation with both the BVAS and the risk of end-stage renal disease. BVAS, the Birmingham Vasculitis Activity Score, had a correlation coefficient of 0.39, almost 0.4. You know, not fabulous, but significant and good enough, saying that there's probably something there. And the risk of end-stage kidney disease was about 18% higher in the presence of this specific histone.
And again I like it because it's a citrullinated product that has a relationship then to CCP. And that rheumatoid factor EGPA thing makes me think we should be doing rheumatoid factor and CCP and ANA testing in patients with GPA and MPA. I think it tells us that there's a lot going on, that there's heightened immunologic activity and it could be a potentially useful marker. Right now you have to order a CCP or a rheumatoid factor to get maybe the same value. I don't believe that this is commercially available as a lab test for your patients.
A study of perioperative risk when you're using biologics and DMARDs was undertaken through a TriNetX study. As you know, TriNetX is a network of many many many electronic health records where you can do studies that you wouldn't normally be able to do. They link up all the clinical data. They then try to normalize it by doing propensity matching. Some of these TriNetX studies are very very good. Some of them are, you know, I think a stretch.
This one reiterates a point that was made by Dr. Susan Goodman of HSS at RheumNow Live, where she talked about should you continue therapy — biologics, DMARDs — in patients undergoing surgery. The ACR guidelines say yes. This TriNetX study looked at almost 8,000 patients on DMARDs and 2,600 of those people were on biologic DMARDs, and they looked at these RA patients who are undergoing elective hand surgery and what the influence of being on the drug — meaning continuing it or not continuing it.
One-third of the patients under study were continuing their biologic DMARD during hand surgery. And they showed no significant difference as far as key outcomes that the surgeons worry about, that being wound healing and soft tissue infections. Wound healing was the same in both groups — 1.4% — soft tissue infections was either 2 or 1.5%, not significantly different.
You should continue patients on DMARDs and biologics who are undergoing surgery, and to stop it is a bit goofy, especially since these drugs have long half-lives. To really be off the drug would put the patient at risk for flare and inflammation, which is far worse for surgical risk than being on these drugs. Inflammation drives infection risk, not biologics, not DMARDs.
The FDA accepted Genentech's application to extend its indication on ocrelizumab — which as you know is an anti-CD20 monoclonal antibody — recently, what, eight, nine months ago? No, back in September I believe it was approved for lupus nephritis. Now, because they've done the phase three ALLEGORY study showing that ocrelizumab significantly reduces disease activity as measured by general lupus measures of disease activity, that is going to be now their extended indication. They've submitted it, it's not yet approved, but it looks good based on this data, and we should look forward to that in the future.
As you may know, INCEPTION is an ankylosing spondylitis, or axial spondyloarthritis, cohort study. In this specific study that we reported, 631 patients who had ankylosing spondylitis — sorry, axial spondyloarthritis — did not have hypertension, were started on non-steroidals and compared to axSpA patients with no hypertension who did not take non-steroidals, following them over 10 years, and found no significant increase in the risk of incident hypertension. So in early axSpA, non-steroidals with 10-year follow-up don't seem to cause hypertension. They had a total of 88
cases out of 631. And again it was not significant. I bring it up because I don't think many of our fellows or younger rheumatologists are using non-steroidals. I think you've been taught that they're dangerous or they really don't work or whatever, but honestly, what do you have to treat pain, especially early on, especially before you start them on other more aggressive therapies for axSpA? I still use non-steroidals except for when I can't use them and shouldn't use them and there are contraindications, right? Age is a relative contraindication but obviously no hematologic, cardiac, and GI reasons would be to avoid non-steroidals as adjunctive therapy in all your patients, not just axial spondylitis.
So one of the issues I think that we worry about in axSpA is x-ray progression. We really don't have great studies on that because unlike RA and PsA where you could see x-ray progression in as little as 16 weeks and certainly within one or two years, x-ray progression and the methodology used to prove that in axSpA is slow, slow — you need really two, five, ten year studies. So I like this study that looked at x-ray progression over time in a large cohort of 3,400 AS patients, 75% male, 84% B27 positive, and they looked at the influence of comorbidity. We know comorbidity and other disorders is a bad player for disease severity, and such was shown here — patients who had greater than two comorbidities had a much higher rate of x-ray progression. Also the comorbidities specifically of psoriasis and uveitis were associated with more x-ray progression in AS patients.
Again, the question is, this data — most other people including primary care do not. Who's managing the comorbidity? You should be managing the comorbidity, at least starting the management and ensuring proper management if you're not going to take it on wholeheartedly going forward. It is a big, big issue throughout all the disorders that we treat with inflammatory arthritis.
A big concern — and I learned from Christina Charles-Scaman at RheumNow Live two years ago when she lectured on dermatomyositis — is that ILD is a bad player throughout the connective tissue disease and autoimmune disease spectrum. PsA — well, it's rare in PsA, right — in RA, in lupus, and especially in systemic sclerosis. I mean, the outcomes are really bad, and that's why we devoted a whole month to interstitial lung disease back in September on RheumNow. But Christina showed me that dermatomyositis patients with ILD do really, really well, and you just have to treat them and you can turn around their — it can respond.
So I like this study coming out of China, which is a target emulation trial of MDA5-positive dermatomyositis with ILD. Dermatomyositis — bad. MDA5-positive — even worse. As you know, MDA5 has bad skin disease and bad progressive lung disease as part of the autoantibody association. So what they did was they studied 106 patients who were taking upadacitinib and 328 who were taking tofacitinib and looked at their outcomes, especially the devastating outcome — one being six-month risk of being transplant-free. It's a fairly short follow-up but the numbers in the outcomes were good: 72% and 67% for upadacitinib and tofacitinib respectively. And that shows you, one, that dermatomyositis can respond. Two, it likes to respond to JAK inhibition, and there's a lot of evidence of that, not just this study, but this study sort of supports the pre-existing evidence.
And all this is encouraging because we are now on the verge of the FDA approving a JAK inhibitor. I think it's brepocitinib that we talked about last week — the New England Journal paper in dermatomyositis. Looks very good. And we can expect — I think, I hope — that it'll get approved by the FDA within the next six months.
So in this study, upadacitinib was non-inferior to tofacitinib, meaning they're about the same in MDA5-positive dermatomyositis with ILD.
Other poor outcomes that we worry about — antiphospholipid patients — a lot of things can go wrong there. But thrombocytopenia: we always talk about the triad — recurrent fetal loss, thrombotic events, and thrombocytopenia. I've got to say I haven't seen a lot of that in association with APS. So this was a retrospective study of 432 patients with APS and looked at the influence of thrombocytopenia. Any thrombocytopenia was seen in 142, or 33% — a third. That seems — maybe I'm not looking hard enough, or maybe I'm not looking longitudinally at those patients. But 13% had severe thrombocytopenia, meaning a platelet count of less than 50,000. Who did that happen in? It happened in the APS patients who were classified as having ITP or CAPS — catastrophic antiphospholipid syndrome. And when it was present, it was associated with significantly higher mortality rates.
When this happens, I think it's time to call in the cavalry, the hematologist, and to get aggressive on the management.
of these patients. And there are good new guidelines on that, are there not? That you could look up and help to guide you as well.
Uh, I know rheumatologists and physicians in general over time have been often bothered by direct-to-consumer advertising on television. You know, it is a thing in the United States. It's not in Canada, although American TV goes over the border and that is infuriating, I guess, to some. And the thing is a recent report shows that yes, again DTC is up this year compared to last year. If you look at the top 10 pharma companies on ad spending, that DTC was up to almost $3 billion, up from 2.1 billion last year — $3 billion in 2025, 2.1 in 2024. The total amount spent on DTC from the pharmaceutical industry — I think I saw that it was 35 or 39 billion in 2025. It's a lot, right?
But here's the kicker: the top three spenders in DTC are your drugs. Number one, Skyrizi, 440 million. Number two, Tremfya, 431 million. And number three, Rinvoq, 376 million. You know this because you watch TV. Why do they let this happen? Is it a good thing or a bad thing? I've actually followed this information. I've got a good lecture on this topic. And you know it infuriates physicians because patients come in and ask inappropriately about should I be on Tremfya when I have osteoarthritis, right? Obviously that makes no sense and that means you have to now devote time to this. But the FDA, who has studied this in many ways, including back to when they approved this over 20 years ago, has shown that because of DTC, patients will now discuss with their physicians either drugs or diseases that they would not have normally discussed. And there's very strong evidence for that. And that's why DTC is a part of your medical life.
What may not be a part of your medical life is rare diseases — autoinflammatory diseases like hyper-IgD syndrome, which is due to a genetic defect in mevalonate kinase. It's an MVK deficiency or defect. It's rare. It's autosomal recessive. It's an autoinflammatory disorder where, because of this gene defect, there's exaggerated innate immunity, activation of the inflammasome, that leads to lots and lots of IL-1 beta and probably IL-18 and IL-6 and other things, but mainly IL-1 beta. And they present — in its milder forms, actually, you know there are severe forms of mevalonate kinase deficiency that give a lot of developmental problems and whatnot — but the hyper-IgD syndrome, the periodic febrile syndrome, usually presents in kids as a febrile disorder. It can present in adults and there are actually a number of reports, and this particular report that we put up was a discussion of an adult and the syndrome.
Again, how do these people present? It's usually periodic fever, but it's not like Still's disease or Schnitzler syndrome, which is daily fever — daily quotidian fevers, right, especially in Still's. Here they get fever — they call it a periodic febrile syndrome because they get 3 to 7 days of fever that recur every several weeks, sometimes two times a month. But there's no predictability, no true periodicity.
But what is important diagnostically is two things. One, that the fever bouts are recurrent and they last 3 to 7 days — and that's in contrast to Still's, which is every day; contrast to TRAPS, which is 2 weeks of fever, 10 days to 14 days, right — so 3 to 7 days. And the other big red flag is that they don't meet criteria for Still's. And how do you know? Well, you get someone who you think has Still's, you go to StillsNow.com, you look at the Still's disease diagnosis calculator, you check the boxes on the symptoms, and it'll tell you whether you meet Yamaguchi, Cush, or ILAR criteria for Still's disease — and that's for kids or adults. And if you don't, you're now stuck mislabeling this patient, and that's your invitation to do genetic testing for an autoinflammatory monogenic disorder, which would include MVK deficiency, right.
Again, they present with fever, although not as high as the others — like 101, 102 — just for a few days and up to a week. They have GI symptoms, oral ulcers, myalgia, arthralgia, and they can get serositis. Again, it looks a lot like the other autoinflammatory patients that you've seen. Consider doing the genetic testing.
Uh, consider using monotherapy or combination therapy in RA. You want to get me riled up? Tell me how important monotherapy is in RA and I'm going to tell you — really, the disease I spent my whole life studying and battling and trying to treat — you think is going to be treated by one drug with one mechanism of action? What are you, out of your mind? And I truly believe that to be true. Nonetheless, here's a network meta-analysis report of 31 studies looking at 13 different conventional synthetic DMARDs — traditional oral DMARDs — asking the question: does monotherapy work, using as an outcome does it benefit or —
x-ray progression scores when done annually, and the answer is yes — leflunomide, sulfasalazine, and gold were better than placebo and equal to methotrexate. Congratulations — methotrexate, sulfasalazine, leflunomide, and gold that nobody uses anymore does work as monotherapy. The big fault in this study is why are they looking at monotherapy alone and not comparing it to combination?
I did, after looking at this and reporting this, and you know combination therapy — methotrexate with any combination — Jim O'Dell and the RAIN network proved that methotrexate plus any biologic, tons of studies have proven that combination is the way to go. Hence, and I do this and I'm just thinking about this now, I see a brand new RA, I usually start them on methotrexate and then I order labs and I bring them back. Um, maybe that's good for the very first visit just to make sure everything's good, and then at your second visit, 4 weeks later, why are you not putting them on combination therapy?
I've written about the fact that everybody with RA should also be on hydroxychloroquine. I don't care what you're on, it has the same benefits in RA as it has in lupus. Or instead of adding hydroxychloroquine to methotrexate, use a triple DMARD therapy of the RAIN network, or put them on methotrexate and a biologic. You can always withdraw therapy later on. But why not be aggressive right from the outset? Again, combination works better than mono. Congratulations. Mono does work. But that's 1980s thinking in RA management, is it not?
There was a report this last week from JAMA Network Open about a large cohort of giant cell arteritis patients who were treated with aspirin. So this is a retrospective French study of 14,500 patients over age 50 newly diagnosed with GCA, and a portion of the group got aspirin in low dose and the others did not, and they looked at cardiovascular outcomes — MACE, major adverse cardiovascular events — at one year and at three years. The patients treated with low-dose aspirin had better outcomes, 14% or 22% less — better cardiovascular and all-caused mortality outcomes. That's impressive.
Why would you not then put everyone on aspirin? Well, that's the flip side to the study that showed there was a significant increase in bleeding from the GI tract. And that was only seen in the first year, not in the 3 years. In sub-analyses they showed that the biggest protective effect for the low-dose aspirin group was for MACE in women, where there was a 22% benefit, and also in GCA patients who also had diabetes.
So do you use aspirin or not? I would, unless there was a contraindication to it — and you know the contraindications — and age could be one; age plus GI plus renal plus, obviously you're not going to be putting them on aspirin. But aspirin does have some protective effect, and you know 12 to 20% is nothing to discard — 14, excuse me, to 22% is nothing to discard as being an insignificant benefit. I'd walk a mile for that.
Um, so the big downer of the week was rheumatology salaries. Medscape came up with its annual report on physician salaries, congratulating us physicians — I'm patting myself on the back 'cause I'm one of those — with a roughly 3% increase in salaries overall, with eight specialties earning more than $500,000 per year. Who are these people? And we know they're not rheumatologists who haven't invested in Bitcoin.
So, um, yeah, the bad news is a survey of almost 6,000 physicians, only 1% of whom, by the way, were rheumatologists, showed [snorts] that rheumatology ranked in the bottom four of overall annual salaries in the United States. That was $284,000 according to this Medscape survey. Um, Doximity did a similar survey showing that it was about the same, maybe about $20,000–$30,000 less. But the other bad news from Doximity and other reports is that the lowest paid are pediatric rheumatologists. I'm sorry, they're the second lowest paid. I think it was — I can't remember who it was — I think it might have been physiatry that might have been the second lowest paid. Um, and that's sad. Their average salary was $231,000 per year.
So, you know, should we cry? Should we invest in Bitcoin? No. Again, you got the best job ever. Rheumatologists are happy for a lot of reasons. One is the quality of the interaction. Two is the intellectual stimulation. Three is that you're well paid. Four [snorts] is that you love your job. If you want more money, there's a lot of ways to make more money. Get your own website, start your own blog and your own podcast. Good luck — maybe you'll make some more money. But there's a lot of other things, and a lot of rheumatologists do have side gigs to augment their income. And by the way, that's a nationwide salary. If you look at that Medscape article, salaries differ significantly throughout the country. They're highest actually on the West Coast. Um, and there are other things in there that
tell you about how you can do better. One of the biggest problems is — first off, the other thing they said is rheumatologists expect their salary to be the same this year as it was last year. I mean, we're not — there were several specialties, I think there were eight of them, that had significantly more than 5% increase in salary expectations for next year. Rheumatology is not one. We're expecting the same next year as we got this year, as we got last year. And last year it was again $284,000.
But they, you know, they made some points in there, including that most physicians are not very good at negotiating salary. You should think about that if you want to increase your salary. Anyway, hope you enjoyed this podcast. I did. We'll talk next week. Take care.
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