Seronegative RA Disease Activity (7.17.2026) Save
Transcription
It's July 17th, 2026. This is the RheumNow podcast. Hi, I'm Dr. Jack Cush, executive editor of RheumNow.com. I'm coming to you from the FSR meeting in Orlando, Florida Society of Rheumatology. Always an excellent meeting. I lectured here today on seropositive and seronegative RA. Which one should you worry about? And tomorrow I'm going to be lecturing on Moneyball rheumatology. I think you can find that on the podcast.
So today we're going to talk about predicting cancer in dermatomyositis patients, saliva as home testing, and some scleroderma updates.
Let's begin with genicular artery embolization, GAE. I've talked about it before. There's been some encouraging data about its use in problematic knee OA. All the reports I found and published on RheumNow in the last two years have been kind of positive, leading me to believe this was a potential underutilized therapy. However, there's a real reporting bias. If you look at the data and where others have looked at the data and reviewed the subject, it's kind of hit and miss. This particular report was actually a 12-month sham-controlled trial of GAE in painful knee OA, and you know what, pain got better in both groups but was not better with the intervention, genicular artery embolization. So if I've intimated in the past that maybe this was a good idea, I think I'm recalling that. I want a do-over.
Some data on RA — the ARCTIC trial looked at seronegative and seropositive patients. The ARCTIC trial was a 234-patient DMARD-naive study with less than two years of RA where they were enrolled and followed and they looked at different outcomes. Anyway, in this sub-study, they looked at what happened to those who had seronegative RA at enrollment. And usually seronegative RA is not included in clinical trials, so that's kind of new here. 15% of their patients were seronegative. They compared them to seropositives and what they looked like at enrollment. And this was one of the points of my lecture today. Seronegatives have more disease at the onset and at baseline because they don't have the privilege of having a positive test to make it an easier diagnosis. Hence, you need more disease. In this study, that was exactly the case. At enrollment, seronegatives had higher swollen joint counts, 17 versus 8; higher DAS-28 scores, 3.9 versus 3.4; higher ultrasound scores, 55 versus 25; and higher MD global assessments, 49 versus 39 — all of those being significant. Interestingly, no difference in HAQ scores or Sharp scores.
But again, seronegative is an interesting subset, especially at the outset, and they probably — and there is clear data on that — they have a delay in diagnosis, but once they get into your hands you have no delay in treating them, that's for certain.
An international consortium from 10 European countries and almost 4,000 RA patients looked at the associations of RA with major adverse cardiovascular events, called MACE. This was between 1985 and 2012, 27 years. A total of 184 events. The MACE risk was really associated with disease activity, the DAS-28 scores. If you had an elevated DAS-28, it had an 18% increase, and that was significant. But it was not associated with, in this case, rheumatoid factor positivity or anti-CCP positivity. There are studies that do show seropositivity, especially in high titers, does increase the risk of cardiovascular events and cardiovascular death, but not in this study. In this study it was MACE. Other studies have suggested that the increase in cardiovascular risk with anti-CCP is in fact related to disease activity. So I sort of believe this study. I think it's a well-done study.
Steroid use in 574 newly diagnosed RA patients. This is a review. What do you think? How many newly diagnosed RA patients are on steroids? You know, in clinical trials, the average number of patients entering a clinical trial — to get into a clinical trial, you have to have active disease — is about 50–60%. These are newly diagnosed. In this study, 75% received steroids in the first year. 55% were on steroids at their very first visit. Half of these people also received intraarticular glucocorticoids. In this study, they did not show an association of steroid use at low dose — 5 to 10 milligrams a day, or less than 10 milligrams a day, I should say, or up to 10 milligrams a day, I should say — was not associated with increased risk of infection. A little bit increased, but not significantly.
So, a meta-analysis of infection in patients with idiopathic inflammatory myopathy. I've said many times in the past when asked to talk about this, there's probably more steroid complications with inflammatory myositis than there is with systemic lupus. Lupus, you get variable degrees of steroids. Inflammatory myositis, boom, everybody gets 80 milligrams to start with. At least that's the dose Dr. Zé taught us. That's a Zé-ism. And I still think it's the right dose to start with. But because of steroids
because of immunosuppression. In this study of almost 15,000 patients, the prevalence was 24% for infection, most of those being respiratory including PJP, aspergillosis, and then herpes zoster being also another prevalent pathogen. Risk factors for infection with idiopathic inflammatory myopathy includes increasing age, being male, a curse of being male, don't I know it, diabetes, hypertension, and having MDA5 positive disease where with MDA5 positive, there's a 3.4-fold increased risk and rapidly progressing lung disease part of the MDA5 story. And again, once you get the lung involved, that's when you get all that pneumonia and PJP and that's where all the dirty stuff happens with these folks.
Speaking of infection, one of the most common infections in our immunosuppressed patients is something we don't often talk about and that is atypical mycobacterial infections, better termed non-tuberculous mycobacterial infections, NTM. A retrospective study of 1,420 patients with NTM infections between 2012 and 2024 showed that 4.6% of them or 66 cases had RA. In 55 of those cases, NTM was diagnosed after RA. Why am I telling you this? Well, NTM can be mild, can be severe, but having RA imparts a higher risk of respiratory death, a fourfold higher risk of respiratory death, and a lower 5-year survival, 75% versus 93%. Most NTM infections are not as severe or need not be as severe as pulmonary TB, but they're often undiagnosed. And because they're undiagnosed, there can be morbidity and mortality associated with that. Some of that increase in death rate and lowered survival is partly explained by ILD in these RA patients and systemic inflammation adding to risk.
The way to prevent infection of course would be with vaccination. A study of the Shingrix vaccine, the recombinant zoster vaccine, in 76 immunosuppressed systemic sclerosis patients compared to 304 controls — these patients and controls all received two RZV doses. There were very high seroconversion rates. It works. It's great. But the point of the paper was that it's not as good in the scleroderma patients as it is in controls. It's 93% versus 99.7%. I'm sorry, that's still pretty good. Even for the scleroderma patients, it's a shade lower. They had lower overall antibody levels, but when they looked at cell-mediated immunity, it was equal between the groups. Overall, the patients with scleroderma had lower adverse event rates related to the use of the Shingrix vaccine, 74% versus 86%. Everybody gets some kind of side effects, if not just muscle soreness and whatnot.
Speaking of scleroderma, a recent review looked at 20-year trends on drug use in scleroderma, showing that in a cohort of 6,583 scleroderma patients followed for a 20-year period from 2005 to 2025, endothelin receptor antagonists and prostanoids and prostacyclin drugs went from really not being used — 3% 20 years ago — to being used in 28% currently. While calcium channel blockers and phosphodiesterase 5 inhibitors have remained flat, the use of cyclophosphamide has been replaced by greater reliance on mycophenolate first and then rituximab, and now there's more use of nintedanib. Steroids thankfully have decreased from 50% down to 18%, and that's a good move by you the rheumatologist.
Lastly, a study looked at scleroderma and malignancy risk. We've reported this before and this is pretty much more of the same. Yes, there's a higher risk of malignancy in systemic sclerosis. 31 studies, 32,000 patients showed a SIR — standardized incidence ratio — where you compare the risk of malignancy in the disease state scleroderma to a population risk. The SIR here is 1.66, confidence intervals 1.32 to 2.08 — a 66% increase in malignancies in systemic sclerosis. Highest were esophageal cancers, liver, cervical, lung, and hematologic malignancies including lymphoma, leukemia, and other hematologic malignancies. The SIR range was 3.35 — so all those other ones that were high actually range from an SIR of 3.35, threefold, to almost 14-fold, 13.95. The time from scleroderma diagnosis to cancer diagnosis in this study was a mean of 7.4 years. So it doesn't take forever.
I did report an update — I think it's a New England Journal — on the management of restless leg syndrome. You know, most of your patients have a sleep problem. If you can diagnose restless leg syndrome, oh my goodness, that's so great because there are so many good therapies that you can use. You just need to diagnose it, and that's understanding it. This is a really good review article that you should look at. So whether it's chronic or intermittent restless leg syndrome, the article points out that you don't need to do a sleep study, you don't need to do polysomnography, which is an extra time and expense and a hassle to set up, but they do say as a first step check the iron levels. RLS is associated with iron deficiency, and you don't even need to
be anemic, and then when that's present, boom, then you basically replace it and fix the problem. You should consider removing the exacerbators of RLS, alcohol being one of the prime ones. You should recommend walking, massage, heat. Drugs that they like are carbidopa-levodopa combo, pramipexole or ropinirole. And if necessary, low potency opioids are highly effective.
I like this report that came out of the FDA. It's the 120-year anniversary and the current acting director of the FDA did a nice two-page review of the history of the FDA and its role in protecting your health. It's a good overview. It starts at the turn of the century when the FDA was known as the Bureau of Chemistry, and because of, you know, crazy sales of potions and things that were killing people. The, uh, was the Pure Drug and Food Act. In 1906, in 1930 the FDA got its name. In 1938, the Food Drug and Cosmetics Act expanded the role of the FDA. And of course, you know, in the 1960s, the FDA was involved in denying thalidomide, and think of all that that did in protecting patient safety.
When I was on the FDA advisory committees, when I went through my orientation, they recommended a book that I recommend to you. I've read this book three times in the last 20 years. It's called Protecting America's Health. It's by Richard Hilts. I have the link in the show notes. I think you'd like that.
As you know, this is gout month. We had a lot of good gout content this week. Great article by Dr. Johnston today about the association between gout and renal disease. That's a really good read. I like this quote from Mary Wortley Montagu. Like people with three names. People wish their enemies dead, but I do not. I say give them the gout, give them the stone. She sounds like fun, doesn't she?
In 2010, colchicine fell under patent protection and the price rose 16-fold. Used to be pennies and went to like 5 cents, went to $5 or more. The out-of-pocket cost to patients increased almost fivefold. Colchicine decreased 27% while allopurinol, steroids, and gout visits to the ER and to the rheumatologist all increased as a result of this legislative move. I stopped using colchicine in 2010. I barely ever use it now. I know many of you like it, but that's my protest. I can easily manage gout and other disorders without it. I got a few, so don't get on me for not using it. But I was out to make a point and I'm using it here on this platform.
I liked a few reports this week, one of which I wrote, but not this one. That you can make a diagnosis of gout by retinal scanning. There's an interesting report that using retinal scanning, just looking at photographs of the fundus — high quality photographs — the study in over 107,000 patients showed you can make diagnoses with good certainty. Receiver operating curves, AUCs: diabetes 83, gout 83, osteoporosis 78, hypertension 74, hyperlipidemia 74, and thyroid disease 69. Wouldn't — I mean, that should be a part of every visit. You go in, your medical assistant does a nondilated picture of the fundus, it gets scanned by AI, your risks are put into your chart, it could be used as follow-up. Again, medicine is changing. You should be a part of the change.
Should you be advocating home testing for gout? You know, such a thing exists. So I wrote an article this week about saliva and uric acid testing because I read the Journal of Bioresources and Bioproducts — had to write that down because I didn't remember it. That describes — and these are, I think, Japanese investigators — that describe how you can use filter paper that's soaked in fluorescent microparticles that change color in the presence of uric acid. The darker the paper, the more the uric acid. And they can very accurately quantify this and show good correlation between serum levels. The article talks about how you can do this at home and in your garage almost. I don't think we're quite ready for that, but this led me to look for home testing via saliva.
And there is one out there called MyFit Strip. MyFit Strip. And I guess it's MyFit products. It's basically like a urine test strip where you put saliva on it, and again it's got an accuracy that's probably like 0.8 or something like that, or correlation with serums. And it's really quite good. It's good for serial assessment and whatnot. A kit with 25 strips costs about $25, meaning you can do this at $1 a clip each time you want to test it. Why not do it?
Our last report is on spotting cancer in patients with dermatomyositis. There was an article this week that tested the international IMACS guidelines. We wrote it. We've talked about that before. Ooid and colleagues presented this at ACR. It was a plenary session. I gave him a hard time about it, but I think it was a great article, a great report. It's been a publication. I think it was published in 2023, where it draws a line
and saying we should be doing these tests and you should test on the basis of risk. Don't do much in the way of PE for people at low risk. You do more and more for people at higher risk. Right? Using the IMACS guidelines, a study of 413 patients with known inflammatory myositis, including clinically active amyopathic dermatomyositis. They found that 6 point something percent of people had an ultimate cancer risk, and that the application of these guidelines in high-risk people had a yield of 8.8%. That was pretty good. In intermediate risk, it was 5.5. In low risk, it was 2.5. Maybe you want to look at those guidelines and incorporate those into your practice as to who and how you screen your myositis patients.
That's it for this week on the podcast. Tune in for more. Go to the website to check out these citations and more. Check out our great gout content. We had a fabulous Tuesday night rheumatology this week with Sara Tedeschi, John Fitzgerald, and Nicola Dalbeth talking about urate deposition and imaging, both ultrasound and DECT, and how to diagnose gout. It's a great one hour. These people are brilliant. They wouldn't let me get a word in edgewise, which is probably why you should listen to it.
Next week, our webinar is going to be equally good. We're going to be talking about — Lisa Stamp's going to be on this one. I think Mike Pillinger is on this one and Ted Mikuls, and I can't remember who the fourth person was. My apologies. We're going to be talking about upgrading and modernizing your approach to current urate-lowering therapy. What are you doing with allopurinol and febuxostat that actually is out of date according to the gout mavens? Tune in on Tuesday night to find out. Take care.
So today we're going to talk about predicting cancer in dermatomyositis patients, saliva as home testing, and some scleroderma updates.
Let's begin with genicular artery embolization, GAE. I've talked about it before. There's been some encouraging data about its use in problematic knee OA. All the reports I found and published on RheumNow in the last two years have been kind of positive, leading me to believe this was a potential underutilized therapy. However, there's a real reporting bias. If you look at the data and where others have looked at the data and reviewed the subject, it's kind of hit and miss. This particular report was actually a 12-month sham-controlled trial of GAE in painful knee OA, and you know what, pain got better in both groups but was not better with the intervention, genicular artery embolization. So if I've intimated in the past that maybe this was a good idea, I think I'm recalling that. I want a do-over.
Some data on RA — the ARCTIC trial looked at seronegative and seropositive patients. The ARCTIC trial was a 234-patient DMARD-naive study with less than two years of RA where they were enrolled and followed and they looked at different outcomes. Anyway, in this sub-study, they looked at what happened to those who had seronegative RA at enrollment. And usually seronegative RA is not included in clinical trials, so that's kind of new here. 15% of their patients were seronegative. They compared them to seropositives and what they looked like at enrollment. And this was one of the points of my lecture today. Seronegatives have more disease at the onset and at baseline because they don't have the privilege of having a positive test to make it an easier diagnosis. Hence, you need more disease. In this study, that was exactly the case. At enrollment, seronegatives had higher swollen joint counts, 17 versus 8; higher DAS-28 scores, 3.9 versus 3.4; higher ultrasound scores, 55 versus 25; and higher MD global assessments, 49 versus 39 — all of those being significant. Interestingly, no difference in HAQ scores or Sharp scores.
But again, seronegative is an interesting subset, especially at the outset, and they probably — and there is clear data on that — they have a delay in diagnosis, but once they get into your hands you have no delay in treating them, that's for certain.
An international consortium from 10 European countries and almost 4,000 RA patients looked at the associations of RA with major adverse cardiovascular events, called MACE. This was between 1985 and 2012, 27 years. A total of 184 events. The MACE risk was really associated with disease activity, the DAS-28 scores. If you had an elevated DAS-28, it had an 18% increase, and that was significant. But it was not associated with, in this case, rheumatoid factor positivity or anti-CCP positivity. There are studies that do show seropositivity, especially in high titers, does increase the risk of cardiovascular events and cardiovascular death, but not in this study. In this study it was MACE. Other studies have suggested that the increase in cardiovascular risk with anti-CCP is in fact related to disease activity. So I sort of believe this study. I think it's a well-done study.
Steroid use in 574 newly diagnosed RA patients. This is a review. What do you think? How many newly diagnosed RA patients are on steroids? You know, in clinical trials, the average number of patients entering a clinical trial — to get into a clinical trial, you have to have active disease — is about 50–60%. These are newly diagnosed. In this study, 75% received steroids in the first year. 55% were on steroids at their very first visit. Half of these people also received intraarticular glucocorticoids. In this study, they did not show an association of steroid use at low dose — 5 to 10 milligrams a day, or less than 10 milligrams a day, I should say, or up to 10 milligrams a day, I should say — was not associated with increased risk of infection. A little bit increased, but not significantly.
So, a meta-analysis of infection in patients with idiopathic inflammatory myopathy. I've said many times in the past when asked to talk about this, there's probably more steroid complications with inflammatory myositis than there is with systemic lupus. Lupus, you get variable degrees of steroids. Inflammatory myositis, boom, everybody gets 80 milligrams to start with. At least that's the dose Dr. Zé taught us. That's a Zé-ism. And I still think it's the right dose to start with. But because of steroids
because of immunosuppression. In this study of almost 15,000 patients, the prevalence was 24% for infection, most of those being respiratory including PJP, aspergillosis, and then herpes zoster being also another prevalent pathogen. Risk factors for infection with idiopathic inflammatory myopathy includes increasing age, being male, a curse of being male, don't I know it, diabetes, hypertension, and having MDA5 positive disease where with MDA5 positive, there's a 3.4-fold increased risk and rapidly progressing lung disease part of the MDA5 story. And again, once you get the lung involved, that's when you get all that pneumonia and PJP and that's where all the dirty stuff happens with these folks.
Speaking of infection, one of the most common infections in our immunosuppressed patients is something we don't often talk about and that is atypical mycobacterial infections, better termed non-tuberculous mycobacterial infections, NTM. A retrospective study of 1,420 patients with NTM infections between 2012 and 2024 showed that 4.6% of them or 66 cases had RA. In 55 of those cases, NTM was diagnosed after RA. Why am I telling you this? Well, NTM can be mild, can be severe, but having RA imparts a higher risk of respiratory death, a fourfold higher risk of respiratory death, and a lower 5-year survival, 75% versus 93%. Most NTM infections are not as severe or need not be as severe as pulmonary TB, but they're often undiagnosed. And because they're undiagnosed, there can be morbidity and mortality associated with that. Some of that increase in death rate and lowered survival is partly explained by ILD in these RA patients and systemic inflammation adding to risk.
The way to prevent infection of course would be with vaccination. A study of the Shingrix vaccine, the recombinant zoster vaccine, in 76 immunosuppressed systemic sclerosis patients compared to 304 controls — these patients and controls all received two RZV doses. There were very high seroconversion rates. It works. It's great. But the point of the paper was that it's not as good in the scleroderma patients as it is in controls. It's 93% versus 99.7%. I'm sorry, that's still pretty good. Even for the scleroderma patients, it's a shade lower. They had lower overall antibody levels, but when they looked at cell-mediated immunity, it was equal between the groups. Overall, the patients with scleroderma had lower adverse event rates related to the use of the Shingrix vaccine, 74% versus 86%. Everybody gets some kind of side effects, if not just muscle soreness and whatnot.
Speaking of scleroderma, a recent review looked at 20-year trends on drug use in scleroderma, showing that in a cohort of 6,583 scleroderma patients followed for a 20-year period from 2005 to 2025, endothelin receptor antagonists and prostanoids and prostacyclin drugs went from really not being used — 3% 20 years ago — to being used in 28% currently. While calcium channel blockers and phosphodiesterase 5 inhibitors have remained flat, the use of cyclophosphamide has been replaced by greater reliance on mycophenolate first and then rituximab, and now there's more use of nintedanib. Steroids thankfully have decreased from 50% down to 18%, and that's a good move by you the rheumatologist.
Lastly, a study looked at scleroderma and malignancy risk. We've reported this before and this is pretty much more of the same. Yes, there's a higher risk of malignancy in systemic sclerosis. 31 studies, 32,000 patients showed a SIR — standardized incidence ratio — where you compare the risk of malignancy in the disease state scleroderma to a population risk. The SIR here is 1.66, confidence intervals 1.32 to 2.08 — a 66% increase in malignancies in systemic sclerosis. Highest were esophageal cancers, liver, cervical, lung, and hematologic malignancies including lymphoma, leukemia, and other hematologic malignancies. The SIR range was 3.35 — so all those other ones that were high actually range from an SIR of 3.35, threefold, to almost 14-fold, 13.95. The time from scleroderma diagnosis to cancer diagnosis in this study was a mean of 7.4 years. So it doesn't take forever.
I did report an update — I think it's a New England Journal — on the management of restless leg syndrome. You know, most of your patients have a sleep problem. If you can diagnose restless leg syndrome, oh my goodness, that's so great because there are so many good therapies that you can use. You just need to diagnose it, and that's understanding it. This is a really good review article that you should look at. So whether it's chronic or intermittent restless leg syndrome, the article points out that you don't need to do a sleep study, you don't need to do polysomnography, which is an extra time and expense and a hassle to set up, but they do say as a first step check the iron levels. RLS is associated with iron deficiency, and you don't even need to
be anemic, and then when that's present, boom, then you basically replace it and fix the problem. You should consider removing the exacerbators of RLS, alcohol being one of the prime ones. You should recommend walking, massage, heat. Drugs that they like are carbidopa-levodopa combo, pramipexole or ropinirole. And if necessary, low potency opioids are highly effective.
I like this report that came out of the FDA. It's the 120-year anniversary and the current acting director of the FDA did a nice two-page review of the history of the FDA and its role in protecting your health. It's a good overview. It starts at the turn of the century when the FDA was known as the Bureau of Chemistry, and because of, you know, crazy sales of potions and things that were killing people. The, uh, was the Pure Drug and Food Act. In 1906, in 1930 the FDA got its name. In 1938, the Food Drug and Cosmetics Act expanded the role of the FDA. And of course, you know, in the 1960s, the FDA was involved in denying thalidomide, and think of all that that did in protecting patient safety.
When I was on the FDA advisory committees, when I went through my orientation, they recommended a book that I recommend to you. I've read this book three times in the last 20 years. It's called Protecting America's Health. It's by Richard Hilts. I have the link in the show notes. I think you'd like that.
As you know, this is gout month. We had a lot of good gout content this week. Great article by Dr. Johnston today about the association between gout and renal disease. That's a really good read. I like this quote from Mary Wortley Montagu. Like people with three names. People wish their enemies dead, but I do not. I say give them the gout, give them the stone. She sounds like fun, doesn't she?
In 2010, colchicine fell under patent protection and the price rose 16-fold. Used to be pennies and went to like 5 cents, went to $5 or more. The out-of-pocket cost to patients increased almost fivefold. Colchicine decreased 27% while allopurinol, steroids, and gout visits to the ER and to the rheumatologist all increased as a result of this legislative move. I stopped using colchicine in 2010. I barely ever use it now. I know many of you like it, but that's my protest. I can easily manage gout and other disorders without it. I got a few, so don't get on me for not using it. But I was out to make a point and I'm using it here on this platform.
I liked a few reports this week, one of which I wrote, but not this one. That you can make a diagnosis of gout by retinal scanning. There's an interesting report that using retinal scanning, just looking at photographs of the fundus — high quality photographs — the study in over 107,000 patients showed you can make diagnoses with good certainty. Receiver operating curves, AUCs: diabetes 83, gout 83, osteoporosis 78, hypertension 74, hyperlipidemia 74, and thyroid disease 69. Wouldn't — I mean, that should be a part of every visit. You go in, your medical assistant does a nondilated picture of the fundus, it gets scanned by AI, your risks are put into your chart, it could be used as follow-up. Again, medicine is changing. You should be a part of the change.
Should you be advocating home testing for gout? You know, such a thing exists. So I wrote an article this week about saliva and uric acid testing because I read the Journal of Bioresources and Bioproducts — had to write that down because I didn't remember it. That describes — and these are, I think, Japanese investigators — that describe how you can use filter paper that's soaked in fluorescent microparticles that change color in the presence of uric acid. The darker the paper, the more the uric acid. And they can very accurately quantify this and show good correlation between serum levels. The article talks about how you can do this at home and in your garage almost. I don't think we're quite ready for that, but this led me to look for home testing via saliva.
And there is one out there called MyFit Strip. MyFit Strip. And I guess it's MyFit products. It's basically like a urine test strip where you put saliva on it, and again it's got an accuracy that's probably like 0.8 or something like that, or correlation with serums. And it's really quite good. It's good for serial assessment and whatnot. A kit with 25 strips costs about $25, meaning you can do this at $1 a clip each time you want to test it. Why not do it?
Our last report is on spotting cancer in patients with dermatomyositis. There was an article this week that tested the international IMACS guidelines. We wrote it. We've talked about that before. Ooid and colleagues presented this at ACR. It was a plenary session. I gave him a hard time about it, but I think it was a great article, a great report. It's been a publication. I think it was published in 2023, where it draws a line
and saying we should be doing these tests and you should test on the basis of risk. Don't do much in the way of PE for people at low risk. You do more and more for people at higher risk. Right? Using the IMACS guidelines, a study of 413 patients with known inflammatory myositis, including clinically active amyopathic dermatomyositis. They found that 6 point something percent of people had an ultimate cancer risk, and that the application of these guidelines in high-risk people had a yield of 8.8%. That was pretty good. In intermediate risk, it was 5.5. In low risk, it was 2.5. Maybe you want to look at those guidelines and incorporate those into your practice as to who and how you screen your myositis patients.
That's it for this week on the podcast. Tune in for more. Go to the website to check out these citations and more. Check out our great gout content. We had a fabulous Tuesday night rheumatology this week with Sara Tedeschi, John Fitzgerald, and Nicola Dalbeth talking about urate deposition and imaging, both ultrasound and DECT, and how to diagnose gout. It's a great one hour. These people are brilliant. They wouldn't let me get a word in edgewise, which is probably why you should listen to it.
Next week, our webinar is going to be equally good. We're going to be talking about — Lisa Stamp's going to be on this one. I think Mike Pillinger is on this one and Ted Mikuls, and I can't remember who the fourth person was. My apologies. We're going to be talking about upgrading and modernizing your approach to current urate-lowering therapy. What are you doing with allopurinol and febuxostat that actually is out of date according to the gout mavens? Tune in on Tuesday night to find out. Take care.
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