Bad Actor Cofactor (10.17.2025) Save
Dr. Jack Cush reviews the news and journal reports, discusses pediatric reports, pregnancy data, diet and nutrition and more.
Transcription
It's 10/17/2025. This is a RheumNow podcast. Hi. I'm doctor Jack Cush, executive editor of roomnow.com. It's one week till ACR.
We've got a big plan for coverage starting next week. But this week on the podcast, we discuss pediatric stuff, pregnancy stuff, diet and nutrition stuff. I'm going totally soft. Am I not? Don't worry.
I'm gonna throw in a few double blind, randomized kind of nonsense things for you just as well. I like this first report, because it kind of addresses an issue that no one really has addressed in my mind, and that is with JAK inhibitors, you sometimes see creatinine bumps. You sometimes see see some benign CK emia, meaning occasional CPK elevations, without ever any reports of myositis or muscle problems. So, this is a small report out of Lancet Rheumatology just published, where they studied fifteen patients with active RA who were at risk for sarcopenia. A sarcopenia risk meant you had a high CRP, a reduced grip strength, some other evidence of weakness.
There's one other criterion. And they were treated with a JAK inhibitor as a new therapy. Thirteen out of fifteen had never seen a biologic or targeted synthetic, and they received tofacitinib in the usual dose. And they studied them at one month, three months, six months. They did before and after muscle biopsies.
They looked at what's going on in muscle in JAK inhibitor patients, and interestingly they found everybody got better by one month as far as their DAS28 ESR scores. But that at six months, they showed that muscle mass had significantly improved in these patients by 242 square centimeters. That was about a 4% increase in muscle mass. That was significant at point zero one seven. The increase in muscle mass interestingly was less if they were on a nonsteroidal.
We'll come back to that. And they also showed a significant increase in serum creatinines. On average, they gave it millimoles. I converted it to milligrams per deciliter. The median change was zero point six point zero six milligrams per deciliter.
Small, but significant across the board. At the same time, while these patients got better, serum cytokine levels dropped including IL six, IL one, and TNF. Interferon didn't change. I think IL 10 was the other one that didn't change. There was no change in CPK, myoglobin, LDH, and AST.
So this says that by controlling inflammation, they increase their muscle mass. Now, is it because they controlled inflammation? They move more? They got more muscle mass and that's why they're doing better? But they also showed an increase in creatinine.
And in this case, maybe the point is that increases in creatinine may be due to newly generated muscle. And then maybe at times you get an increase in CK for the same reason. It's a very low frequency event as you know. I've never had to discontinue a JAK because of small increases in CK. Interestingly, being on a nonsteroidal with the JAK, did that give you better control of pain and inflammation, more activity, more muscle development?
Interesting to postulate on why that happened. Nice report. Congratulations to those, authors. BMJ this week had a systematic review telling you and proving to you the things that you already know and say to your patients. They did a meta analysis and systematic review of 217 RCTs, fifteen, sixteen thousand patients looking at the effects of exercise on knee OA outcomes.
And they showed pretty clearly with moderate evidence, if not better, that aerobic exercise is the way to go, as exemplified by studies on walking, cycling, and swimming. There are other things that gave benefit that was more short term, but the aerobic is what shined through in this study. So walking, cycling, and swimming. You know, cycling and swimming is great for they got really damaged knees and can't do the weight load bearing that walking would imply, require. But, again, these are, pretty strong evidence for the advice that you've been giving.
This week, I had a case of osteonecrosis, led me to look up osteonecrosis on my own textbook, rheumatology.com. The causes of osteonecrosis include the ones you know and a few you didn't know, trauma, high dose steroids, alcoholism, renal failure, organ transplantation, lupus, bad lupus, prothrombotic state including sickle cell and, other hemoglobinopathies, radiation, pancreatitis, gout I didn't know, pregnancy I knew, hyperlipidemia I wasn't unsure of, and Caisson's disease, decompression sickness for those of you who like to go deep deep into the water and ocean. Okay. A pediatric study from JAMA looked at surprising statistic, not necessarily rheumatologic, but it deals with cannabis. A study of basically young adults in the Journal of Pediatrics, almost 1,500 young adults, when surveyed a quarter of them, twenty two percent claimed to use either cannabis or alcohol for sleep.
What? Alcohol the worst thing in the world for sleep. Cannabis, I thought not too bad, but this paper shed some doubt upon it. In their survey, eighteen percent said cannabis was used for sleep, seven percent alcohol. There was some overlap there.
And both of these substances have been shown to interfere with the quality of sleep or the ability to stay asleep. That's clearly what alcohol does hands down. I'm not directly aware of cannabis affecting the quality or the duration of sleep, but they said so in the article and it's JAMA Dermatology JAMA Pediatrics. So for those who use cannabis in the last year, forty one percent said they used it for the purpose of sleep. It's a trend with the wider more available use of cannabis.
Is it not? Another study on pregnancy and outcomes in the offspring was a cohort study of one point five million mother child pairs, and they looked at the influence of antenatal exposure to steroids. And they found that if the mom took steroids between weeks twenty eight, actually it's weeks thirty two up to full term, there was an increased risk of respiratory and non respiratory infections. And and that lasted until the offspring, the child, was up to 21 years of age. The incidence rates here was sixty five versus forty per one thousand patient years, and that's for preterm deliveries, and thirty versus eighteen per one thousand patient years for full term delivery.
So the use of steroids in women who are pregnant, according to this, may have a long term significant effect in the offspring's risk of developing future infections. Now these most of these are nonsense infections. We're not talking about people with, you know, meningitis and sepsis. Right? They they didn't they did not report that.
Another pregnancy report was a single center report on hundred and eighty nine women with IMiDs. A hundred and thirty one RA, twenty nine SPA, twenty nine PSA. Live births were pretty good. Best for SPA, ninety percent. Next best for RA at seventy six percent.
Not so good, but up there seventy percent for PSA. Preterm deliveries was sixteen percent, twelve percent, and seven percent for RA, SPA, PSA respectively. IUGR, intrauterine growth retardation, seen in thirty one of the one hundred thirty one RA patients, but not seen in SPA and PSA. C sections were seen or used in about a third, and I think that the I like this information about how many of these pregnancies used TNF inhibitors during pregnancy. Twelve percent of RA, you could do better than that, but forty eight percent of SPA and thirty one percent of PSAs.
I think that outcomes are doing better as we've come to understand how to best control the disease in the state of pregnancy. Another report on ILD. We do know that about a third or more of non IPF ILD will progress over time, which means that two thirds won't. Right? And subsets, it's only as much as forty percent that won't, but still that's a high number.
Not all ILD will be a rapid progressor with a ten percent change in FVC in a year. So, this study, they assessed a number of different outcomes. It's actually a retrospective study, 10 European centers, three zero three patients. A third, thirty seven percent progressed as defined by a greater than ten percent decline in FVC in one year. They came up with a predictors for progression.
Age, gender, BMI, FVC, NKL6, a new biomarker that are being used a lot by the pulmonologist, not so much by us rheumatologists. The five predictors were better than the biomarker KL6 alone. The five predictors had a 70 excuse me, a 55% sensitivity, 73% specificity, and 67% accuracy. These are good things to look at in your patients with ILD. A study on vasculitis tertiary center looked at their one hundred and forty seven GPA patients followed for eighteen months, fifty five deaths, and a hundred and seventy nine relapses.
Think about that. One hundred and forty seven GPAs, fifty five deaths, a third, boom, with eighteen months follow-up. That's the mean, died, and one hundred and seventy nine relapses in one hundred and seventeen patients. That's an average relapse rate of one point five relapses per patient. So, the predictors of relapse and the predictors of mortality were about the same, about a twofold increase.
The risk factors were age more than 55, being male, an elevated creatinine, and neurologic involvement or CNS involvement, either at baseline or development over time. Not good. GPA still is a challenge, but this could be old data, not may not be based on more current aggressive, proven regimens to better control GPA outcomes. PSA and psoriatic arthritis, a very large study, I think this is in JAMA Dermatology, showed that fibromyalgia when present in psoriasis and psoriatic arthritis is linked to greater complexity and shorter biologic survival. Retrospective study where the psoriatic patients, sixty one thousand of them were matched one to four with two hundred and forty four thousand controls without psoriasis.
The prevalence of psoriasis was about fifty percent higher than the controls, one point four five. It was three percent, three point three percent. I like to say that in the general population, fiber miles is five to 6% in my opinion, but this says it's lower. In psoriatic arthritis patients, when they looked at the presence of fibromyalgia, it complicated things big big time. They needed more biologics.
They were had the biologics they did use had less survival. FM patient FM PSA patients, six year survival versus PSA without FM, ten year biologic survival, and an overall increase, almost a doubling in the rate of switching required. Again, it's a bad actor when it's a co factor. That sounds like the title of this podcast. You know, I never know the title of the podcast until I do the podcast, and then something goofy I say becomes the title.
It's a bad actor when it's a cofactor. Alright. Look for that. Now you know why it's a title. Interesting things on nutrition this week.
Scientific American. Nice paper that you might want to give to your patients who are all into nutraceuticals. It's got a really well written piece on the beneficial effects immunologic and inflammation wise of omega three fatty acids. Vitamin d, which I had to read because I got a bugaboo, in my shoe about vitamin d, but it had good data in there about the immunologic benefits, and as you all know, curcumin. It's a good basic review that I would refer you to.
Three more reports. Again, Arc, JAMA Dermatology had a the published the Medispo study. Medispo study. It's a small study, 38 patients, sixteen weeks with a dietary intervention being the Mediterranean diet. So half the group got a Mediterranean diet intervention with dietitian counseling for sixteen weeks and, a big bucket of virgin olive oil, and the controls just got a control I don't I can't what was it?
A I can't remember what the control diet was, but it was maybe like a low fat diet or something like that. 38 patients, and almost all of them completed the study. When they looked at the psoriasis area, severity index, the PASI scores, at the week sixteens, it was significant for the dietary intervention group minus 3.4 versus zero in the controls. That was significant at less than point zero zero one. The Posse 75 was achieved by four Posse 75 change was achieved by forty seven percent of those on the Mediterranean diet and none in the control group.
Also, on a Mediterranean diet, they had a significant lowering of hemoglobin a one c. And that was significant because A1C has been shown to correlate with psoriasis activity. Didn't know that. Had to read a derm journal to figure that out. A GI journal, looks at IBD in the pediatric population and associated musculoskeletal symptoms.
This is actually an Italian rheumatology and GI study, and they had in this study oh, I think the number was a hundred and eleven. I can't see it right. I didn't write it down. But they had a good cohort size of pediatric IBD, two thirds of them with Crohn's, one third with ulcerative colitis. And of the musculoskeletal manifestations, seventy three percent arthralgia, sixty nine percent arthritis.
This article tells you a lot of things that you probably knew, but it confirms them I think in a good volumetric way. The other things that were important was inflammatory back pain in twenty six percent, enthesitis in eleven percent, and dactylitis in six percent. No difference in musculoskeletal frequency between Crohn's and ulcerative colitis. Peripheral arthritis was much more common than axial seventy seven percent versus fourteen percent. The kinds of arthritis are the ones you would expect.
Most of them, more than half oligoarthritis, with a quarter each presenting as either monoarthritis or polyarthritis. Not unexpectedly, the main lab finding was acute phase reactants, sed rate, CRP, and fecal calprotectin elevated in seventy four to sixty percent, and those acute phase reactants were more often higher in Crohn's disease than ulcerative colitis. Interesting. ANA positivity was seen in a quarter, and that was associated with a greater risk of extended chronic arthritis. Lastly, ferritin I found interesting because it was more likely to be low in this pediatric IBD with MSK symptoms than to be high.
So, I would think ferritin might be elevated because of inflammation. It was only high in seven percent, but it was low in thirty two percent. So, that could be inflammation, that could be IBD related GI bleeding, a number of factors. Anyway, I like that one. Last report is has been teased at at past ACR and EULAR meetings, teletacecept.
Teletacept, as you know, is the dual inhibitor of B cells by inhibiting BLIS in April. Ron van Vohlenhofen was the lead author on a study conducted in China in a phase three, three thirty five active SLE patients who stayed on their background standard therapies. They received one to one either teletacept or placebo as a once weekly injection for a year. The year results favor telotacicept. The primary endpoint was an SRI four achieved in two thirds, sixty seven percent, versus one third on placebo.
That was highly significant. The four point reduction in the Salina Sleet Eye was achieved to seventy percent on teletacept and forty percent on placebo. The downside is that there were more adverse events with teletacept than placebo. Overall, seventy five percent versus fifty percent. Most of those were nonsense like URIs.
Right? But and they weren't there was no statistic for that was meaningful for serious adverse events. But the teletastocept group did have more reduced IgG levels and IgM levels, sixteen percent versus one point two percent for IgG, fifteen percent versus zero point six percent for IgM. And also the teletastocept had a twelve point six percent ISR rate versus placebo 0.6. So this is this looks good.
And there was a phase two before this. And you know teletacept has hinted at being effective in RA and also in Sjogren's. So it's development is early, but it's encouraging, and we hope to see more data on this. You wanna see more data? Follow us on RheumNow next week.
We'll be giving you some previews of what's happening at ACR, starts a week from Sunday. I think that's on the October 26 and goes through the twenty ninth. We've got a big lineup, a lot of big reports. You'd be sure you follow us. My recommendations, if you wanna stay up on what's going on on the ACR during your breaks, just follow the Twitter feed from AtriumNow.
But if you want a daily kinda update, do the daily recaps. They're gonna be at 5PM, I think, central time, 6PM eastern time, every day live streamed on RheumNow, on the website, on our YouTube channel, on Facebook, YouTube, and also LinkedIn and Twitter. So you can see that report every day of what was the highlight of the day for each of the four days. And then after the meeting, tune in and watch the video on the topic reports. We got a topic report on RA, a topic report on PSA and SPA.
This year, a topic report on CAR T cell therapy. What? Be there. Be square. Talk next week.
We've got a big plan for coverage starting next week. But this week on the podcast, we discuss pediatric stuff, pregnancy stuff, diet and nutrition stuff. I'm going totally soft. Am I not? Don't worry.
I'm gonna throw in a few double blind, randomized kind of nonsense things for you just as well. I like this first report, because it kind of addresses an issue that no one really has addressed in my mind, and that is with JAK inhibitors, you sometimes see creatinine bumps. You sometimes see see some benign CK emia, meaning occasional CPK elevations, without ever any reports of myositis or muscle problems. So, this is a small report out of Lancet Rheumatology just published, where they studied fifteen patients with active RA who were at risk for sarcopenia. A sarcopenia risk meant you had a high CRP, a reduced grip strength, some other evidence of weakness.
There's one other criterion. And they were treated with a JAK inhibitor as a new therapy. Thirteen out of fifteen had never seen a biologic or targeted synthetic, and they received tofacitinib in the usual dose. And they studied them at one month, three months, six months. They did before and after muscle biopsies.
They looked at what's going on in muscle in JAK inhibitor patients, and interestingly they found everybody got better by one month as far as their DAS28 ESR scores. But that at six months, they showed that muscle mass had significantly improved in these patients by 242 square centimeters. That was about a 4% increase in muscle mass. That was significant at point zero one seven. The increase in muscle mass interestingly was less if they were on a nonsteroidal.
We'll come back to that. And they also showed a significant increase in serum creatinines. On average, they gave it millimoles. I converted it to milligrams per deciliter. The median change was zero point six point zero six milligrams per deciliter.
Small, but significant across the board. At the same time, while these patients got better, serum cytokine levels dropped including IL six, IL one, and TNF. Interferon didn't change. I think IL 10 was the other one that didn't change. There was no change in CPK, myoglobin, LDH, and AST.
So this says that by controlling inflammation, they increase their muscle mass. Now, is it because they controlled inflammation? They move more? They got more muscle mass and that's why they're doing better? But they also showed an increase in creatinine.
And in this case, maybe the point is that increases in creatinine may be due to newly generated muscle. And then maybe at times you get an increase in CK for the same reason. It's a very low frequency event as you know. I've never had to discontinue a JAK because of small increases in CK. Interestingly, being on a nonsteroidal with the JAK, did that give you better control of pain and inflammation, more activity, more muscle development?
Interesting to postulate on why that happened. Nice report. Congratulations to those, authors. BMJ this week had a systematic review telling you and proving to you the things that you already know and say to your patients. They did a meta analysis and systematic review of 217 RCTs, fifteen, sixteen thousand patients looking at the effects of exercise on knee OA outcomes.
And they showed pretty clearly with moderate evidence, if not better, that aerobic exercise is the way to go, as exemplified by studies on walking, cycling, and swimming. There are other things that gave benefit that was more short term, but the aerobic is what shined through in this study. So walking, cycling, and swimming. You know, cycling and swimming is great for they got really damaged knees and can't do the weight load bearing that walking would imply, require. But, again, these are, pretty strong evidence for the advice that you've been giving.
This week, I had a case of osteonecrosis, led me to look up osteonecrosis on my own textbook, rheumatology.com. The causes of osteonecrosis include the ones you know and a few you didn't know, trauma, high dose steroids, alcoholism, renal failure, organ transplantation, lupus, bad lupus, prothrombotic state including sickle cell and, other hemoglobinopathies, radiation, pancreatitis, gout I didn't know, pregnancy I knew, hyperlipidemia I wasn't unsure of, and Caisson's disease, decompression sickness for those of you who like to go deep deep into the water and ocean. Okay. A pediatric study from JAMA looked at surprising statistic, not necessarily rheumatologic, but it deals with cannabis. A study of basically young adults in the Journal of Pediatrics, almost 1,500 young adults, when surveyed a quarter of them, twenty two percent claimed to use either cannabis or alcohol for sleep.
What? Alcohol the worst thing in the world for sleep. Cannabis, I thought not too bad, but this paper shed some doubt upon it. In their survey, eighteen percent said cannabis was used for sleep, seven percent alcohol. There was some overlap there.
And both of these substances have been shown to interfere with the quality of sleep or the ability to stay asleep. That's clearly what alcohol does hands down. I'm not directly aware of cannabis affecting the quality or the duration of sleep, but they said so in the article and it's JAMA Dermatology JAMA Pediatrics. So for those who use cannabis in the last year, forty one percent said they used it for the purpose of sleep. It's a trend with the wider more available use of cannabis.
Is it not? Another study on pregnancy and outcomes in the offspring was a cohort study of one point five million mother child pairs, and they looked at the influence of antenatal exposure to steroids. And they found that if the mom took steroids between weeks twenty eight, actually it's weeks thirty two up to full term, there was an increased risk of respiratory and non respiratory infections. And and that lasted until the offspring, the child, was up to 21 years of age. The incidence rates here was sixty five versus forty per one thousand patient years, and that's for preterm deliveries, and thirty versus eighteen per one thousand patient years for full term delivery.
So the use of steroids in women who are pregnant, according to this, may have a long term significant effect in the offspring's risk of developing future infections. Now these most of these are nonsense infections. We're not talking about people with, you know, meningitis and sepsis. Right? They they didn't they did not report that.
Another pregnancy report was a single center report on hundred and eighty nine women with IMiDs. A hundred and thirty one RA, twenty nine SPA, twenty nine PSA. Live births were pretty good. Best for SPA, ninety percent. Next best for RA at seventy six percent.
Not so good, but up there seventy percent for PSA. Preterm deliveries was sixteen percent, twelve percent, and seven percent for RA, SPA, PSA respectively. IUGR, intrauterine growth retardation, seen in thirty one of the one hundred thirty one RA patients, but not seen in SPA and PSA. C sections were seen or used in about a third, and I think that the I like this information about how many of these pregnancies used TNF inhibitors during pregnancy. Twelve percent of RA, you could do better than that, but forty eight percent of SPA and thirty one percent of PSAs.
I think that outcomes are doing better as we've come to understand how to best control the disease in the state of pregnancy. Another report on ILD. We do know that about a third or more of non IPF ILD will progress over time, which means that two thirds won't. Right? And subsets, it's only as much as forty percent that won't, but still that's a high number.
Not all ILD will be a rapid progressor with a ten percent change in FVC in a year. So, this study, they assessed a number of different outcomes. It's actually a retrospective study, 10 European centers, three zero three patients. A third, thirty seven percent progressed as defined by a greater than ten percent decline in FVC in one year. They came up with a predictors for progression.
Age, gender, BMI, FVC, NKL6, a new biomarker that are being used a lot by the pulmonologist, not so much by us rheumatologists. The five predictors were better than the biomarker KL6 alone. The five predictors had a 70 excuse me, a 55% sensitivity, 73% specificity, and 67% accuracy. These are good things to look at in your patients with ILD. A study on vasculitis tertiary center looked at their one hundred and forty seven GPA patients followed for eighteen months, fifty five deaths, and a hundred and seventy nine relapses.
Think about that. One hundred and forty seven GPAs, fifty five deaths, a third, boom, with eighteen months follow-up. That's the mean, died, and one hundred and seventy nine relapses in one hundred and seventeen patients. That's an average relapse rate of one point five relapses per patient. So, the predictors of relapse and the predictors of mortality were about the same, about a twofold increase.
The risk factors were age more than 55, being male, an elevated creatinine, and neurologic involvement or CNS involvement, either at baseline or development over time. Not good. GPA still is a challenge, but this could be old data, not may not be based on more current aggressive, proven regimens to better control GPA outcomes. PSA and psoriatic arthritis, a very large study, I think this is in JAMA Dermatology, showed that fibromyalgia when present in psoriasis and psoriatic arthritis is linked to greater complexity and shorter biologic survival. Retrospective study where the psoriatic patients, sixty one thousand of them were matched one to four with two hundred and forty four thousand controls without psoriasis.
The prevalence of psoriasis was about fifty percent higher than the controls, one point four five. It was three percent, three point three percent. I like to say that in the general population, fiber miles is five to 6% in my opinion, but this says it's lower. In psoriatic arthritis patients, when they looked at the presence of fibromyalgia, it complicated things big big time. They needed more biologics.
They were had the biologics they did use had less survival. FM patient FM PSA patients, six year survival versus PSA without FM, ten year biologic survival, and an overall increase, almost a doubling in the rate of switching required. Again, it's a bad actor when it's a co factor. That sounds like the title of this podcast. You know, I never know the title of the podcast until I do the podcast, and then something goofy I say becomes the title.
It's a bad actor when it's a cofactor. Alright. Look for that. Now you know why it's a title. Interesting things on nutrition this week.
Scientific American. Nice paper that you might want to give to your patients who are all into nutraceuticals. It's got a really well written piece on the beneficial effects immunologic and inflammation wise of omega three fatty acids. Vitamin d, which I had to read because I got a bugaboo, in my shoe about vitamin d, but it had good data in there about the immunologic benefits, and as you all know, curcumin. It's a good basic review that I would refer you to.
Three more reports. Again, Arc, JAMA Dermatology had a the published the Medispo study. Medispo study. It's a small study, 38 patients, sixteen weeks with a dietary intervention being the Mediterranean diet. So half the group got a Mediterranean diet intervention with dietitian counseling for sixteen weeks and, a big bucket of virgin olive oil, and the controls just got a control I don't I can't what was it?
A I can't remember what the control diet was, but it was maybe like a low fat diet or something like that. 38 patients, and almost all of them completed the study. When they looked at the psoriasis area, severity index, the PASI scores, at the week sixteens, it was significant for the dietary intervention group minus 3.4 versus zero in the controls. That was significant at less than point zero zero one. The Posse 75 was achieved by four Posse 75 change was achieved by forty seven percent of those on the Mediterranean diet and none in the control group.
Also, on a Mediterranean diet, they had a significant lowering of hemoglobin a one c. And that was significant because A1C has been shown to correlate with psoriasis activity. Didn't know that. Had to read a derm journal to figure that out. A GI journal, looks at IBD in the pediatric population and associated musculoskeletal symptoms.
This is actually an Italian rheumatology and GI study, and they had in this study oh, I think the number was a hundred and eleven. I can't see it right. I didn't write it down. But they had a good cohort size of pediatric IBD, two thirds of them with Crohn's, one third with ulcerative colitis. And of the musculoskeletal manifestations, seventy three percent arthralgia, sixty nine percent arthritis.
This article tells you a lot of things that you probably knew, but it confirms them I think in a good volumetric way. The other things that were important was inflammatory back pain in twenty six percent, enthesitis in eleven percent, and dactylitis in six percent. No difference in musculoskeletal frequency between Crohn's and ulcerative colitis. Peripheral arthritis was much more common than axial seventy seven percent versus fourteen percent. The kinds of arthritis are the ones you would expect.
Most of them, more than half oligoarthritis, with a quarter each presenting as either monoarthritis or polyarthritis. Not unexpectedly, the main lab finding was acute phase reactants, sed rate, CRP, and fecal calprotectin elevated in seventy four to sixty percent, and those acute phase reactants were more often higher in Crohn's disease than ulcerative colitis. Interesting. ANA positivity was seen in a quarter, and that was associated with a greater risk of extended chronic arthritis. Lastly, ferritin I found interesting because it was more likely to be low in this pediatric IBD with MSK symptoms than to be high.
So, I would think ferritin might be elevated because of inflammation. It was only high in seven percent, but it was low in thirty two percent. So, that could be inflammation, that could be IBD related GI bleeding, a number of factors. Anyway, I like that one. Last report is has been teased at at past ACR and EULAR meetings, teletacecept.
Teletacept, as you know, is the dual inhibitor of B cells by inhibiting BLIS in April. Ron van Vohlenhofen was the lead author on a study conducted in China in a phase three, three thirty five active SLE patients who stayed on their background standard therapies. They received one to one either teletacept or placebo as a once weekly injection for a year. The year results favor telotacicept. The primary endpoint was an SRI four achieved in two thirds, sixty seven percent, versus one third on placebo.
That was highly significant. The four point reduction in the Salina Sleet Eye was achieved to seventy percent on teletacept and forty percent on placebo. The downside is that there were more adverse events with teletacept than placebo. Overall, seventy five percent versus fifty percent. Most of those were nonsense like URIs.
Right? But and they weren't there was no statistic for that was meaningful for serious adverse events. But the teletastocept group did have more reduced IgG levels and IgM levels, sixteen percent versus one point two percent for IgG, fifteen percent versus zero point six percent for IgM. And also the teletastocept had a twelve point six percent ISR rate versus placebo 0.6. So this is this looks good.
And there was a phase two before this. And you know teletacept has hinted at being effective in RA and also in Sjogren's. So it's development is early, but it's encouraging, and we hope to see more data on this. You wanna see more data? Follow us on RheumNow next week.
We'll be giving you some previews of what's happening at ACR, starts a week from Sunday. I think that's on the October 26 and goes through the twenty ninth. We've got a big lineup, a lot of big reports. You'd be sure you follow us. My recommendations, if you wanna stay up on what's going on on the ACR during your breaks, just follow the Twitter feed from AtriumNow.
But if you want a daily kinda update, do the daily recaps. They're gonna be at 5PM, I think, central time, 6PM eastern time, every day live streamed on RheumNow, on the website, on our YouTube channel, on Facebook, YouTube, and also LinkedIn and Twitter. So you can see that report every day of what was the highlight of the day for each of the four days. And then after the meeting, tune in and watch the video on the topic reports. We got a topic report on RA, a topic report on PSA and SPA.
This year, a topic report on CAR T cell therapy. What? Be there. Be square. Talk next week.
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