Mentshlichkeit (8.7.2026) Save
Dr. Jack Cush reviews the news and recent journal reports on RheumNow.com
Transcription
It's 08/07/2026. This is the RheumNow podcast. Yes, you're here again. I'm Jack Cush, glad to join you. We're gonna review the news from this past week.
A lot of interesting things did come up and were posted for your educational pleasure. Let's begin with a study from Beer. That's the British Dermatology Biologics Registry called Bad Beer. We haven't really talked about that, but they're just as good as the BSRBR, which is a biologics registry for rheumatologists and, for biologics. Anyway, Bad Beer has a registry of almost nineteen thousand psoriasis patients.
They looked at the incidence of serious, infectious events, SIEs. The number is, drum roll please, twenty eight SIEs per 1,000 patient years. Let me do the conversion for you, that's two point eight per 100 patient years. I've talked about those terms before, that's a low number and we've said before that, psoriatic tend to have lower rates of SIEs compared to for instance RA and inflammatory bowel patients, and there may be factors behind it, but those are just the facts. Generally less than three per 100 patient years.
I thought that that was interesting. The other interesting factor in this report was the rate was higher if you had a prior SIE. That's a very well known phenomenon in the infectious disease world. If you had a previous SIE, meningitis, pneumonia, sepsis, and you were hospitalized for it, guess what? Your odds of getting it again are way up and your odds of dying for it second time around are also now substantial.
Anyway, if you had a prior SIE, now the rate goes to seventy nine per one thousand, twenty eight to seventy nine, that's almost two and a half fold higher, that's important. They found the rates were lowest with, rizenkizumab, when they compared it to bredalumab or etanercept or other standard therapies. Rizenkizumab, the IL-twenty three inhibitor had roughly a twenty six to twenty percent lower rate. Now, those are more recent drugs compared to more older drugs. Maybe there's better patient selection, hard to know.
Nonetheless, these are good numbers. The death rate from an SIE is one point eight per one thousand patient years or less than, zero point two per 100 patient years, right? Speaking of infection, Cassie Calabrese from the Cleveland Clinic Foundation had a nice piece, that she published this week, giving an overview of vaccinating, patients with immune mediated inflammatory disorders or IMiDs. She basically says that you need a risk based approach, knowing what's high, benefit and who needs it most. And for instance, she says the use of Shingrix or the recombinant Zoster vaccine is indicated for all individuals regardless of age, going on a JAK inhibitor or going on anifrolumab.
I like that, I endorse that a 100%. She says you need to time, the use of a COVID vaccine in your patients who are on or going to consider treatment with rituximab, meaning they're on rituximab and you give a COVID or any vaccine, the human response is gonna stink. You need to get them at the nadir or before you start them, it's really important that you time vaccinations, especially the COVID vaccine. She strongly recommends annual flu and PCV20 or twenty one for all of our patients who are immunosuppressed, and she does recommend sort of a selective use of the vaccine against, RSV, being highly indicated in the elderly over age 75 or younger individuals who have risk factors, chronic lung disease and chronic kidney disease. I saw an interesting, article about nonsteroidals, and their effect in age related macular degeneration, from an ophthalmology journal.
Age related macular degeneration is, as they put it in their paper, which was gonna say that nonsteroidals are protective. They made the point that it's probably an inflammatory condition. I went a little bit further on this. I think most experts don't think that age related macular degeneration is inflammatory in its origins, but inflammation, especially chronic inflammation plays a role, and this sounds to me like what we see with osteoarthritis. It's a degenerative condition, so is age related macular degeneration, AMD, and it is modified by and spurned by at times inflammation.
Anyway, in this study, it was a TriNetX study from 2015 to 2024, nine year study, looking at people who did not individuals via their electronic medical records, who did not have AMD and compared, about six hundred and thirty five thousand who took a non steroidal versus six hundred and thirty five thousand who did not take a non steroidal and guess what? Non steroidal use significantly lowered the risk of future AMD at six months, lowered it by almost seventy percent and going all the way out to five years lowered it almost by fifty percent. So, it basically has a protective effect of about forty two percent overall over a five year span. This was not as strong, but still significant if they were just taking aspirin. Stronger and more significant if you're taking selective nonsteroidals with about a 59% protective effect.
So, another reason why some patients really might need to be on or wouldn't be a bad idea if they were on, nonsteroidals. Again, there are no trials proving this point, this is TriNetX sort of a target emulation trial using, cohort data to prove the point. There was a rebroadcast, if you will, of the TREAT earlier study, which you know was an early intervention study in clinically suspect arthralgia patients who had evidence of subclinical joint inflammation. They did not need to be seropositive to be in the study, and in this study done in The Netherlands, they were treated with twelve months of methotrexate or not. Two hundred and thirty six patients with CSA, they showed that methotrexate was preventative, but only in seronegative RA, where, in that population getting methotrexate only nine percent developed RA versus placebo where thirty five percent developed RA.
If you looked at seropositive patients, it didn't matter, fifty eight and sixty five percent developed seropositive RA on placebo or on methotrexate. I put this up because I think it's proof of something I've been lecturing about lately, which is the differences between seronegative and seropositive RA. They are definitely different and seronegative is definitely not more benign, but this shows you, maybe at a deeper, not yet understood level that these response rates are also indicating there's something truly different between those disorders. Think about it. JAMA had a nice review this week about sleep health and obesity, they are linked, there's a bi directional relationship.
If you have obesity, you're more likely to get sleep problems. If you have sleep problems, you're more likely to get obesity. Pretty simple, right? Insufficient sleep and poor sleep quality associated with weight gain, less healthy diets, and a higher risk of obesity, and then we go back the other way as well. It's a nice review in JAMA.
University of Alberta reported on a study looking at a predictive survey called GCAPS or GCAPS, and I posted for you on there the survey questions that are used to know whether someone who you suspect is having GCA should receive a more aggressive workup and biopsy. So, in their study of sixty two newly referred suspected GCA patients, GCA was ultimately diagnosed in thirty nine of those individuals, and of those that were diagnosed, fifty percent had a high, GCaPS screening score, only thirty eight with intermediate disease only thirteen percent, or low risk, by the GCaPPS score. So, using the GCaPPS score, you can, maybe predict who needs further evaluation. One more fact, in intermediate or high risk GCAP score had a sensitivity of ninety seven percent, specificity of thirty percent, positive predictive value of seventy percent. Those are strong numbers, especially sensitivity.
Specificity, maybe not so much. What's in the GCAP score? Again, I think it comes from Scotland. It's age, sex, duration of symptoms, CRP, headache, PMR, jaw claudication, fever, type of field loss, temporal artery changes on fundoscopy, cranial nerve palsies, and peripheral artery changes, and you got a zero, one, two, or three score, you need a GCAP score of 10 or more to be high risk and definitely deserving of a biopsy and further evaluation. You might want to look at that if you're a GCA person.
Another study this week looked at males with SLE in a cohort of over 400 patients at thirty seven males, and what was unique about the males compared to females, again, this is only less than ten percent of the population, is that they had a higher prevalence of renal disease class four and class five lupus nephritis, was seen in fifty percent of those patients that was higher than the other populations. The males also had an higher incidence of Plaquenil related retinal toxicity. Sixty two percent of their patients overall were on hydroxychloroquine and of those twenty two percent had to discontinue the hydroxychloroquine who were male. So, I've always said that since you're not female, if you're gonna get lupus and you're male, you better have you're gonna more likely to have more lupus features and more serious lupus and that's borne out by many studies in the past. This study, I think, reiterates that.
Another study of lupus, six fifty seven multi ethnic lupus patients, use a machine learning tool to show that fourteen percent had organic brain disease and thirty percent had neuropsychiatric damage. The biggest predictor of organic brain disease was steroids. Are also a big predictor of neuropsychiatric damage, but other predictors of neuropsychiatric damage were MD global fatigue, pain, and again, glucocorticoids, especially glucocorticoid dose and how long you use it. Again, I think we find, the management of lupus and CNS disease is problematic. The more we know, the better we know.
Another study this week looked at cerebral atrophy. I mean, you scanned all your patients with lupus, you'd find cerebral atrophy more than you would expect, but it doesn't always correlate with neuropsychiatric lupus or lupus cerebritis. Anyway, in this study, they found that it was associated with, total of seventy patients, mean age 40, disease duration twelve years. They found that cerebral atrophy was associated with age, number 10% higher, higher education levels was associated with this and then cerebral atrophy in their study was associated with neuropsychiatric lupus, a four point six fold higher risk. They found cerebral atrophy at fifty three percent, but most of it was mild.
Three quarters of those who had cerebral atrophy, it was said to be mild. So, point is don't freak out when you see cerebral atrophy, think about whether it's related to age, or being, having too much education, but I guess maybe you should worry about, you know, a future risk of neuropsychiatric disease. ITP is a problem and how you manage is a problem. I came across a study this week looking at the use of baricitinib. In this study, they were using, everybody got Danazole, the, hormonal therapy for ITP.
Two hundred sixteen patients. This is not, and half of them were treated with placebo, the other half was treated with baricitinib plus Danazole. Six month study, they found a durable response, that was higher, and I guess this is a correction of, the platelet counts in forty five percent of the combo patient group versus twenty percent on Danazole only, suggesting that JAK inhibitor therapy could be an effective therapy for patients with refractory ITP. Again, I want to underscore that was refractory, meaning they had failed corticosteroids and other measures. This week, the world US News and World Report published its annual, listing of the top, 20 best rheumatology hospitals in The United States and I think other than, you know, five and six or six and seven doing a flip here, the listing is the same as last year.
Here's the top 10. Number one, Johns Hopkins. Number two, Cleveland Clinic. Number three, the HSS Columbia Cornell Association number four, Mayo Clinic five, the Brigham and Women's number six, Mass General Hospital. I think the Brigham and Mass General Hospital have emerged into MGB, that's a new entity, so that's before this survey.
UCSF number seven, UCLA number eight, NYU Langone number nine, and Michigan, University of Michigan, Medical Center number 10. Good to know. Two more reports, Gem had an, I thought, really interesting review worth reading on hip fracture, something that does come across your desk. It is a major global health, problem, fourteen million worldwide, 280,000 United States, higher in women, much more so than men. And again, what they wanted you to take away was RA and steroids are dual risk factors, both impair bone, strength and increase fall risk, suggesting that RA patients are high priority populations for, FRACS based screening.
They point to studies showing IV zolundronic acid post hip fracture reduces both the risk of new fracture by thirty five percent and significantly reduces future mortality. Again, something they bring up in this article is the number of people who have hip fractures who are not assessed for osteoporosis after their hip fractures is criminal, you know, and you need to remind everybody in the ER and who's an orthopedist and those amongst your patients, I don't care what their age is, you do need to do an assessment for whether or not you're going to intervene with drugs that will strengthen bone. They remind everyone that discontinuing denosumab, denosumab will cause a rapid rebound in bone loss and also a vertebral fracture risk and that you need to bridge that with future alternative anti resorptive therapies. They point out something I'm not really aware of, in all the places I've worked, we have not had fracture liaison services or ortho geriatric home management clinics, that patients, elderly that have hip fracture should be referred to fracture liaison services. Look it up, find out, you have one or, an orthopedic geriatric, specialist in your area.
And lastly, that patients should be assessed by the fracture risk assessment tool also known as FRACS, especially if they're on glucocorticoids, it is the most validated tool providing a ten year risk of future major, hip and osteoporotic fractures. A hip FRACS score of greater than 3% automatically means you need to be on pharmacotherapy for that. Lastly, we had a tribute to, great friends, great mentor, great scientific leader, Doctor. Dan Kastner from the NIH, the father of autoimmunity, he coined the term. He started his career working on FMF, did a lot of work, traveled to a lot of places, spent a lot of time in Israel, getting to the roots of the MEFV gene, variants that are associated with that disease.
And he went on to describe so many other conditions, including, the cryopyranopathies, Savvy, Dada, Candle, and more recently working with other researchers to describe the Vexus syndrome. It's worth a read, if only to read the comments by his colleagues, friends, those he trained, those he worked alongside with. One comment on Facebook called him the healer, mentor, and master of kindness. That's really true. Another said he was a brilliant scientist but a deeply humble, generous mentor, renaissance physician whose empathy for patients rivaled his scientific rigor.
Again, not everyone knows Dan's scientific achievements, but his dealings with patients were special. He was one of them. He'd sit on the floor with them and ask them, why do you wear those crazy socks? I mean, he was great at this. Fred Miller, started his training at the NIH the same time as Dan remembers him most for his wisdom and calm, insightful and considerate demeanor.
He had this positive spirit and unwavering belief in the potential of others and in his work environment created a place where people were excited to learn rather than being intimidated to work in a place like the NIH. Michelle Petrie had a real short but definitely resonating comment. That voice, that big booming voice, Dan, was in the room before we could see him. He had this great, great baritone. Ron Laxner of of in Toronto said he remembers him for his menschlikite.
And pardon me if for if I'm I'm not Yiddish enough to say that right, but menschlikite, it's a Yiddish word that describes your humanness and dedication to others. Susan Chenoweth said he had this infectious passion that went well beyond that brilliant mind that led to so many transformative scientific discoveries. Lastly, John Kay put a tribute up and included his caricature of Dan and his spectacular eyebrows, that were better than Andy Rooney's, and usually left an impression that was bore some sort of comment by someone. He was proud of those eyebrows and John reminded us that it was an honor to his mentor when he got to the NIH, John Decker, which I did not know that story because at the time I was considering going into rheumatology, I wrote John Decker about his report on Still's disease and the man called me back. I was a resident.
I was, I don't know, 23 or 25 or something, and I was shocked that the guy from the NIH just called me back about, you know, this project. So, Dan chose well to model after John Decker and, John Decker would be immensely proud of the effects that Dan has had on rheumatology, innumerable researchers, countless numbers of patients and the discipline overall. To me, he's not the father of auto inflammatory disease, He's, I think he's the godfather of rheumatology. It's hard to come up with anyone who has had as much of an impact on our field as Dan Castor. Take care.
A lot of interesting things did come up and were posted for your educational pleasure. Let's begin with a study from Beer. That's the British Dermatology Biologics Registry called Bad Beer. We haven't really talked about that, but they're just as good as the BSRBR, which is a biologics registry for rheumatologists and, for biologics. Anyway, Bad Beer has a registry of almost nineteen thousand psoriasis patients.
They looked at the incidence of serious, infectious events, SIEs. The number is, drum roll please, twenty eight SIEs per 1,000 patient years. Let me do the conversion for you, that's two point eight per 100 patient years. I've talked about those terms before, that's a low number and we've said before that, psoriatic tend to have lower rates of SIEs compared to for instance RA and inflammatory bowel patients, and there may be factors behind it, but those are just the facts. Generally less than three per 100 patient years.
I thought that that was interesting. The other interesting factor in this report was the rate was higher if you had a prior SIE. That's a very well known phenomenon in the infectious disease world. If you had a previous SIE, meningitis, pneumonia, sepsis, and you were hospitalized for it, guess what? Your odds of getting it again are way up and your odds of dying for it second time around are also now substantial.
Anyway, if you had a prior SIE, now the rate goes to seventy nine per one thousand, twenty eight to seventy nine, that's almost two and a half fold higher, that's important. They found the rates were lowest with, rizenkizumab, when they compared it to bredalumab or etanercept or other standard therapies. Rizenkizumab, the IL-twenty three inhibitor had roughly a twenty six to twenty percent lower rate. Now, those are more recent drugs compared to more older drugs. Maybe there's better patient selection, hard to know.
Nonetheless, these are good numbers. The death rate from an SIE is one point eight per one thousand patient years or less than, zero point two per 100 patient years, right? Speaking of infection, Cassie Calabrese from the Cleveland Clinic Foundation had a nice piece, that she published this week, giving an overview of vaccinating, patients with immune mediated inflammatory disorders or IMiDs. She basically says that you need a risk based approach, knowing what's high, benefit and who needs it most. And for instance, she says the use of Shingrix or the recombinant Zoster vaccine is indicated for all individuals regardless of age, going on a JAK inhibitor or going on anifrolumab.
I like that, I endorse that a 100%. She says you need to time, the use of a COVID vaccine in your patients who are on or going to consider treatment with rituximab, meaning they're on rituximab and you give a COVID or any vaccine, the human response is gonna stink. You need to get them at the nadir or before you start them, it's really important that you time vaccinations, especially the COVID vaccine. She strongly recommends annual flu and PCV20 or twenty one for all of our patients who are immunosuppressed, and she does recommend sort of a selective use of the vaccine against, RSV, being highly indicated in the elderly over age 75 or younger individuals who have risk factors, chronic lung disease and chronic kidney disease. I saw an interesting, article about nonsteroidals, and their effect in age related macular degeneration, from an ophthalmology journal.
Age related macular degeneration is, as they put it in their paper, which was gonna say that nonsteroidals are protective. They made the point that it's probably an inflammatory condition. I went a little bit further on this. I think most experts don't think that age related macular degeneration is inflammatory in its origins, but inflammation, especially chronic inflammation plays a role, and this sounds to me like what we see with osteoarthritis. It's a degenerative condition, so is age related macular degeneration, AMD, and it is modified by and spurned by at times inflammation.
Anyway, in this study, it was a TriNetX study from 2015 to 2024, nine year study, looking at people who did not individuals via their electronic medical records, who did not have AMD and compared, about six hundred and thirty five thousand who took a non steroidal versus six hundred and thirty five thousand who did not take a non steroidal and guess what? Non steroidal use significantly lowered the risk of future AMD at six months, lowered it by almost seventy percent and going all the way out to five years lowered it almost by fifty percent. So, it basically has a protective effect of about forty two percent overall over a five year span. This was not as strong, but still significant if they were just taking aspirin. Stronger and more significant if you're taking selective nonsteroidals with about a 59% protective effect.
So, another reason why some patients really might need to be on or wouldn't be a bad idea if they were on, nonsteroidals. Again, there are no trials proving this point, this is TriNetX sort of a target emulation trial using, cohort data to prove the point. There was a rebroadcast, if you will, of the TREAT earlier study, which you know was an early intervention study in clinically suspect arthralgia patients who had evidence of subclinical joint inflammation. They did not need to be seropositive to be in the study, and in this study done in The Netherlands, they were treated with twelve months of methotrexate or not. Two hundred and thirty six patients with CSA, they showed that methotrexate was preventative, but only in seronegative RA, where, in that population getting methotrexate only nine percent developed RA versus placebo where thirty five percent developed RA.
If you looked at seropositive patients, it didn't matter, fifty eight and sixty five percent developed seropositive RA on placebo or on methotrexate. I put this up because I think it's proof of something I've been lecturing about lately, which is the differences between seronegative and seropositive RA. They are definitely different and seronegative is definitely not more benign, but this shows you, maybe at a deeper, not yet understood level that these response rates are also indicating there's something truly different between those disorders. Think about it. JAMA had a nice review this week about sleep health and obesity, they are linked, there's a bi directional relationship.
If you have obesity, you're more likely to get sleep problems. If you have sleep problems, you're more likely to get obesity. Pretty simple, right? Insufficient sleep and poor sleep quality associated with weight gain, less healthy diets, and a higher risk of obesity, and then we go back the other way as well. It's a nice review in JAMA.
University of Alberta reported on a study looking at a predictive survey called GCAPS or GCAPS, and I posted for you on there the survey questions that are used to know whether someone who you suspect is having GCA should receive a more aggressive workup and biopsy. So, in their study of sixty two newly referred suspected GCA patients, GCA was ultimately diagnosed in thirty nine of those individuals, and of those that were diagnosed, fifty percent had a high, GCaPS screening score, only thirty eight with intermediate disease only thirteen percent, or low risk, by the GCaPPS score. So, using the GCaPPS score, you can, maybe predict who needs further evaluation. One more fact, in intermediate or high risk GCAP score had a sensitivity of ninety seven percent, specificity of thirty percent, positive predictive value of seventy percent. Those are strong numbers, especially sensitivity.
Specificity, maybe not so much. What's in the GCAP score? Again, I think it comes from Scotland. It's age, sex, duration of symptoms, CRP, headache, PMR, jaw claudication, fever, type of field loss, temporal artery changes on fundoscopy, cranial nerve palsies, and peripheral artery changes, and you got a zero, one, two, or three score, you need a GCAP score of 10 or more to be high risk and definitely deserving of a biopsy and further evaluation. You might want to look at that if you're a GCA person.
Another study this week looked at males with SLE in a cohort of over 400 patients at thirty seven males, and what was unique about the males compared to females, again, this is only less than ten percent of the population, is that they had a higher prevalence of renal disease class four and class five lupus nephritis, was seen in fifty percent of those patients that was higher than the other populations. The males also had an higher incidence of Plaquenil related retinal toxicity. Sixty two percent of their patients overall were on hydroxychloroquine and of those twenty two percent had to discontinue the hydroxychloroquine who were male. So, I've always said that since you're not female, if you're gonna get lupus and you're male, you better have you're gonna more likely to have more lupus features and more serious lupus and that's borne out by many studies in the past. This study, I think, reiterates that.
Another study of lupus, six fifty seven multi ethnic lupus patients, use a machine learning tool to show that fourteen percent had organic brain disease and thirty percent had neuropsychiatric damage. The biggest predictor of organic brain disease was steroids. Are also a big predictor of neuropsychiatric damage, but other predictors of neuropsychiatric damage were MD global fatigue, pain, and again, glucocorticoids, especially glucocorticoid dose and how long you use it. Again, I think we find, the management of lupus and CNS disease is problematic. The more we know, the better we know.
Another study this week looked at cerebral atrophy. I mean, you scanned all your patients with lupus, you'd find cerebral atrophy more than you would expect, but it doesn't always correlate with neuropsychiatric lupus or lupus cerebritis. Anyway, in this study, they found that it was associated with, total of seventy patients, mean age 40, disease duration twelve years. They found that cerebral atrophy was associated with age, number 10% higher, higher education levels was associated with this and then cerebral atrophy in their study was associated with neuropsychiatric lupus, a four point six fold higher risk. They found cerebral atrophy at fifty three percent, but most of it was mild.
Three quarters of those who had cerebral atrophy, it was said to be mild. So, point is don't freak out when you see cerebral atrophy, think about whether it's related to age, or being, having too much education, but I guess maybe you should worry about, you know, a future risk of neuropsychiatric disease. ITP is a problem and how you manage is a problem. I came across a study this week looking at the use of baricitinib. In this study, they were using, everybody got Danazole, the, hormonal therapy for ITP.
Two hundred sixteen patients. This is not, and half of them were treated with placebo, the other half was treated with baricitinib plus Danazole. Six month study, they found a durable response, that was higher, and I guess this is a correction of, the platelet counts in forty five percent of the combo patient group versus twenty percent on Danazole only, suggesting that JAK inhibitor therapy could be an effective therapy for patients with refractory ITP. Again, I want to underscore that was refractory, meaning they had failed corticosteroids and other measures. This week, the world US News and World Report published its annual, listing of the top, 20 best rheumatology hospitals in The United States and I think other than, you know, five and six or six and seven doing a flip here, the listing is the same as last year.
Here's the top 10. Number one, Johns Hopkins. Number two, Cleveland Clinic. Number three, the HSS Columbia Cornell Association number four, Mayo Clinic five, the Brigham and Women's number six, Mass General Hospital. I think the Brigham and Mass General Hospital have emerged into MGB, that's a new entity, so that's before this survey.
UCSF number seven, UCLA number eight, NYU Langone number nine, and Michigan, University of Michigan, Medical Center number 10. Good to know. Two more reports, Gem had an, I thought, really interesting review worth reading on hip fracture, something that does come across your desk. It is a major global health, problem, fourteen million worldwide, 280,000 United States, higher in women, much more so than men. And again, what they wanted you to take away was RA and steroids are dual risk factors, both impair bone, strength and increase fall risk, suggesting that RA patients are high priority populations for, FRACS based screening.
They point to studies showing IV zolundronic acid post hip fracture reduces both the risk of new fracture by thirty five percent and significantly reduces future mortality. Again, something they bring up in this article is the number of people who have hip fractures who are not assessed for osteoporosis after their hip fractures is criminal, you know, and you need to remind everybody in the ER and who's an orthopedist and those amongst your patients, I don't care what their age is, you do need to do an assessment for whether or not you're going to intervene with drugs that will strengthen bone. They remind everyone that discontinuing denosumab, denosumab will cause a rapid rebound in bone loss and also a vertebral fracture risk and that you need to bridge that with future alternative anti resorptive therapies. They point out something I'm not really aware of, in all the places I've worked, we have not had fracture liaison services or ortho geriatric home management clinics, that patients, elderly that have hip fracture should be referred to fracture liaison services. Look it up, find out, you have one or, an orthopedic geriatric, specialist in your area.
And lastly, that patients should be assessed by the fracture risk assessment tool also known as FRACS, especially if they're on glucocorticoids, it is the most validated tool providing a ten year risk of future major, hip and osteoporotic fractures. A hip FRACS score of greater than 3% automatically means you need to be on pharmacotherapy for that. Lastly, we had a tribute to, great friends, great mentor, great scientific leader, Doctor. Dan Kastner from the NIH, the father of autoimmunity, he coined the term. He started his career working on FMF, did a lot of work, traveled to a lot of places, spent a lot of time in Israel, getting to the roots of the MEFV gene, variants that are associated with that disease.
And he went on to describe so many other conditions, including, the cryopyranopathies, Savvy, Dada, Candle, and more recently working with other researchers to describe the Vexus syndrome. It's worth a read, if only to read the comments by his colleagues, friends, those he trained, those he worked alongside with. One comment on Facebook called him the healer, mentor, and master of kindness. That's really true. Another said he was a brilliant scientist but a deeply humble, generous mentor, renaissance physician whose empathy for patients rivaled his scientific rigor.
Again, not everyone knows Dan's scientific achievements, but his dealings with patients were special. He was one of them. He'd sit on the floor with them and ask them, why do you wear those crazy socks? I mean, he was great at this. Fred Miller, started his training at the NIH the same time as Dan remembers him most for his wisdom and calm, insightful and considerate demeanor.
He had this positive spirit and unwavering belief in the potential of others and in his work environment created a place where people were excited to learn rather than being intimidated to work in a place like the NIH. Michelle Petrie had a real short but definitely resonating comment. That voice, that big booming voice, Dan, was in the room before we could see him. He had this great, great baritone. Ron Laxner of of in Toronto said he remembers him for his menschlikite.
And pardon me if for if I'm I'm not Yiddish enough to say that right, but menschlikite, it's a Yiddish word that describes your humanness and dedication to others. Susan Chenoweth said he had this infectious passion that went well beyond that brilliant mind that led to so many transformative scientific discoveries. Lastly, John Kay put a tribute up and included his caricature of Dan and his spectacular eyebrows, that were better than Andy Rooney's, and usually left an impression that was bore some sort of comment by someone. He was proud of those eyebrows and John reminded us that it was an honor to his mentor when he got to the NIH, John Decker, which I did not know that story because at the time I was considering going into rheumatology, I wrote John Decker about his report on Still's disease and the man called me back. I was a resident.
I was, I don't know, 23 or 25 or something, and I was shocked that the guy from the NIH just called me back about, you know, this project. So, Dan chose well to model after John Decker and, John Decker would be immensely proud of the effects that Dan has had on rheumatology, innumerable researchers, countless numbers of patients and the discipline overall. To me, he's not the father of auto inflammatory disease, He's, I think he's the godfather of rheumatology. It's hard to come up with anyone who has had as much of an impact on our field as Dan Castor. Take care.
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