Mentschlichkeit (8.7.2026) Save
Transcription
It's August 7th, 2026. This is the RheumNow podcast. Yes, you're here again. I'm Jack Cush. Glad to join you. We're going to 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 BADBIR. That's the British Dermatology Biologics Registry called BADBIR. 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, BADBIR has a registry of almost 19,000 psoriasis patients. They looked at the incidence of serious infectious events, SIEs. The number is — drum roll, please — 28 SIEs per 1,000 patient years. Let me do the conversion for you. That's 2.8 per 100 patient years. I've talked about those terms before. That's a low number. And we've said before that psoriatics tend to have lower rates of SIEs compared to, for instance, RA and inflammatory bowel patients. 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 from it a second time around are also now substantial. Anyway, if you had a prior SIE, now the rate goes to 79 per 10,000 — 28 to 79. That's almost two and a half fold higher. That's important.
They found the rates were lowest with risankizumab when they compared it to bimekizumab or etanercept or other standard therapies. Risankizumab, the IL-23 inhibitor, had roughly a 26 to 20% lower rate. Now those are more recent drugs compared to older drugs. Maybe there's better patient selection. Hard to know. Nonetheless, these are good numbers. The death rate from an SIE is 1.8 per 1,000 patient years, or less than 0.2 per 100 patient years.
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. For instance, she says the use of Shingrix, 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 100%.
She says you need to time the use of a COVID vaccine in your patients who are on or going to consider a treatment with rituximab. Meaning they're on rituximab and you give a COVID or any vaccine — the humoral response is going to 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 PCV21 for all of our patients who are immunosuppressed, and she does recommend a selective use of the vaccine against RSV, being highly indicated in the elderly over age 75 or younger individuals who have risk factors including chronic lung disease and chronic kidney disease.
I saw an interesting article about non-steroidals and their effect in age-related macular degeneration from an ophthalmology journal. Age-related macular degeneration — as they put it in their paper, which was going to say that non-steroidals 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 spurred by at times, inflammation.
Anyway, in this study, it was a retrospective study from 2015 to 2024, a 9-year study looking at individuals via their electronic medical records who did not have AMD, and compared about 635,000 who took a non-steroidal versus 635,000 who did not take a non-steroidal. And guess what? Non-steroidal use significantly lowered the risk of future AMD — at 6 months, lowered it by almost 70%, and going all the way out to 5 years, lowered it almost by 50%. So it basically has a protective effect of about 42% overall over a 5-year span.
This was not as strong but still significant if they were just taking aspirin, stronger and more significant if they were taking selective non-steroidals, with about a 59% protective effect. So, another reason why some patients really might need to be on, or it wouldn't be a bad idea if they were
on, uh, non-steroidals. Again, there are no trials proving this point. This is a target emulation trial using uh, cohort data to prove the point.
Uh, there was a rebroadcast, if you will, of the TREAT earlier study, which you know was an uh, 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 12 months of methotrexate or not. 236 patients with CSA. Um, they showed that methotrexate was preventative but only in seronegative RA, where um, in that population getting methotrexate only 9% developed RA versus placebo where 35% developed RA. If you looked at seropositive patients, it didn't matter. 58 and 65% developed seropositive RA on placebo or on methotrexate. I put this up because I think it's proof of uh, something I've been lecturing about lately, which is the differences between seronegative and seropositive — they are definitely different and seronegative is definitely not more benign. Um, but this shows you uh, 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 bidirectional 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? Uh, insufficient sleep and poor sleep quality is 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. Uh, and I posted for you on there the uh, the survey questions that are used um, to know whether someone who you suspect is having GCA should receive a more aggressive workup and biopsy. So in their study of 62 newly referred suspected GCA patients, GCA was ultimately diagnosed in 39 of those individuals. Um, and of those that were diagnosed, 50% had a high GCAPS screening score. Only 38% with intermediate disease, only 13% um, or low risk uh, by the GCAPS score. So using the GCAPS score, you can um, maybe predict who needs further evaluation. One more fact: an intermediate or high risk GCAPS score had a sensitivity of 97%, specificity of 30%, positive predictive value of 70%. Um, those are strong numbers, especially sensitivity. Specificity maybe not so much. What's in the GCAPS score? Again, I think it comes from Scotland. It's uh, age, sex, duration of symptoms, CRP, headache, PMR, jaw claudication, fever, um, type of visual field loss, temporal artery changes on fundoscopy, cranial nerve palsies, and peripheral artery changes. And you get a 0, 1, 2, or 3 score. You need a GCAPS 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.
Uh, another study this week looked at males with SLE in a cohort of over 400 patients. They had 37 males. And what was unique about the males compared to females — again this is only, less than 10% of the population — is that they had a higher prevalence of renal disease. Class 4 and class 5 lupus nephritis um, was seen in 50% of those patients. That was higher than the other populations. The males also had a higher incidence of plaquenil-related retinal toxicity. 62% of their patients overall were on hydroxychloroquine and of those 22% had to discontinue the hydroxychloroquine who were male. So um, I've always said that since you're not female, if you're going to get lupus and you're male, you're 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.
Uh, another study of lupus — 657 multiethnic lupus patients — uh, used a machine learning tool to show that 14% had organic uh, brain disease and 30% had neuropsychiatric damage. Um, the biggest predictor of organic brain disease was steroids. 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 uh, the management of lupus and CNS disease is problematic. The more we know the better we know.
Um, another study this week looked at cerebral atrophy. I mean, if you scanned all your patients with lupus, you'd find cerebral atrophy uh, more than you would expect, but it doesn't always correlate with um, neuropsychiatric lupus or lupus cerebritis. Anyway, in this study, they found that it was associated with um, total of 70 patients, mean age 40, uh, disease duration 12 years. Uh,
they found that uh cerebral atrophy was associated with age number one. uh 10% higher um higher education levels um was associated with uh this uh and then cerebral atrophy in their study was associated with neuropsychiatric lupus a 4.6-fold six-fold higher risk. They found cerebral atrophy at uh 53% but most of it was mild. Um 3/4 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 Danazol um the hormonal therapy for ITP 216 patients this is not and half of them were treated with placebo the other half was treated with baricitinib plus Danazol six-month study they found a durable response um that was higher and I this is a correction of uh the platelet counts in 45% of the combo patient group versus 20% on Danazol 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 US News and World Report published its annual um listing of the top uh 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 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 um 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 merged 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 um University of Michigan uh medical center number 10. Good to know.
Uh two more reports. Uh JAMA had an I thought a really interesting review worth reading on hip fracture. Something that does come across your desk. It is a major global health uh problem. 14 million worldwide, 280,000 in the United States. Higher in women, much more so than men. Um, and again, what they wanted you to take away was RA and steroids are dual risk factors. Both impair uh bone strength and increase fall risk, suggesting that RA patients are high priority populations for uh FRAX-based screening. They point to studies showing IV zoledronic acid post hip fracture reduces both the risk of new fracture by 35% 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 that 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 will cause a a 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. I in all the places I've worked, we have not had fracture liaison services or ortho geriatric co-management clinics. Um that patients, especially elderly, that have hip fracture should be referred to fracture liaison services. Look it up, find out. You might you might have one or u an orthopedic geriatric uh specialist in your area. And lastly, that patients should be assessed by the fracture risk assessment tool, also known as FRAX, uh especially if they're on glucocorticoids. It is the most validated tool, providing a 10-year risk of uh future major uh hip and osteoporotic fractures. A FRAX score of greater than 3% automatically means you need to be on pharmacotherapy for that.
Lastly, we had a tribute to uh great friends, great mentor, great scientific leader, Dr. 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 um variants that are associated with that disease. And he went on to describe so many other conditions you know including um you know uh the cryopyrinopathies uh uh SAVI DADA um CANDLE um and and more recently working with other researchers to describe the VEXAS syndrome. Um it's worth a read if only to read the comments by his colleagues, friends, those he trained, those he worked alongside with. Um 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 many people, 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, who 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 Petri had a real short but definitely resonating comment. That voice, that big booming, that big booming voice, Dan was in the room before we could see him. He had this great great baritone.
Ron Laxer of Toronto said he remembers him for his menschkeit. And pardon me if I'm not Yiddish enough to say that right, but menschkeit is a Yiddish word that describes your humanness and dedication to others.
Susan Shinoi said he had this infectious passion that went well beyond that brilliant mind that led to so many transformative scientific discoveries.
And lastly, John K 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 could 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 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 autoinflammatory disease. 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 Kastner. Take care.
Let's begin with a study from BADBIR. That's the British Dermatology Biologics Registry called BADBIR. 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, BADBIR has a registry of almost 19,000 psoriasis patients. They looked at the incidence of serious infectious events, SIEs. The number is — drum roll, please — 28 SIEs per 1,000 patient years. Let me do the conversion for you. That's 2.8 per 100 patient years. I've talked about those terms before. That's a low number. And we've said before that psoriatics tend to have lower rates of SIEs compared to, for instance, RA and inflammatory bowel patients. 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 from it a second time around are also now substantial. Anyway, if you had a prior SIE, now the rate goes to 79 per 10,000 — 28 to 79. That's almost two and a half fold higher. That's important.
They found the rates were lowest with risankizumab when they compared it to bimekizumab or etanercept or other standard therapies. Risankizumab, the IL-23 inhibitor, had roughly a 26 to 20% lower rate. Now those are more recent drugs compared to older drugs. Maybe there's better patient selection. Hard to know. Nonetheless, these are good numbers. The death rate from an SIE is 1.8 per 1,000 patient years, or less than 0.2 per 100 patient years.
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. For instance, she says the use of Shingrix, 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 100%.
She says you need to time the use of a COVID vaccine in your patients who are on or going to consider a treatment with rituximab. Meaning they're on rituximab and you give a COVID or any vaccine — the humoral response is going to 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 PCV21 for all of our patients who are immunosuppressed, and she does recommend a selective use of the vaccine against RSV, being highly indicated in the elderly over age 75 or younger individuals who have risk factors including chronic lung disease and chronic kidney disease.
I saw an interesting article about non-steroidals and their effect in age-related macular degeneration from an ophthalmology journal. Age-related macular degeneration — as they put it in their paper, which was going to say that non-steroidals 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 spurred by at times, inflammation.
Anyway, in this study, it was a retrospective study from 2015 to 2024, a 9-year study looking at individuals via their electronic medical records who did not have AMD, and compared about 635,000 who took a non-steroidal versus 635,000 who did not take a non-steroidal. And guess what? Non-steroidal use significantly lowered the risk of future AMD — at 6 months, lowered it by almost 70%, and going all the way out to 5 years, lowered it almost by 50%. So it basically has a protective effect of about 42% overall over a 5-year span.
This was not as strong but still significant if they were just taking aspirin, stronger and more significant if they were taking selective non-steroidals, with about a 59% protective effect. So, another reason why some patients really might need to be on, or it wouldn't be a bad idea if they were
on, uh, non-steroidals. Again, there are no trials proving this point. This is a target emulation trial using uh, cohort data to prove the point.
Uh, there was a rebroadcast, if you will, of the TREAT earlier study, which you know was an uh, 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 12 months of methotrexate or not. 236 patients with CSA. Um, they showed that methotrexate was preventative but only in seronegative RA, where um, in that population getting methotrexate only 9% developed RA versus placebo where 35% developed RA. If you looked at seropositive patients, it didn't matter. 58 and 65% developed seropositive RA on placebo or on methotrexate. I put this up because I think it's proof of uh, something I've been lecturing about lately, which is the differences between seronegative and seropositive — they are definitely different and seronegative is definitely not more benign. Um, but this shows you uh, 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 bidirectional 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? Uh, insufficient sleep and poor sleep quality is 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. Uh, and I posted for you on there the uh, the survey questions that are used um, to know whether someone who you suspect is having GCA should receive a more aggressive workup and biopsy. So in their study of 62 newly referred suspected GCA patients, GCA was ultimately diagnosed in 39 of those individuals. Um, and of those that were diagnosed, 50% had a high GCAPS screening score. Only 38% with intermediate disease, only 13% um, or low risk uh, by the GCAPS score. So using the GCAPS score, you can um, maybe predict who needs further evaluation. One more fact: an intermediate or high risk GCAPS score had a sensitivity of 97%, specificity of 30%, positive predictive value of 70%. Um, those are strong numbers, especially sensitivity. Specificity maybe not so much. What's in the GCAPS score? Again, I think it comes from Scotland. It's uh, age, sex, duration of symptoms, CRP, headache, PMR, jaw claudication, fever, um, type of visual field loss, temporal artery changes on fundoscopy, cranial nerve palsies, and peripheral artery changes. And you get a 0, 1, 2, or 3 score. You need a GCAPS 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.
Uh, another study this week looked at males with SLE in a cohort of over 400 patients. They had 37 males. And what was unique about the males compared to females — again this is only, less than 10% of the population — is that they had a higher prevalence of renal disease. Class 4 and class 5 lupus nephritis um, was seen in 50% of those patients. That was higher than the other populations. The males also had a higher incidence of plaquenil-related retinal toxicity. 62% of their patients overall were on hydroxychloroquine and of those 22% had to discontinue the hydroxychloroquine who were male. So um, I've always said that since you're not female, if you're going to get lupus and you're male, you're 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.
Uh, another study of lupus — 657 multiethnic lupus patients — uh, used a machine learning tool to show that 14% had organic uh, brain disease and 30% had neuropsychiatric damage. Um, the biggest predictor of organic brain disease was steroids. 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 uh, the management of lupus and CNS disease is problematic. The more we know the better we know.
Um, another study this week looked at cerebral atrophy. I mean, if you scanned all your patients with lupus, you'd find cerebral atrophy uh, more than you would expect, but it doesn't always correlate with um, neuropsychiatric lupus or lupus cerebritis. Anyway, in this study, they found that it was associated with um, total of 70 patients, mean age 40, uh, disease duration 12 years. Uh,
they found that uh cerebral atrophy was associated with age number one. uh 10% higher um higher education levels um was associated with uh this uh and then cerebral atrophy in their study was associated with neuropsychiatric lupus a 4.6-fold six-fold higher risk. They found cerebral atrophy at uh 53% but most of it was mild. Um 3/4 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 Danazol um the hormonal therapy for ITP 216 patients this is not and half of them were treated with placebo the other half was treated with baricitinib plus Danazol six-month study they found a durable response um that was higher and I this is a correction of uh the platelet counts in 45% of the combo patient group versus 20% on Danazol 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 US News and World Report published its annual um listing of the top uh 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 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 um 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 merged 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 um University of Michigan uh medical center number 10. Good to know.
Uh two more reports. Uh JAMA had an I thought a really interesting review worth reading on hip fracture. Something that does come across your desk. It is a major global health uh problem. 14 million worldwide, 280,000 in the United States. Higher in women, much more so than men. Um, and again, what they wanted you to take away was RA and steroids are dual risk factors. Both impair uh bone strength and increase fall risk, suggesting that RA patients are high priority populations for uh FRAX-based screening. They point to studies showing IV zoledronic acid post hip fracture reduces both the risk of new fracture by 35% 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 that 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 will cause a a 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. I in all the places I've worked, we have not had fracture liaison services or ortho geriatric co-management clinics. Um that patients, especially elderly, that have hip fracture should be referred to fracture liaison services. Look it up, find out. You might you might have one or u an orthopedic geriatric uh specialist in your area. And lastly, that patients should be assessed by the fracture risk assessment tool, also known as FRAX, uh especially if they're on glucocorticoids. It is the most validated tool, providing a 10-year risk of uh future major uh hip and osteoporotic fractures. A FRAX score of greater than 3% automatically means you need to be on pharmacotherapy for that.
Lastly, we had a tribute to uh great friends, great mentor, great scientific leader, Dr. 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 um variants that are associated with that disease. And he went on to describe so many other conditions you know including um you know uh the cryopyrinopathies uh uh SAVI DADA um CANDLE um and and more recently working with other researchers to describe the VEXAS syndrome. Um it's worth a read if only to read the comments by his colleagues, friends, those he trained, those he worked alongside with. Um 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 many people, 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, who 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 Petri had a real short but definitely resonating comment. That voice, that big booming, that big booming voice, Dan was in the room before we could see him. He had this great great baritone.
Ron Laxer of Toronto said he remembers him for his menschkeit. And pardon me if I'm not Yiddish enough to say that right, but menschkeit is a Yiddish word that describes your humanness and dedication to others.
Susan Shinoi said he had this infectious passion that went well beyond that brilliant mind that led to so many transformative scientific discoveries.
And lastly, John K 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 could 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 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 autoinflammatory disease. 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 Kastner. Take care.
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