Moral Distress (3.27.2026) Save
Transcription
Hello everyone. It is March 27, 2026 and this is the RheumNow podcast. Hi, I'm Dr. Jack Cush with RheumNow.com. This week on the podcast, a lot of good information designed to alleviate moral distress. In doing so, we'll be covering fibromyalgia in psoriatic arthritis. A Lyme vaccine is back. Were we not waiting for this? And the hidden but tangible benefits of patient surveys, particularly the MD hack. Let's begin with moral distress.
Moral distress. I just love this title. It was from a JAMA paper, which was a survey, and actually the title of the piece in JAMA was "Moral Distress and Occupational Burnout in US Physicians," published this last week in JAMA Network Open. The idea here is that moral distress is sort of clinical scenarios coupled with ethical concerns modified by personal factors. Your own strengths, weaknesses, feeling powerful or powerless, and external factors like your institution, your boss, and whatnot leads to a lot of moral distress while on the job. They have a tool that measures this. And by the way, it's measurable in medical students, in physicians, in health care workers.
So JAMA published a study of 5,700 physicians and found that the moral distress score, the mean moral distress score on a 0 to 10 scale with greater than four being high moral distress, was 3.29. Uh oh. Almost high moral distress in 5,741 physicians. But almost 40% of them said that they had high levels of moral distress. And this was more amongst physicians than amongst other US workers, and this is outside of health care. There was a very strong correlation between rising moral distress scores and burnout scores, intent to leave the job, intent to reduce workforce hours. And each of those got worse for each one-point increase in the moral distress thermometer or score.
Um, you know, I don't know what to think about this. I know that burnout and these issues are getting talked about now. They were really never talked about when I was a fellow. I think if you did talk about them, you were a crybaby and given more work to do as a reward for your presumed or voiced moral distress. But I think that these tools need to be measured, need to be followed, need to be addressed because medicine needs to be something that you're really happy with. And if you're not happy with it, then I think you can probably make more money or do more important things somewhere else. And the job as you choose or as defined needs to be one that is free of moral distress, is not going to lead to burnout. We do know that the biggest driver of burnout is sort of the administration of medicine, the electronic health record, all the things that we have to do, must do, and do it all in less than 10 minutes. Just not good.
Um, on a positive note, sed rates and CRPs — who's not happy when talking about sed rates and CRPs? They're cheap, they're easy, and they're just chock-full of good information that we can use. An economic analysis of sed rate and CRP testing was done. It was really a very lengthy article trying to look at the many ways you could do this. And the bottom line was, was it better to do sed rate and CRP together as opposed to doing each one individually? When they considered cost efficacy, misdiagnosis, follow-up costs, re-evaluations, overall health care costs, sed rate with a CRP was highly cost-effective, reduced misdiagnosis, and reduced follow-up care costs. Um, I think that's what you're all doing now. It's good to know that you've got actually good evidence backing you up in case someone's calling you on the carpet giving you moral distress about ordering too much in the way of sed rates and CRPs.
Jeff Curtis and colleagues this week published a claims data analysis using real-world safety data on tofacitinib and a variety of biologics in 48,000 patients with psoriatic arthritis. 3,100 were on tofacitinib, 27,000 on TNF inhibitors, 20,000 on IL-17 targeted drugs, the IL-23 inhibitor risankizumab almost 4,400, and ustekinumab almost 4,500. When they looked at the safety of all these drugs together and how it compared to TNF, the crude incidence rates really overlap considerably, saying basically there's no increased risk of tofacitinib for serious infections, MI and stroke, or cancer. But there's always a but, isn't there? Tofacitinib did have a significant increased risk of VTE, venous thromboembolic events, compared to all the others.
What were the rates we're talking about here? For serious infections, it was about two per 100 patient years. That's quite low, and those are in line with what you see in psoriatic arthritis, which has lower numbers than you have in RA and IBD. The rates for MI and stroke were 27 to 61 per 10,000 — or no, per thousand. VTE also very low, 17 to 42 per thousand, and cancer was 74 to 106 per thousand. So again, this is sort of one of these studies that's post-oral surveillance asking the repeated question: is it really risky, is it really
risky. Well, the study actually answered the question, but this study tells you it doesn't seem to be different from the other drugs. And if you look at the event rates, it's really quite unusual, right? It's quite rare. So that's important to know.
Sometimes to get the answers on the diseases we treat, we need large data. We look at registries, network analyses, meta-analyses. You know what? Those are not grade A evidence. Those are supportive evidence. Those are hypothesis-generating forms of data.
Truveta is a network of EMRs and you can do incredible research with the Truveta network cohort studies. This is retrospective data. They control for it by doing propensity matching. Sometimes well done, sometimes not so well done. This particular study was a Truveta cohort analysis of adult psoriatic arthritis patients — 123,000 — that were propensity matched to non-PsA controls. And yeah, you already know that PsA and psoriasis have a significantly higher cardiovascular morbidity risk. MACE events are hazard ratio 1.74, cardiovascular mortality almost double at hazard ratio 1.95, heart failure the same at 1.96, MI 1.71, and CVA 1.49. All significantly elevated.
Maybe the important part of this report was what was the influence of therapy. Did biologics or conventional DMARDs lower risk? And it was clear that biologics reduce MACE risk by 5% and cardiovascular mortality risk by — I want to say it was 8% — compared to conventional DMARDs like methotrexate or apremilast or whatever. So I think these drugs — we know from the RA literature that methotrexate and effective control with methotrexate lowers cardiovascular risk, right? But the biologics might be better, and I think you're seeing the same here with psoriatic arthritis therapies.
Speaking of psoriatic arthritis, I like this particular report that looked at the prevalence of fibromyalgia in PsA. It is the confounding factor that will screw up a lot of things. They found the median prevalence to be 18%, but it ranged — I think from 10 to 60% — in different cohort studies. Overall, across the board, patients with PsA who had coexistent fibromyalgia had higher disease activity scores, and those disease activity scores were from fibromyalgia and not inflammation and synovitis. Fibromyalgia, when present in PsA, was associated with worse disease outcomes, including failure to achieve low disease activity state and also failure to respond to therapy. But the important point is if you don't see it, you're going to think that the disease activity is from the disease and not something else. You must look for fibromyalgia in all clinic visits. That's a tender point exam and asking about sleep and then looking at their survey — you know, they mark up their surveys quite a bit — with notalgia.
Uh, a new revelation this week, and I don't know how important it is, but we now have — in the works, not yet FDA approved, but positive data reported by Pfizer and its co-developer, can't remember their name, sorry, starts with a V. The VALOR study was using a six-valent surface protein-based Lyme disease vaccine. It's called VLA15 compared to placebo. Patients were — and the studies were done in adults including adolescents in endemic regions where Lyme disease is prevalent. They got four doses at month zero, two, somewhere between five and nine, and then 12 months later. They looked at the number of people who developed Lyme disease during those times and then after the 12 months. And VLA15 did reduce Lyme disease risk by almost 73% at 28 days after the fourth dose, but when they looked in that second year period — second phase period — the protection rate was 15.8% and it fell short of the prespecified 20% margin needed to say that this was successful. But in this study they had fewer than expected cases of Lyme disease. So it was felt, by the press release from Pfizer, that this was positive data and that this would move forward.
Is this important? How much Lyme disease do you see? Do you need it in your area? According to the companies, there are 470-something thousand cases of Lyme in the United States every year. And you know, we had a LYMErix vaccine approved — I think it was a GSK product approved in 1998. That stayed on the market for a little bit, but because the vaccine wasn't being used and there were some concerns about safety, it was taken off the market — why we're developing this now. Again, they're going to have to really show safety, are they not? And meeting at least a benchmark minimal level of vaccine efficacy.
Dr. Ruscetti and colleagues in Italy have published in Lancet Rheumatology a really nice article — an important article — about disease activity being defined for patients with adult Still's disease. They use two different cohorts. They have an Italian cohort of 187 patients; part was used for development of criteria and the other part was for validation. And then 41 patients from a
canakinumab in Still's disease — a study called CONSIDER. They said that active Still's disease is based on five criteria and they didn't give the cutoffs here. So I'll just assume it's the classic fever of greater than 39 degrees centigrade, but it's fever plus one of the following: skin rash, arthritis, patient global greater than two out of 10, CRP greater than 10. Or you could have active disease if you didn't have fever but you had any of the other three — rash, arthritis, patient global, CRP.
Now again, Still's disease — you've got to have not just fever but high fever, not just rash but the evanescent salmon pink rash that comes and goes, not arthritis but polyarthritis — monoarthritis ain't working. Patient global I get. CRP should be sky-high, not 1 milligram per deciliter or 10 milligrams per liter.
So anyway, they showed correlations that were strong, and they showed that these criteria had an AUC — depending on whether it was the development, validation, or confirmation — AUCs of 0.93, 0.85, 0.88. Again, they should be congratulated for doing something that's very hard to do, which is study a disease that's rare and come up with useful guidelines that can be used in clinical trials that will better evaluate future therapies.
Ted Pincus, as you know, has championed the use of the HAQII score and the MD-HAQ score, working with his investigators at Rush. They have an ongoing study and they published the results of the MD-HAQ being done in 1,300-plus patients in the rheumatology clinic with a variety of rheumatology diagnoses. None of these patients had primary fibromyalgia. Nonetheless, in those 1,337 patients, they found using MD-HAQ they could identify 30% with anxiety, 24% with depression, a quarter with fibromyalgia, and 44% who had any one of those three.
In that 44%, those people had — guess what? — higher pain scores, seven versus four out of 10; higher RAPID3 scores, 17 versus 8.2. 8.2 is active; 17 is highly active. And that was compared to patients who did not have either fibromyalgia, anxiety, or depression. And those results were highly significant.
If you're not doing an MD-HAQ or a HAQ score in your practice, or a survey, I think you're really making a big mistake. Number one, it's no skin off your back — or if you're a knuckle or whatever you take skin off of. The patient does it. They do it in the waiting room. I won't see a patient who hasn't filled out my one-page, you know, RheumNow follow-up evaluation form, which includes: give me a zero to 10 HAQ pain score, give me a zero to 10 disease activity score. I do the eight-question HAQ. The MD-HAQ is 10 questions. And then I have all my other review of systems things and a few other things I ask them to fill out. I won't see a patient unless that's filled out — sorry — because I can look at that and in a nanosecond know where we're going on this visit. It's incredibly informative and it does help you to identify things you may not be asking about, including anxiety, depression, and fibromyalgia.
Okay, I'll get off my high horse and go back to reporting about a retrospective study on 135 lupus nephritis patients where they had 195 renal biopsies scored in the usual ways with activity and chronicity index. The point of this paper was: look beyond the glomeruli in lupus nephritis, because it's the interstitial fibrosis and tubular atrophy that predict the poor outcomes. They showed in their patients that had either moderate to severe interstitial fibrosis with tubular atrophy very strong correlations with non-renal response and progression to end-stage renal disease — a ninefold increased risk. Those factors were also influenced by age, the duration of lupus, prior number of lupus flares, and higher chronicity indexes. But I think they correctly point out something we've said for rheumatoid — we don't talk about the fibrotic stage of disease and how damaging and disabling and horrific it is — and it is exactly the same in other tissues like the kidney, especially in lupus nephritis.
Another study this week was a systematic review of 31 RCTs over 17,000 patients looking at predictors of response and trying to make the point that the traditional measures are better than biomarkers. Now, they only looked at one biomarker and that's the interferon signal. They looked at a lot of different biologics that were being used — it had anti-BAFF, JAK inhibitors, BTK inhibitors, the alpha interferon inhibitors — and basically they showed that when you use biologics in lupus, guess what, they all got better. The SRI-4 response was significantly higher than placebo, 26% higher, and that was significant even though it's only a relative risk of 1.26. But clinical responses they showed were significantly correlated with: one, serologic measures of active disease — by that they meant double-stranded DNA with low complements — and that
was higher than um than I just said with a relative risk of 1.45 and high baseline SLEDAI scores of greater of 10 or higher relative risk of 1.22 — that also being significant. Um, not significant was interferon um uh as a as a marker for disease activity and we know that it hasn't worked out well even in drugs where interferon alpha is the target of the therapy and that would be anifrolumab but anyway you're doing the right thing but the day is going to come — they I don't think they really looked at the right biomarkers here they really you know interferon great but you know uh Andrea Fava and and Michelle Petri has shown you know IL-16 in the urine is CD163 you know um other you know um macrophage biomarkers actually have great correlation with clinical outcomes renal damage renal outcomes activity index much better than proteinuria for instance much better than even double stranded DNA we need to see those biomarkers in play in rheumatology.
RA we know is a devastating disease it is associated with disability is associated with work loss. But did you know that as RA starts, it's already doing the damage? In this study, they compared 3,850 RA patients to their same sex siblings. And this was a study that went on between 2006 and 2020. They found that work loss in incident RA began as much as 13 months before the diagnosis of RA and peaked a year later. Um, and over this time frame, it was really bad during that first decade and it's gotten better in the last decade. So, what they found was that work loss was highly skewed, meaning that it wasn't all patients amongst that 3,800 RA patient cohort that had this problem. It's a small portion of them that contributed the most amount of work lost days, but the point is it begins early. It's not a disability thing that happens in the third, fourth, or tenth year of disease activity.
Speaking of RA, a nice study from uh Alberta looked at 546 RA patients being cared for in primary care practices. And what they showed uh in the multiple years of the study that at least 40% of RA patients in primary care will receive at least one prednisone prescription by the primary care doctor. They excluded people in the study who received you know um brief courses like for a cold or bronchitis or something like that. These are people that went on chronic prednisone. Um, 41% of people um were treated with both prednisone and a DMARD and that seems about right. Um and then of the people that went on prednisone, the prednisone um was being used a median of 124 days before the DMARD which is I think not good and not the way you should manage RA — meaning manage it with you know um what's that that's four months uh before they go on a DMARD or get referred for a DMARD — and then again in the primary care practices um when DMARDs were initiated two-thirds of them stayed on prednisone for more than a year and you're guilty of that too. There's good data showing rheumatologists do the same thing. Even though you're using steroid sparing therapy evidence that we actually steroid spare reduce steroids go off steroids isn't as great as the EULAR guidelines would allow us to believe. I think it is incumbent upon you that when you prescribe a steroid it should come with an expiration date.
So, um, one more thing on, uh, steroids. I did a survey, um, on Twitter this week. I I asked the question, an RA patient on 7.5 milligrams a day of prednisone needs to go for major surgery, i.e. uh, a hip replacement, let's say. What do you advise regarding the prednisone dose before surgery? What do you do with prednisone? And um 61% of you — a hundred people responded to this — 61% got it right, which is don't change anything. You're allowed to stay on the same dose of prednisone and go to surgery. But 37% of you said, you know, wean it down to five or less or go off — with many many saying go off the steroids. And that's wrong because the patient's going to flare. Flare is going to cause inflammation. Inflammation will drive infectious risk. You don't need to be below the endogenous cortisol production level and you don't need to uh cover people with stress doses of steroids. That's uh you know that was in Susan Goodman's lecture at RheumNow Live about the orthopedic ACR guidelines on how to manage drugs in people going for major surgery.
The last report this week that I'll cover was the EULAR 2025 update to Behçet's. Uh EULAR um last published its uh its guidelines on Behçet's in 2018. Uh they they are a real big revision. There are no recommendations from the previous version. Their seven recommendations have uh have been significantly modified. Overall, um, these new guidelines were based on over 7,000 articles, 16 studies, seven randomized trials. They came up with five overarching principles and 12 new recommendations. Maybe the the newest one is a preference for monoclonal TNF uh inhibitors in patients who have Behçet's with eye, vascular, or CNS or nervous system involvement. And
I can kind of endorse that, but I don't endorse TNF inhibitor use in Behçet's, especially for mucocutaneous disease arthritis. I've never been impressed with that at all, and I'm not convinced. But vascular — yes, they do say colchicine is the mainstay for mucocutaneous disease. Colchicine should be used as first-line therapy for acute arthritis. But patients who have either recurrent or chronic disease, immunosuppressives may be required.
And they go over the immunosuppressors. And immunosuppressors have to be used in patients with uveitis. And again they sort of come out front and say TNF might be their preferred agent there. They also make some comments about organ disease needing more aggressive therapy, thrombotic disease needing immunosuppressors and steroids, and plus or minus the use of anticoagulants based on the scenario, that GI involvement in Behçet's needs to be based on endoscopy. And that one of the agents that you can use with GI involvement in Behçet's is 5-ASA and drugs like that.
Anyway, that's it for this week on the podcast. Hope you enjoyed this. We'll talk to you next week. You can go to the website, find the citations for the reports I talked about here. Please give us a good review when you're reviewing and scoring podcasts that you like. We would appreciate that. We'll talk next week.
Moral distress. I just love this title. It was from a JAMA paper, which was a survey, and actually the title of the piece in JAMA was "Moral Distress and Occupational Burnout in US Physicians," published this last week in JAMA Network Open. The idea here is that moral distress is sort of clinical scenarios coupled with ethical concerns modified by personal factors. Your own strengths, weaknesses, feeling powerful or powerless, and external factors like your institution, your boss, and whatnot leads to a lot of moral distress while on the job. They have a tool that measures this. And by the way, it's measurable in medical students, in physicians, in health care workers.
So JAMA published a study of 5,700 physicians and found that the moral distress score, the mean moral distress score on a 0 to 10 scale with greater than four being high moral distress, was 3.29. Uh oh. Almost high moral distress in 5,741 physicians. But almost 40% of them said that they had high levels of moral distress. And this was more amongst physicians than amongst other US workers, and this is outside of health care. There was a very strong correlation between rising moral distress scores and burnout scores, intent to leave the job, intent to reduce workforce hours. And each of those got worse for each one-point increase in the moral distress thermometer or score.
Um, you know, I don't know what to think about this. I know that burnout and these issues are getting talked about now. They were really never talked about when I was a fellow. I think if you did talk about them, you were a crybaby and given more work to do as a reward for your presumed or voiced moral distress. But I think that these tools need to be measured, need to be followed, need to be addressed because medicine needs to be something that you're really happy with. And if you're not happy with it, then I think you can probably make more money or do more important things somewhere else. And the job as you choose or as defined needs to be one that is free of moral distress, is not going to lead to burnout. We do know that the biggest driver of burnout is sort of the administration of medicine, the electronic health record, all the things that we have to do, must do, and do it all in less than 10 minutes. Just not good.
Um, on a positive note, sed rates and CRPs — who's not happy when talking about sed rates and CRPs? They're cheap, they're easy, and they're just chock-full of good information that we can use. An economic analysis of sed rate and CRP testing was done. It was really a very lengthy article trying to look at the many ways you could do this. And the bottom line was, was it better to do sed rate and CRP together as opposed to doing each one individually? When they considered cost efficacy, misdiagnosis, follow-up costs, re-evaluations, overall health care costs, sed rate with a CRP was highly cost-effective, reduced misdiagnosis, and reduced follow-up care costs. Um, I think that's what you're all doing now. It's good to know that you've got actually good evidence backing you up in case someone's calling you on the carpet giving you moral distress about ordering too much in the way of sed rates and CRPs.
Jeff Curtis and colleagues this week published a claims data analysis using real-world safety data on tofacitinib and a variety of biologics in 48,000 patients with psoriatic arthritis. 3,100 were on tofacitinib, 27,000 on TNF inhibitors, 20,000 on IL-17 targeted drugs, the IL-23 inhibitor risankizumab almost 4,400, and ustekinumab almost 4,500. When they looked at the safety of all these drugs together and how it compared to TNF, the crude incidence rates really overlap considerably, saying basically there's no increased risk of tofacitinib for serious infections, MI and stroke, or cancer. But there's always a but, isn't there? Tofacitinib did have a significant increased risk of VTE, venous thromboembolic events, compared to all the others.
What were the rates we're talking about here? For serious infections, it was about two per 100 patient years. That's quite low, and those are in line with what you see in psoriatic arthritis, which has lower numbers than you have in RA and IBD. The rates for MI and stroke were 27 to 61 per 10,000 — or no, per thousand. VTE also very low, 17 to 42 per thousand, and cancer was 74 to 106 per thousand. So again, this is sort of one of these studies that's post-oral surveillance asking the repeated question: is it really risky, is it really
risky. Well, the study actually answered the question, but this study tells you it doesn't seem to be different from the other drugs. And if you look at the event rates, it's really quite unusual, right? It's quite rare. So that's important to know.
Sometimes to get the answers on the diseases we treat, we need large data. We look at registries, network analyses, meta-analyses. You know what? Those are not grade A evidence. Those are supportive evidence. Those are hypothesis-generating forms of data.
Truveta is a network of EMRs and you can do incredible research with the Truveta network cohort studies. This is retrospective data. They control for it by doing propensity matching. Sometimes well done, sometimes not so well done. This particular study was a Truveta cohort analysis of adult psoriatic arthritis patients — 123,000 — that were propensity matched to non-PsA controls. And yeah, you already know that PsA and psoriasis have a significantly higher cardiovascular morbidity risk. MACE events are hazard ratio 1.74, cardiovascular mortality almost double at hazard ratio 1.95, heart failure the same at 1.96, MI 1.71, and CVA 1.49. All significantly elevated.
Maybe the important part of this report was what was the influence of therapy. Did biologics or conventional DMARDs lower risk? And it was clear that biologics reduce MACE risk by 5% and cardiovascular mortality risk by — I want to say it was 8% — compared to conventional DMARDs like methotrexate or apremilast or whatever. So I think these drugs — we know from the RA literature that methotrexate and effective control with methotrexate lowers cardiovascular risk, right? But the biologics might be better, and I think you're seeing the same here with psoriatic arthritis therapies.
Speaking of psoriatic arthritis, I like this particular report that looked at the prevalence of fibromyalgia in PsA. It is the confounding factor that will screw up a lot of things. They found the median prevalence to be 18%, but it ranged — I think from 10 to 60% — in different cohort studies. Overall, across the board, patients with PsA who had coexistent fibromyalgia had higher disease activity scores, and those disease activity scores were from fibromyalgia and not inflammation and synovitis. Fibromyalgia, when present in PsA, was associated with worse disease outcomes, including failure to achieve low disease activity state and also failure to respond to therapy. But the important point is if you don't see it, you're going to think that the disease activity is from the disease and not something else. You must look for fibromyalgia in all clinic visits. That's a tender point exam and asking about sleep and then looking at their survey — you know, they mark up their surveys quite a bit — with notalgia.
Uh, a new revelation this week, and I don't know how important it is, but we now have — in the works, not yet FDA approved, but positive data reported by Pfizer and its co-developer, can't remember their name, sorry, starts with a V. The VALOR study was using a six-valent surface protein-based Lyme disease vaccine. It's called VLA15 compared to placebo. Patients were — and the studies were done in adults including adolescents in endemic regions where Lyme disease is prevalent. They got four doses at month zero, two, somewhere between five and nine, and then 12 months later. They looked at the number of people who developed Lyme disease during those times and then after the 12 months. And VLA15 did reduce Lyme disease risk by almost 73% at 28 days after the fourth dose, but when they looked in that second year period — second phase period — the protection rate was 15.8% and it fell short of the prespecified 20% margin needed to say that this was successful. But in this study they had fewer than expected cases of Lyme disease. So it was felt, by the press release from Pfizer, that this was positive data and that this would move forward.
Is this important? How much Lyme disease do you see? Do you need it in your area? According to the companies, there are 470-something thousand cases of Lyme in the United States every year. And you know, we had a LYMErix vaccine approved — I think it was a GSK product approved in 1998. That stayed on the market for a little bit, but because the vaccine wasn't being used and there were some concerns about safety, it was taken off the market — why we're developing this now. Again, they're going to have to really show safety, are they not? And meeting at least a benchmark minimal level of vaccine efficacy.
Dr. Ruscetti and colleagues in Italy have published in Lancet Rheumatology a really nice article — an important article — about disease activity being defined for patients with adult Still's disease. They use two different cohorts. They have an Italian cohort of 187 patients; part was used for development of criteria and the other part was for validation. And then 41 patients from a
canakinumab in Still's disease — a study called CONSIDER. They said that active Still's disease is based on five criteria and they didn't give the cutoffs here. So I'll just assume it's the classic fever of greater than 39 degrees centigrade, but it's fever plus one of the following: skin rash, arthritis, patient global greater than two out of 10, CRP greater than 10. Or you could have active disease if you didn't have fever but you had any of the other three — rash, arthritis, patient global, CRP.
Now again, Still's disease — you've got to have not just fever but high fever, not just rash but the evanescent salmon pink rash that comes and goes, not arthritis but polyarthritis — monoarthritis ain't working. Patient global I get. CRP should be sky-high, not 1 milligram per deciliter or 10 milligrams per liter.
So anyway, they showed correlations that were strong, and they showed that these criteria had an AUC — depending on whether it was the development, validation, or confirmation — AUCs of 0.93, 0.85, 0.88. Again, they should be congratulated for doing something that's very hard to do, which is study a disease that's rare and come up with useful guidelines that can be used in clinical trials that will better evaluate future therapies.
Ted Pincus, as you know, has championed the use of the HAQII score and the MD-HAQ score, working with his investigators at Rush. They have an ongoing study and they published the results of the MD-HAQ being done in 1,300-plus patients in the rheumatology clinic with a variety of rheumatology diagnoses. None of these patients had primary fibromyalgia. Nonetheless, in those 1,337 patients, they found using MD-HAQ they could identify 30% with anxiety, 24% with depression, a quarter with fibromyalgia, and 44% who had any one of those three.
In that 44%, those people had — guess what? — higher pain scores, seven versus four out of 10; higher RAPID3 scores, 17 versus 8.2. 8.2 is active; 17 is highly active. And that was compared to patients who did not have either fibromyalgia, anxiety, or depression. And those results were highly significant.
If you're not doing an MD-HAQ or a HAQ score in your practice, or a survey, I think you're really making a big mistake. Number one, it's no skin off your back — or if you're a knuckle or whatever you take skin off of. The patient does it. They do it in the waiting room. I won't see a patient who hasn't filled out my one-page, you know, RheumNow follow-up evaluation form, which includes: give me a zero to 10 HAQ pain score, give me a zero to 10 disease activity score. I do the eight-question HAQ. The MD-HAQ is 10 questions. And then I have all my other review of systems things and a few other things I ask them to fill out. I won't see a patient unless that's filled out — sorry — because I can look at that and in a nanosecond know where we're going on this visit. It's incredibly informative and it does help you to identify things you may not be asking about, including anxiety, depression, and fibromyalgia.
Okay, I'll get off my high horse and go back to reporting about a retrospective study on 135 lupus nephritis patients where they had 195 renal biopsies scored in the usual ways with activity and chronicity index. The point of this paper was: look beyond the glomeruli in lupus nephritis, because it's the interstitial fibrosis and tubular atrophy that predict the poor outcomes. They showed in their patients that had either moderate to severe interstitial fibrosis with tubular atrophy very strong correlations with non-renal response and progression to end-stage renal disease — a ninefold increased risk. Those factors were also influenced by age, the duration of lupus, prior number of lupus flares, and higher chronicity indexes. But I think they correctly point out something we've said for rheumatoid — we don't talk about the fibrotic stage of disease and how damaging and disabling and horrific it is — and it is exactly the same in other tissues like the kidney, especially in lupus nephritis.
Another study this week was a systematic review of 31 RCTs over 17,000 patients looking at predictors of response and trying to make the point that the traditional measures are better than biomarkers. Now, they only looked at one biomarker and that's the interferon signal. They looked at a lot of different biologics that were being used — it had anti-BAFF, JAK inhibitors, BTK inhibitors, the alpha interferon inhibitors — and basically they showed that when you use biologics in lupus, guess what, they all got better. The SRI-4 response was significantly higher than placebo, 26% higher, and that was significant even though it's only a relative risk of 1.26. But clinical responses they showed were significantly correlated with: one, serologic measures of active disease — by that they meant double-stranded DNA with low complements — and that
was higher than um than I just said with a relative risk of 1.45 and high baseline SLEDAI scores of greater of 10 or higher relative risk of 1.22 — that also being significant. Um, not significant was interferon um uh as a as a marker for disease activity and we know that it hasn't worked out well even in drugs where interferon alpha is the target of the therapy and that would be anifrolumab but anyway you're doing the right thing but the day is going to come — they I don't think they really looked at the right biomarkers here they really you know interferon great but you know uh Andrea Fava and and Michelle Petri has shown you know IL-16 in the urine is CD163 you know um other you know um macrophage biomarkers actually have great correlation with clinical outcomes renal damage renal outcomes activity index much better than proteinuria for instance much better than even double stranded DNA we need to see those biomarkers in play in rheumatology.
RA we know is a devastating disease it is associated with disability is associated with work loss. But did you know that as RA starts, it's already doing the damage? In this study, they compared 3,850 RA patients to their same sex siblings. And this was a study that went on between 2006 and 2020. They found that work loss in incident RA began as much as 13 months before the diagnosis of RA and peaked a year later. Um, and over this time frame, it was really bad during that first decade and it's gotten better in the last decade. So, what they found was that work loss was highly skewed, meaning that it wasn't all patients amongst that 3,800 RA patient cohort that had this problem. It's a small portion of them that contributed the most amount of work lost days, but the point is it begins early. It's not a disability thing that happens in the third, fourth, or tenth year of disease activity.
Speaking of RA, a nice study from uh Alberta looked at 546 RA patients being cared for in primary care practices. And what they showed uh in the multiple years of the study that at least 40% of RA patients in primary care will receive at least one prednisone prescription by the primary care doctor. They excluded people in the study who received you know um brief courses like for a cold or bronchitis or something like that. These are people that went on chronic prednisone. Um, 41% of people um were treated with both prednisone and a DMARD and that seems about right. Um and then of the people that went on prednisone, the prednisone um was being used a median of 124 days before the DMARD which is I think not good and not the way you should manage RA — meaning manage it with you know um what's that that's four months uh before they go on a DMARD or get referred for a DMARD — and then again in the primary care practices um when DMARDs were initiated two-thirds of them stayed on prednisone for more than a year and you're guilty of that too. There's good data showing rheumatologists do the same thing. Even though you're using steroid sparing therapy evidence that we actually steroid spare reduce steroids go off steroids isn't as great as the EULAR guidelines would allow us to believe. I think it is incumbent upon you that when you prescribe a steroid it should come with an expiration date.
So, um, one more thing on, uh, steroids. I did a survey, um, on Twitter this week. I I asked the question, an RA patient on 7.5 milligrams a day of prednisone needs to go for major surgery, i.e. uh, a hip replacement, let's say. What do you advise regarding the prednisone dose before surgery? What do you do with prednisone? And um 61% of you — a hundred people responded to this — 61% got it right, which is don't change anything. You're allowed to stay on the same dose of prednisone and go to surgery. But 37% of you said, you know, wean it down to five or less or go off — with many many saying go off the steroids. And that's wrong because the patient's going to flare. Flare is going to cause inflammation. Inflammation will drive infectious risk. You don't need to be below the endogenous cortisol production level and you don't need to uh cover people with stress doses of steroids. That's uh you know that was in Susan Goodman's lecture at RheumNow Live about the orthopedic ACR guidelines on how to manage drugs in people going for major surgery.
The last report this week that I'll cover was the EULAR 2025 update to Behçet's. Uh EULAR um last published its uh its guidelines on Behçet's in 2018. Uh they they are a real big revision. There are no recommendations from the previous version. Their seven recommendations have uh have been significantly modified. Overall, um, these new guidelines were based on over 7,000 articles, 16 studies, seven randomized trials. They came up with five overarching principles and 12 new recommendations. Maybe the the newest one is a preference for monoclonal TNF uh inhibitors in patients who have Behçet's with eye, vascular, or CNS or nervous system involvement. And
I can kind of endorse that, but I don't endorse TNF inhibitor use in Behçet's, especially for mucocutaneous disease arthritis. I've never been impressed with that at all, and I'm not convinced. But vascular — yes, they do say colchicine is the mainstay for mucocutaneous disease. Colchicine should be used as first-line therapy for acute arthritis. But patients who have either recurrent or chronic disease, immunosuppressives may be required.
And they go over the immunosuppressors. And immunosuppressors have to be used in patients with uveitis. And again they sort of come out front and say TNF might be their preferred agent there. They also make some comments about organ disease needing more aggressive therapy, thrombotic disease needing immunosuppressors and steroids, and plus or minus the use of anticoagulants based on the scenario, that GI involvement in Behçet's needs to be based on endoscopy. And that one of the agents that you can use with GI involvement in Behçet's is 5-ASA and drugs like that.
Anyway, that's it for this week on the podcast. Hope you enjoyed this. We'll talk to you next week. You can go to the website, find the citations for the reports I talked about here. Please give us a good review when you're reviewing and scoring podcasts that you like. We would appreciate that. We'll talk next week.
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