SATISFACTION (2.27.2026) Save
Transcription
It's February 27, 2026. This is the RheumNow podcast. Hi, I'm Jack Cush with RheumNow.com. This week on the podcast, IL-17 retention, the many causes of rhabdo, which should you be worried about, and satisfaction with and satisfaction by nurse practitioners.
At the top, JAMA Network Open had a nice article this week about using BIMAAB early rather than late. And they showed in an economic evaluation, not a head-to-head trial, basically as I do these economic cost-efficacy studies, they're used to these Markov modeling simulations with available data and whatnot. And they showed that using the BLISS inhibitor belimumab early versus late was shown to be cost effective and also clinically efficacious in patients with active disease.
Isn't that a game-changer or is it not? When and where do we use what we think are our best therapies, especially when our best therapies are really expensive? A number of years ago, I asked a few RA mavens, you know, if it's your mother or your mother-in-law, what are you using? Methotrexate or a JAK inhibitor? And for their mothers, they were wanting to use a JAK inhibitor as first drug. Even though JAK inhibitors are not in any guidelines currently listed as first-line therapy, methotrexate always is.
And the same applies here to lupus. Will we get to a point where the efficacy of a new expensive therapy far exceeds our expectations such that we must use it? We should use it. I think this kind of data, economic analyses about its utility, are important if they're backed up by the actual data that shows that using it earlier gives you better long-term outcomes. So this is an economic evaluation. We'd want better long-term outcomes, less renal death, less dialysis, less death, less hospitalization, less steroid use. You know, that's the studies we need to see. But I think this is a very good first step.
BMC Rheumatology did an analysis — and it was a survey of 143 women with a variety of different rheumatic diseases. These were young women of childbearing potential between the ages of 18 and 45, and they showed that only two-thirds of them, 63%, were using effective contraception. Even amongst those who were previously pregnant, one-third said that they experienced an unplanned pregnancy, suggesting, "Oops, the way I'm doing this is probably not a good idea." And as you know, the ACR guidelines on reproductive health authored by Lisa Sammaritano and a great group of investigators really are strongly in favor of counseling and coaching patients about contraception with our diseases, with our drugs, especially in lupus. So again, I think that this is a little bit of a shame on us for not doing better.
Frontiers in Immunology did a study of the test for rheumatoid arthritis called 14-3-3η. You know, this is one of the many tests that you can use to make a diagnosis of rheumatoid arthritis. There's rheumatoid factor, there's anti-citrullinated or anti-CCP antibodies, and there's also carbamylated protein antibodies. And this 14-3-3η, in a case-control study of control people — people without rheumatoid arthritis, 56 early rheumatoid arthritis, 72 established rheumatoid arthritis — they showed really the diagnostic performance of 14-3-3η was very good with an AUC of 85% for both established disease and early disease.
We know that 14-3-3η like CCP long precedes the onset of disease — you know, maybe not by 10 years like CCP, but pretty close to that in a lot of studies where it's been looked at. They did show that in comparison with CCP, CCP did have a better specificity, with the highest being 96%, and a slightly better likelihood ratio, but 14-3-3η had a higher sensitivity than the other tests that we use, 88%. So this is one of several that you can use, and this is good data suggesting its utility. I don't know that you need to do three or four rheumatoid tests when typically you usually do one or two. That's up for you to decide by looking at the data.
The Taiwan National Registry collects a lot of good data and they did a 20-year analysis of newly diagnosed biologically naive RA patients starting either on a biologic or a targeted synthetic. And in this 20-year period, what — 6,300 on TNF inhibitors, almost 700 on IL-6, 656 on abatacept, over 1,000 on a JAK inhibitor — they looked at over 8,700 patients. And when they looked at malignancy rates between these drugs — now again, you've got to think these are 8,700 newly diagnosed biologically naive patients sick enough to get a biologic. So you have to assume, although they didn't give us data on activity, that they have very active disease. And with the combination of very active disease and these new expensive biologics, is there an increase in malignancies? And they did not show any difference in the malignancy rates between these four drugs, either looking at a 5-year endpoint or out to 18 years.
where the risk of a newly diagnosed malignancy was 2.16% at 5 years, almost less than 3% at 18 years. That's encouraging data. And you know, I've talked about cancer in the past. Your job is to treat the arthritis. Let someone else worry about cancer. There is not a cancer scenario that is going to dictate what drug I'm going to use. And there's far more data about TNF inhibitors and cancer than there is on any other drug. Look it up. Do the research as I have. So I'm going to give the patient the best drug that they need, and I'm not going to be handicapped by cancer, whether it's a worry about cancer because it's in the package label. Everything's in the package label, including blue eyeball, green toenail syndrome. I just made those up, by the way. And if you're worried about cancer, let someone else manage the cancer, and you manage the arthritis with the best drugs available.
JAMA Dermatology published the results of what happens when newly diagnosed psoriasis patients are entered into the Danish derm bio registry and treated with biologics. When they look at bio-naive patients, almost 4,000 of them, which of the many biologics they use in psoriasis — same that you use in psoriatic arthritis — had the best long-term 5-year survival. Number one on the list would surprise you. It was ustekinumab, the IL-12/23 inhibitor, followed by adalimumab and secukinumab not being a close second and third. Of the again over 3,400 who were biologic-experienced, the best performing drugs after 2 years — as far as survival, and that's how they're counting the efficacy and safety of a drug, meaning their long-term survival — number one: deucravacitinib, guselkumab, and risankizumab. So we have a number of IL-23 inhibitors on this list: guselkumab, risankizumab, and ustekinumab, and then also rising to the top, the IL-17s.
Does that help you in the algorithm on what you may use in psoriatic arthritis? What about psoriatic arthritis that has got a lot of skin disease? I think a lot of people have forgotten about ustekinumab and why did it work. I think one of the reasons, kind of hinted at in the article, was that variable dosing — you can start at 45 mg or go to 90 mg — and it looked like most of those people who did really well long-term did go to 90 mg. So something to think about.
While we're on IL-17, there's a newer one in development by Moonlake. It's called sonelokimab. It's a nanobody that inhibits both IL-17A and F. It's marching towards approval. The data looks good in psoriasis and in psoriatic arthritis. They put out a press release this week showing that their phase 2 trials in spondyloarthritis — this is called the Solaris study — it's a small study, 26 patients, but it's encouraging data. They are in phase 3 trials. And they have other phase 2 trials that were also positive, but this is axial spondyloarthritis: over 80% achieved an ASAS40 — that's a high marker, a high benchmark if you will — by week 12. So that's quite encouraging. We want to see more data like that on IL-17 inhibition, especially dual inhibitors like this.
A real-world study of PsA patients looked at retention rates over time and what affects that. I don't know if you follow the data as I have for psoriasis and psoriatic arthritis. It's really dramatic for psoriasis — these drugs work great, but their long-term retention, not so great. And I think one of the reasons is not that the drugs wear out. I think at the first hint of not doing well, there are so many options people switch and bail out maybe too early. I think if you were running a country — let's say you were running the country of Grenada, as I have in the past — and you only had one drug to use or two drugs to use, I'll bet your retention rate on one of those or two drugs would be much better than what's pointed out in these studies. And I'm talking about two-year survivals being, you know, 40% or less.
So in this particular study, what they found was most influential on retention rates being significantly lowered was, number one, smoking. Smoking, especially being a current smoker, showed a significant drop in retention rates. But unlike other studies, obesity did not, in the 2-year time period that they looked at. The hazard ratios were significantly higher for former smokers — 32% higher of dropping out — and 27% higher for current smokers.
When I actually went back to get the citation, I saw that just in the last 6 months there's a whole bunch of retention studies that are out there for both PsA and spondyloarthritis. And at two years, it looks like it's 60%. And that's not good. Retention is worse when there's obesity, when there's prior treatment with biologics or prior drug failures — that's not surprising. It's also best in axial disease, so the converse would be it may be worse in peripheral disease.
So speaking of peripheral disease, the
journal rheumatology this past week published a report from Sophia Romero and a bunch of colleagues in Europe that looked at a number of different trials and specifically looking at peripheral manifestations of axial spondyloarthritis. And what they showed was in trials that involved biologics and targeted synthetics there was only a modest small to modest effect on peripheral symptoms and that means either peripheral arthritis, enthesitis, dactylitis. So when you looked at these trials, many trials only 54% reported data on peripheral arthritis, 64% on enthesitis and dactylitis in only 10% of the studies. Well, does that not happen in a large percentage of axSpA patients? Why isn't it being, you know, collected on all of them? And again, they're saying that the small to moderate effects seen may be due to the under-reporting and under-assessment, if you will, a complete assessment of axial spondyloarthritis. You will get different results for these drugs between peripheral manifestations and axial manifestations. And that's why they should all — and or extra-axial manifestations we should say — that's why they should all be done.
The journal Chest had an issue, a discussion this week about rhabdo. So I found this recent report, a full review. It's really a good one from the journal Chest on rhabdomyolysis. You know, 26,000 cases a year in the United States. Whoa. So muscle damage leading to gigantic CK aldolase enzyme elevations manifesting as weakness, myalgias, you know, swelling, myoglobinuria, electrolyte problems, and then hopefully not acute kidney injury or death. These are the consequences. The common causes from their review — the most common one was exogenous toxins. And I guess that would be obviously drugs, and yeah, statins and alcohol and drugs and toxins. Number two was trauma. Number three is myositis, myopathies, and metabolic bone disease. That's about 10%. Acute kidney injury was seen in 46% and death in 3.4%. They also go into the management of rhabdo and that includes fluids, electrolytes, alkalinization of the urine, use of mannitol, even dialysis and some new research things not necessarily proven.
Whenever I talk about rhabdo, I remember a case I had as a fellow where the chief complaint was patient found log rolling down Lemon Avenue. Log rolling being the form of ambulation. He had to log roll because he couldn't walk because he was weak because he was an IV drug abuser alcoholic who got rhabdo one way or another, but it was so bad he just couldn't walk. So to get from point A to B he was just rolling down Lemon Avenue and they picked him up and his CPK was 56,000. He skirted death but survived and the treatment was pretty much like I just mentioned.
Arthritis Research and Therapy published a review of antimitochondrial antibodies in systemic sclerosis. A retrospective study of 165 patients with that disease, 20% with diffuse disease, a third having ILD, 7% with pulmonary hypertension. Centromere antibodies were 51% in this cohort. 29% had topoisomerase antibodies. 12% had RNA polymerase antibodies and 22% were antimitochondrial antibody positive. What was the clinical scenario associated with that? Either GI or vascular disease, 13-fold higher, including gastric antral vascular ectasia. These patients presumably may be at a higher risk for GI bleeds and manifestations thereof including iron deficiency anemia. Can't say I often do AMA antibody testing and maybe I should.
The Journal of Clinical Medicine — not something I usually read but found a nice review of calcinosis cutis, which you know certainly occurs in systemic sclerosis and dermatomyositis, can be really problematic, can be associated with NXP2 antibodies I believe. But the question always is when they get a lot of calcinosis and they start to ulcerate and it really is ugly — what's your treatment? In their review, number one, and this came out in discussions in the past and on Twitter discussions, surgical intervention, usually excision, curettage, even laser ablation may be useful in removing the calcium deposits and to stop the ulceration and the problems that are intended thereafter.
Medical measures not so good. We'd like to write a prescription or do an infusion. These are partially effective. I would also say mostly ineffective. And if they are effective are only so when used early and with very localized disease. Includes the use of calcium channel blockers, tetracycline, probenecid, immunomodulators, biologic colchicine, sodium thiosulfate, and even JAK inhibitors. Can't say I've got any experience with that, can't say I would recommend that, but that's what was in the review and that's what I'm here to report.
A few more reports — Cell Metabolism talked about GLP-1 targeted therapy, which we know from a New England Journal article of last year pretty efficacious in NASH, and the question is is
it — and pain getting better, arthritis getting better, whatever — lupus, gout, RA, OA getting better because they lost weight, which we know makes everybody better, or are there other mechanisms by which this could occur? In this particular report, a basic science journal looked at a mouse model with obesity. Gave them the — the little mice. That's more than one mouse is me. Oh no, mice. Yeah, there you go. Um, gave them semaglutide and yes, they had less pain. Um, I'd like to see those assessments. What does that look like? The mice had less pain. Um, they also had less osteophytes and better cartilage preservation, all mediated via a weight loss independent pathway. So they basically said that by regulating the GLP-1 receptor AMPK/FBX3 axis, the GLP-1 reprograms chondrocyte metabolism from glycolysis to oxidative phosphorylation under inflammatory conditions, thus resulting in cartilage restoration. I'm obviously reading directly from the abstract and report, but it does give you — and there are other pathways, by the way, that the companies that are making these drugs are actively investigating — that are pointing to weight loss independent mechanisms by which these drugs will be big in our diseases. Stay tuned.
Um, I like this report. I'm ending with a few reports on advanced practice providers. The American College of Chest Physicians announced that they have a program where APPs can receive critical care certification, CCAP certification, by taking an exam that basically validates their experience and competence and enhances their credibility and recognition, as there is an issue with training and certification and competency. If you're looking to hire a — why don't we have this in rheumatology, we should — a recent AMA survey of 502 nurse practitioners, 95% of whom are working for MDs, showed that almost 90% were satisfied in the model that they were in. 90% — half were very satisfied, that was 48%. 94% valued the mentorship. 89% cited patient safety as a key benefit to physician-led care. Um, and 88% liked the liability protection of working in a group led by a physician.
And then I came across this Cochrane analysis that's recent, showing that when nurses are substituted for physicians in both inpatient and outpatient settings, the outcomes are not different. In fact, the outcomes may be better with nurses. And by nurses, I mean advanced practice nurses, clinical nurse specialists, and even RNs. 82 studies, 28,000 patients, 20 countries looking at inpatient and outpatient care in cardiology, diabetes, cancer, OB/GYN, and yes, rheumatology. The meta-analyses showed really no difference between nurse-led care and MD care, with moderate certainty evidence favoring — although not different — favoring the nurse-led care for mortality outcomes, quality of life outcomes, and self-efficacy outcomes. Again, moderate evidence, low certainty evidence for patient safety events and direct costs. You think, well, it's got to be a slam dunk on cost, right? Well, turns out there's maybe other extra training involved for people that are involved in specialty settings, hospital settings, etc. Uh, so that may normalize some of the cost, or the cost difference, if you will.
Again, I put this up because many rheumatologists are not sure that it's worth the expense or the effort to hire an APP. And as I have said in the past, if you don't, if you haven't, you're behind the times — because you'll just, well, you won't be behind the times. There'll be a 6-month to 8-month wait to get into your clinic, which means that you're going to see every fibromyalgia and ache and pain due to the ozone layer as opposed to seeing brand new early RA, brand new vasc.
This week in my clinic, I work in a charity clinic and the wait to get them to see me is not very long. And on Tuesday, the first — I saw four patients. The first three were brand new acute onset gout. No, I'm sorry, recurrent gout, but never seen by a rheumatologist before. First one. Second one was brand new PMR in someone who has an addiction problem with IV drugs. That was interesting. And the third one is just released from the hospital — lupus with nephritis, cytopenias, arthritis, skin involvement, and a serologic mess. And then the fourth one was RA, started on hydroxychloroquine because they had bilateral wrist pain, thumb pain, and a rheumatoid factor of 88. The thumb pain was correctly identified with a Finkelstein maneuver showing the patient has de Quervain's tenosynovitis. No synovitis. The patient doesn't have RA. The patient has bilateral tenosynovitis with fibromyalgia and poor sleep.
Oh, by the way, none of these people waited to get in to see me. And I do work with nurse practitioners in the charity clinic. So, obviously, I think you should as well. That's it for this week. Hope you take good care of yourself. Tune in next week. We'll do it again. Steely Dan said, "Right, get up and do it again."
At the top, JAMA Network Open had a nice article this week about using BIMAAB early rather than late. And they showed in an economic evaluation, not a head-to-head trial, basically as I do these economic cost-efficacy studies, they're used to these Markov modeling simulations with available data and whatnot. And they showed that using the BLISS inhibitor belimumab early versus late was shown to be cost effective and also clinically efficacious in patients with active disease.
Isn't that a game-changer or is it not? When and where do we use what we think are our best therapies, especially when our best therapies are really expensive? A number of years ago, I asked a few RA mavens, you know, if it's your mother or your mother-in-law, what are you using? Methotrexate or a JAK inhibitor? And for their mothers, they were wanting to use a JAK inhibitor as first drug. Even though JAK inhibitors are not in any guidelines currently listed as first-line therapy, methotrexate always is.
And the same applies here to lupus. Will we get to a point where the efficacy of a new expensive therapy far exceeds our expectations such that we must use it? We should use it. I think this kind of data, economic analyses about its utility, are important if they're backed up by the actual data that shows that using it earlier gives you better long-term outcomes. So this is an economic evaluation. We'd want better long-term outcomes, less renal death, less dialysis, less death, less hospitalization, less steroid use. You know, that's the studies we need to see. But I think this is a very good first step.
BMC Rheumatology did an analysis — and it was a survey of 143 women with a variety of different rheumatic diseases. These were young women of childbearing potential between the ages of 18 and 45, and they showed that only two-thirds of them, 63%, were using effective contraception. Even amongst those who were previously pregnant, one-third said that they experienced an unplanned pregnancy, suggesting, "Oops, the way I'm doing this is probably not a good idea." And as you know, the ACR guidelines on reproductive health authored by Lisa Sammaritano and a great group of investigators really are strongly in favor of counseling and coaching patients about contraception with our diseases, with our drugs, especially in lupus. So again, I think that this is a little bit of a shame on us for not doing better.
Frontiers in Immunology did a study of the test for rheumatoid arthritis called 14-3-3η. You know, this is one of the many tests that you can use to make a diagnosis of rheumatoid arthritis. There's rheumatoid factor, there's anti-citrullinated or anti-CCP antibodies, and there's also carbamylated protein antibodies. And this 14-3-3η, in a case-control study of control people — people without rheumatoid arthritis, 56 early rheumatoid arthritis, 72 established rheumatoid arthritis — they showed really the diagnostic performance of 14-3-3η was very good with an AUC of 85% for both established disease and early disease.
We know that 14-3-3η like CCP long precedes the onset of disease — you know, maybe not by 10 years like CCP, but pretty close to that in a lot of studies where it's been looked at. They did show that in comparison with CCP, CCP did have a better specificity, with the highest being 96%, and a slightly better likelihood ratio, but 14-3-3η had a higher sensitivity than the other tests that we use, 88%. So this is one of several that you can use, and this is good data suggesting its utility. I don't know that you need to do three or four rheumatoid tests when typically you usually do one or two. That's up for you to decide by looking at the data.
The Taiwan National Registry collects a lot of good data and they did a 20-year analysis of newly diagnosed biologically naive RA patients starting either on a biologic or a targeted synthetic. And in this 20-year period, what — 6,300 on TNF inhibitors, almost 700 on IL-6, 656 on abatacept, over 1,000 on a JAK inhibitor — they looked at over 8,700 patients. And when they looked at malignancy rates between these drugs — now again, you've got to think these are 8,700 newly diagnosed biologically naive patients sick enough to get a biologic. So you have to assume, although they didn't give us data on activity, that they have very active disease. And with the combination of very active disease and these new expensive biologics, is there an increase in malignancies? And they did not show any difference in the malignancy rates between these four drugs, either looking at a 5-year endpoint or out to 18 years.
where the risk of a newly diagnosed malignancy was 2.16% at 5 years, almost less than 3% at 18 years. That's encouraging data. And you know, I've talked about cancer in the past. Your job is to treat the arthritis. Let someone else worry about cancer. There is not a cancer scenario that is going to dictate what drug I'm going to use. And there's far more data about TNF inhibitors and cancer than there is on any other drug. Look it up. Do the research as I have. So I'm going to give the patient the best drug that they need, and I'm not going to be handicapped by cancer, whether it's a worry about cancer because it's in the package label. Everything's in the package label, including blue eyeball, green toenail syndrome. I just made those up, by the way. And if you're worried about cancer, let someone else manage the cancer, and you manage the arthritis with the best drugs available.
JAMA Dermatology published the results of what happens when newly diagnosed psoriasis patients are entered into the Danish derm bio registry and treated with biologics. When they look at bio-naive patients, almost 4,000 of them, which of the many biologics they use in psoriasis — same that you use in psoriatic arthritis — had the best long-term 5-year survival. Number one on the list would surprise you. It was ustekinumab, the IL-12/23 inhibitor, followed by adalimumab and secukinumab not being a close second and third. Of the again over 3,400 who were biologic-experienced, the best performing drugs after 2 years — as far as survival, and that's how they're counting the efficacy and safety of a drug, meaning their long-term survival — number one: deucravacitinib, guselkumab, and risankizumab. So we have a number of IL-23 inhibitors on this list: guselkumab, risankizumab, and ustekinumab, and then also rising to the top, the IL-17s.
Does that help you in the algorithm on what you may use in psoriatic arthritis? What about psoriatic arthritis that has got a lot of skin disease? I think a lot of people have forgotten about ustekinumab and why did it work. I think one of the reasons, kind of hinted at in the article, was that variable dosing — you can start at 45 mg or go to 90 mg — and it looked like most of those people who did really well long-term did go to 90 mg. So something to think about.
While we're on IL-17, there's a newer one in development by Moonlake. It's called sonelokimab. It's a nanobody that inhibits both IL-17A and F. It's marching towards approval. The data looks good in psoriasis and in psoriatic arthritis. They put out a press release this week showing that their phase 2 trials in spondyloarthritis — this is called the Solaris study — it's a small study, 26 patients, but it's encouraging data. They are in phase 3 trials. And they have other phase 2 trials that were also positive, but this is axial spondyloarthritis: over 80% achieved an ASAS40 — that's a high marker, a high benchmark if you will — by week 12. So that's quite encouraging. We want to see more data like that on IL-17 inhibition, especially dual inhibitors like this.
A real-world study of PsA patients looked at retention rates over time and what affects that. I don't know if you follow the data as I have for psoriasis and psoriatic arthritis. It's really dramatic for psoriasis — these drugs work great, but their long-term retention, not so great. And I think one of the reasons is not that the drugs wear out. I think at the first hint of not doing well, there are so many options people switch and bail out maybe too early. I think if you were running a country — let's say you were running the country of Grenada, as I have in the past — and you only had one drug to use or two drugs to use, I'll bet your retention rate on one of those or two drugs would be much better than what's pointed out in these studies. And I'm talking about two-year survivals being, you know, 40% or less.
So in this particular study, what they found was most influential on retention rates being significantly lowered was, number one, smoking. Smoking, especially being a current smoker, showed a significant drop in retention rates. But unlike other studies, obesity did not, in the 2-year time period that they looked at. The hazard ratios were significantly higher for former smokers — 32% higher of dropping out — and 27% higher for current smokers.
When I actually went back to get the citation, I saw that just in the last 6 months there's a whole bunch of retention studies that are out there for both PsA and spondyloarthritis. And at two years, it looks like it's 60%. And that's not good. Retention is worse when there's obesity, when there's prior treatment with biologics or prior drug failures — that's not surprising. It's also best in axial disease, so the converse would be it may be worse in peripheral disease.
So speaking of peripheral disease, the
journal rheumatology this past week published a report from Sophia Romero and a bunch of colleagues in Europe that looked at a number of different trials and specifically looking at peripheral manifestations of axial spondyloarthritis. And what they showed was in trials that involved biologics and targeted synthetics there was only a modest small to modest effect on peripheral symptoms and that means either peripheral arthritis, enthesitis, dactylitis. So when you looked at these trials, many trials only 54% reported data on peripheral arthritis, 64% on enthesitis and dactylitis in only 10% of the studies. Well, does that not happen in a large percentage of axSpA patients? Why isn't it being, you know, collected on all of them? And again, they're saying that the small to moderate effects seen may be due to the under-reporting and under-assessment, if you will, a complete assessment of axial spondyloarthritis. You will get different results for these drugs between peripheral manifestations and axial manifestations. And that's why they should all — and or extra-axial manifestations we should say — that's why they should all be done.
The journal Chest had an issue, a discussion this week about rhabdo. So I found this recent report, a full review. It's really a good one from the journal Chest on rhabdomyolysis. You know, 26,000 cases a year in the United States. Whoa. So muscle damage leading to gigantic CK aldolase enzyme elevations manifesting as weakness, myalgias, you know, swelling, myoglobinuria, electrolyte problems, and then hopefully not acute kidney injury or death. These are the consequences. The common causes from their review — the most common one was exogenous toxins. And I guess that would be obviously drugs, and yeah, statins and alcohol and drugs and toxins. Number two was trauma. Number three is myositis, myopathies, and metabolic bone disease. That's about 10%. Acute kidney injury was seen in 46% and death in 3.4%. They also go into the management of rhabdo and that includes fluids, electrolytes, alkalinization of the urine, use of mannitol, even dialysis and some new research things not necessarily proven.
Whenever I talk about rhabdo, I remember a case I had as a fellow where the chief complaint was patient found log rolling down Lemon Avenue. Log rolling being the form of ambulation. He had to log roll because he couldn't walk because he was weak because he was an IV drug abuser alcoholic who got rhabdo one way or another, but it was so bad he just couldn't walk. So to get from point A to B he was just rolling down Lemon Avenue and they picked him up and his CPK was 56,000. He skirted death but survived and the treatment was pretty much like I just mentioned.
Arthritis Research and Therapy published a review of antimitochondrial antibodies in systemic sclerosis. A retrospective study of 165 patients with that disease, 20% with diffuse disease, a third having ILD, 7% with pulmonary hypertension. Centromere antibodies were 51% in this cohort. 29% had topoisomerase antibodies. 12% had RNA polymerase antibodies and 22% were antimitochondrial antibody positive. What was the clinical scenario associated with that? Either GI or vascular disease, 13-fold higher, including gastric antral vascular ectasia. These patients presumably may be at a higher risk for GI bleeds and manifestations thereof including iron deficiency anemia. Can't say I often do AMA antibody testing and maybe I should.
The Journal of Clinical Medicine — not something I usually read but found a nice review of calcinosis cutis, which you know certainly occurs in systemic sclerosis and dermatomyositis, can be really problematic, can be associated with NXP2 antibodies I believe. But the question always is when they get a lot of calcinosis and they start to ulcerate and it really is ugly — what's your treatment? In their review, number one, and this came out in discussions in the past and on Twitter discussions, surgical intervention, usually excision, curettage, even laser ablation may be useful in removing the calcium deposits and to stop the ulceration and the problems that are intended thereafter.
Medical measures not so good. We'd like to write a prescription or do an infusion. These are partially effective. I would also say mostly ineffective. And if they are effective are only so when used early and with very localized disease. Includes the use of calcium channel blockers, tetracycline, probenecid, immunomodulators, biologic colchicine, sodium thiosulfate, and even JAK inhibitors. Can't say I've got any experience with that, can't say I would recommend that, but that's what was in the review and that's what I'm here to report.
A few more reports — Cell Metabolism talked about GLP-1 targeted therapy, which we know from a New England Journal article of last year pretty efficacious in NASH, and the question is is
it — and pain getting better, arthritis getting better, whatever — lupus, gout, RA, OA getting better because they lost weight, which we know makes everybody better, or are there other mechanisms by which this could occur? In this particular report, a basic science journal looked at a mouse model with obesity. Gave them the — the little mice. That's more than one mouse is me. Oh no, mice. Yeah, there you go. Um, gave them semaglutide and yes, they had less pain. Um, I'd like to see those assessments. What does that look like? The mice had less pain. Um, they also had less osteophytes and better cartilage preservation, all mediated via a weight loss independent pathway. So they basically said that by regulating the GLP-1 receptor AMPK/FBX3 axis, the GLP-1 reprograms chondrocyte metabolism from glycolysis to oxidative phosphorylation under inflammatory conditions, thus resulting in cartilage restoration. I'm obviously reading directly from the abstract and report, but it does give you — and there are other pathways, by the way, that the companies that are making these drugs are actively investigating — that are pointing to weight loss independent mechanisms by which these drugs will be big in our diseases. Stay tuned.
Um, I like this report. I'm ending with a few reports on advanced practice providers. The American College of Chest Physicians announced that they have a program where APPs can receive critical care certification, CCAP certification, by taking an exam that basically validates their experience and competence and enhances their credibility and recognition, as there is an issue with training and certification and competency. If you're looking to hire a — why don't we have this in rheumatology, we should — a recent AMA survey of 502 nurse practitioners, 95% of whom are working for MDs, showed that almost 90% were satisfied in the model that they were in. 90% — half were very satisfied, that was 48%. 94% valued the mentorship. 89% cited patient safety as a key benefit to physician-led care. Um, and 88% liked the liability protection of working in a group led by a physician.
And then I came across this Cochrane analysis that's recent, showing that when nurses are substituted for physicians in both inpatient and outpatient settings, the outcomes are not different. In fact, the outcomes may be better with nurses. And by nurses, I mean advanced practice nurses, clinical nurse specialists, and even RNs. 82 studies, 28,000 patients, 20 countries looking at inpatient and outpatient care in cardiology, diabetes, cancer, OB/GYN, and yes, rheumatology. The meta-analyses showed really no difference between nurse-led care and MD care, with moderate certainty evidence favoring — although not different — favoring the nurse-led care for mortality outcomes, quality of life outcomes, and self-efficacy outcomes. Again, moderate evidence, low certainty evidence for patient safety events and direct costs. You think, well, it's got to be a slam dunk on cost, right? Well, turns out there's maybe other extra training involved for people that are involved in specialty settings, hospital settings, etc. Uh, so that may normalize some of the cost, or the cost difference, if you will.
Again, I put this up because many rheumatologists are not sure that it's worth the expense or the effort to hire an APP. And as I have said in the past, if you don't, if you haven't, you're behind the times — because you'll just, well, you won't be behind the times. There'll be a 6-month to 8-month wait to get into your clinic, which means that you're going to see every fibromyalgia and ache and pain due to the ozone layer as opposed to seeing brand new early RA, brand new vasc.
This week in my clinic, I work in a charity clinic and the wait to get them to see me is not very long. And on Tuesday, the first — I saw four patients. The first three were brand new acute onset gout. No, I'm sorry, recurrent gout, but never seen by a rheumatologist before. First one. Second one was brand new PMR in someone who has an addiction problem with IV drugs. That was interesting. And the third one is just released from the hospital — lupus with nephritis, cytopenias, arthritis, skin involvement, and a serologic mess. And then the fourth one was RA, started on hydroxychloroquine because they had bilateral wrist pain, thumb pain, and a rheumatoid factor of 88. The thumb pain was correctly identified with a Finkelstein maneuver showing the patient has de Quervain's tenosynovitis. No synovitis. The patient doesn't have RA. The patient has bilateral tenosynovitis with fibromyalgia and poor sleep.
Oh, by the way, none of these people waited to get in to see me. And I do work with nurse practitioners in the charity clinic. So, obviously, I think you should as well. That's it for this week. Hope you take good care of yourself. Tune in next week. We'll do it again. Steely Dan said, "Right, get up and do it again."
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