Referral Rules to Live By (2.20.2026) Save
Transcription
Hello everyone. This is the RheumNow podcast. It is February 20th, 2026. I'm Jack Cush with RheumNow. This week on the podcast, more on combined biologic therapy in psoriatic arthritis. My referral rules when choosing between an orthopedist and a rheumatologist. You might want to argue with me about that. And can I use JAK inhibitors in pregnancy?
First, dermatomyositis and what we see and what we do. This is an interesting study. It's a combination of two different cohorts. Uh, 2,500 from claims data, almost 1,200 from a community-based electronic medical record claims data. And these are all dermatomyositis patients. And they found, as far as some basic benchmarks here, as far as what they observed, myositis panels were done in about half the patients, that 35% had testing for myositis specific associated autoantibodies. Not surprisingly, steroid use was common in roughly 70% between the two. But the most common drugs that were used in dermatomyositis — this was a head-scratcher for me. Hydroxychloroquine led the way, followed by methotrexate, mycophenolate, and then azathioprine. Number one, hydroxychloroquine. Really? What?
Now I have used it in a few people for the skin manifestations of dermatomyositis, but I don't know of any good data about its efficacy in muscle disease, and there's good evidence of hydroxychloroquine causing flares of dermatomyositis. So I find this one surprising. Again, this is observational data. Methotrexate we all kind of agree with, right? Mycophenolate though. Hm. We did report last year a cohort study from University of Pennsylvania about comparing mycophenolate to methotrexate outcomes as far as skin outcomes, and they were roughly the same. Okay, that makes sense. But mycophenolate — I don't have anybody on mycophenolate for dermatomyositis. Azathioprine — I think most of you are using methotrexate or azathioprine. I use a lot of leflunomide and there's only scant data to support that, but my experience says it works really, really well.
The outcomes as far as hospitalization and bad outcomes — these are expressed per 1,000 patient years. Not surprisingly, hospitalization leads the way at 92. Malignancy is next at 15. Malignancy is more common than — 15 versus six per 1,000 patient years — and myocarditis is really rare at only two events. So again, I think I like seeing these kinds of studies, although they are skewed by being observational data, but it sort of lets me think about what I do and how it compares to what's being done out there in the world.
A US biobank registry had lots and lots of patients. Looks at — and again really high numbers here — sought to evaluate the associations between osteoarthritis and osteoarthritis endpoints and sleep. And the osteoarthritis endpoints were knee OA, hip OA, knee replacement, hip replacement. Turns out that all of these were higher in people who had less than six hours of sleep per night. Hm. Moreover, night shift workers — people who worked that, you know, that graveyard shift and who were bouncing around between being night owls and trying to live daytime lives when they weren't working the night shift — these people had a 24% higher risk of knee OA and a 28% higher risk of knee replacement.
So why is that? What's the association here between sleep, bad sleep, and knee? I can't really put it together biologically. I can put it together from the standpoint of people with bad sleep have pain. People with pain seek attention. When you seek attention, you get a diagnosis, and then maybe something happens like a diagnosis or even surgery. But it still underscores the importance of sleep. If you as a rheumatologist are not an expert at sleep, you're really not doing a good job. I'm sorry to call you out on this, but I think it is so integral into what we do. It is such a big driver of pain and fatigue. If you do not assess for it and know what to do about it, you're missing a big chunk of the treatment options for your patient.
JRHEUM had a full read editorial on what HLA-B27 can and cannot tell us. I like this article because I like gene things. It basically tells you the prognostic and therapeutic implications behind B27. And they noted in this paper, B27 is associated with greater structural damage, higher inflammatory burden, better response to TNF inhibitors and IL-17 inhibitors. Now that latter part — that being B27 positive makes you more likely to respond to TNF and IL-17 targeted drugs — I'm not really that familiar with. I looked, and they just referenced one reference by doctors Diodar and Magra, and I couldn't really find much on that. I do know the converse is probably true. If you're B27 negative, you're probably not going to respond as well to those agents. Maybe because the diagnosis is less certain, but I certainly would like to know, and hopefully someone will tell me at some point, if I have a true advantage if you're B27 positive by giving you either a TNF inhibitor or an IL-17
inhibitor and which do I choose? Wouldn't that be a real advantage when it comes to prescribing? I think a real big move this week was the FDA changed its labeling on hormonal therapy. These are primarily estrogen based but sometimes combination estrogen progesterone based therapies. As you know when I was a fellow back in '84 I started — I think in the early '80s this whole issue of hormonal therapy posing risk to patients as far as cardiovascular disease, breast cancer etc was a big thing, became a black box warning and really it dramatically changed post-menopausal management and I got to say most of the women were not very happy about this and it's been shown that most of that data is probably not true and now you're going to see — now you see these box warnings being removed on six products, most of them being estrogen but then there were some progesterone only I think, and there are some topicals, but that's an important move because in the post-menopausal period estrogen and hormonal therapy proved to be very effective at symptom management and as long as it didn't pose a risk, why not do it.
Genentech announced the results of a phase two study of obexelimab, their anti-CD20 monoclonal antibody that we know was approved for lupus in October. This study, the Majesty study, is an open label study comparing obexelimab versus tacrolimus in 142 patients with primary membranous nephropathy and found more complete remissions at 2 years with the anti-CD20 drug. Now again, we know it's approved for lupus. This is going to be a big thing in lupus management. I thought you should know about this. Lupus patients get membranous nephropathy but I don't think there were lupus patients in this study because this was primary membranous nephropathy, but the good news is that it worked and it worked with an important outcome — complete remission at 2 years.
When we were doing in September, I believe it was, our campaign on — there was this argument going around by the experts about the utility of ultrasound in diagnosing ILD. And I thought that was kind of goofy because I thought you needed — I knew the chest X-rays were good, but high-res CTs were much better and really were the gold standard. And there were some reports of this. So I came across a recent study that looked at 73 patients with RA who had mild to moderate disease activity and they did both lung ultrasound and high-res CTs in these patients. Using high-res CT they found ILD in 29% of them, but when they used lung ultrasound it was found in 22%. That would make the sensitivity of lung ultrasound to be 59% and a specificity of 49%. It's noninvasive. There's no X-ray exposure. The ROC on this was good. You know, I think that maybe this could be an early screening procedure. But I must say that both ACR guidelines and the recent EULAR European Respiratory Society guidelines do state that if you're doing screening, the screening procedure of choice is high-res CT. But the lung ultrasound — who'd have thought?
Rotator cuff injuries we know are something that we commonly see. The prevalence of them goes up with age significantly. And this study that I put up this week, it was a study of 602 individuals with shoulder pain who underwent MRI. The average age was 58. Rotator cuff abnormalities were seen in 99% of people. I again was surprised by that number. 25% it was pure tendinopathy. 62% it was a partial tear of the rotator cuff. And 11% — only 11% — were full thickness tears. The point is, as we look at an elderly population with shoulder pain, is it really worth doing a rotator cuff MRI? Maybe if you're going to do surgery, and if that's the case, why should you be doing it? Send it to the shoulder guy and let him decide because he's going to do the surgery. In the meantime, all you can do is rotator cuff exercises, physical therapy, maybe local injections. But I think that this finding that with a mean age of 58, 99% having rotator cuff abnormalities makes me think twice about ordering MRI in the future before I refer or as a reason to refer.
Speaking of referral, someone said in the last two weeks, yeah, this person has this problem and I didn't know whether I should go to orthopedics or rheumatology. So I sort of looked that up. You know, what are the rules here? What's going on in the real world? Obviously, the decisions are either made by patients or by referring doctors, most of whom are either primary care or urgent care, emergency care. And you know what? There's no rules. And most of what's out there is kind of idiotic. You know, it says orthopedics, they get fractures, sprains, strains, and that kind of thing. And that rheumatologists only see autoimmune disease for immunosuppression. Obviously, there's a very big gray area in between. And there's a few papers that look at cohorts that were referred for
evaluation. And you know the ones that went to orthopedics — you know up to 25% or more — they said they should have gone to rheumatology, and that maybe 15% could have gone to rheumatology or orthopedics. And of the ones that went to rheumatology it looked like 90 plus percent should have been rheumatology with only a few percent going either way. So I don't think there are any rules on this. So I came up with my own, and it's for you to argue with me.
Number one, and again, this is something I would say to patients. This is something I would say to my primary care docs who want some instruction. Number one, anyone with a history of trauma, fall, you know, that sort of thing should go to the orthopedist or to emergency medicine, meaning the emergency department at your local hospital. That makes sense — you need to rule out structural damage and serious surgically correctable conditions.
Two, people with nagging or chronic musculoskeletal symptoms — that would mean more than 6 weeks — I think they should first go to a primary care doctor and then let primary care doctors refer to either ortho or rheumatology. And you would say, wait, primary care doctors don't know who to refer to. Well, that's what these rules are for. I'm honoring them. And you know there's what, 59 million people in the United States with osteoarthritis, 10 million with gout, 7 million with fibromyalgia, and 1 million with RA and 1.4 million with psoriatic. Come on. We can't see these people. We need a gatekeeper and primary care should be doing that and doing that well.
Number three, large joints — that's where that's the primary complaint — shoulders, hips, or knees. I say it's a toss-up between ortho and rheum. But if there's a discernible deformity, you know, a genu — an actual deformity, a contracture, or an abnormally enlarged joint — I think orthopedics should be first.
And number four, if it's small joint musculoskeletal problems — hands, fingers, wrist, elbows, ankles, feet, and toes — the rheumatologist is the choice to go to, especially if there are signs of swelling, inflammation, and no history of trauma.
My last recommendation is spinal problems should go to a spinal specialist. Neck, low back, whole back — go to a spine specialist first, a rheumatologist second, or an orthopedist third. I think this one we might want to argue about, but I think rheumatologists are adept at sorting out what needs to go to orthopedics, what may need neurosurgery, and being a good gatekeeper for the system. So anyway, these are my recommendations. I'd like to know what you think about them.
I think another big report came out this week. This was a press release from Lilly about their TOGETHER PSO trial. This is a trial of 274 patients with plaque psoriasis — moderate to severe plaque psoriasis — with obesity, who were then treated either with the IL-17 inhibitor ixekizumab, or the GLP-1 drug tirzepatide, and the combination was compared to IL-17 alone — ixekizumab. This is a phase 3b study. The 32-week endpoint was read out, showing superiority of the combination over the single drug. The primary endpoint here was a combined endpoint of a PASI 100 plus greater than 10% weight loss. That was achieved with the combination drug by 27%. If you were just on ixekizumab, only 6% got better. If you just look at the PASI 100 alone, it's 41% versus 29% — combination versus ixekizumab alone.
This is just like what we reported previously — this is the TOGETHER PSO trial that I'm talking about. Previously reported was the TOGETHER PSA trial that showed the same results, where the combination therapy was 32% versus less than 1% for ixekizumab at 36 weeks. Both these trials are only out as press releases. They're going to be presented at a major medical meeting coming up in the future. We're also waiting on the primary — the full endpoint of the study, which is week 52. I think this is a major advance in therapy.
Lastly, there was a great lecture last week at RWCS by Uma Mahadevan from UCSF on information about pregnancies. I got up and asked her a question. It was interesting to me that the guidelines on drug use during pregnancy look to me like the guidelines for drug use during surgery. One: continue all the DMARDs. Two: maybe either continue or suspend for a brief period — one dosing interval — the biologics. And for surgery the JAK inhibitor question is that you have a brief suspension, but in pregnancy you don't use them, according to Dr. Mahadevan. The reasons — I researched and wrote about in an article — and the bottom line is that the ACR recommendations on reproductive health really didn't have a guideline on this, but they noted that there is no available evidence regarding the use or safety of the new small molecule agents, and they pointed out tofacitinib, baricitinib, and upadacitinib during
pregnancy really for a lack of data but they also point out that um these drugs do cross the placenta and will be in breast milk and the animal preclinical data shows in very high doses that there's teratogenicity and some ugly effects but there are sporadic reports in the literature about they can be successfully used and whatnot um but again I do find it surprising since tofacitinib was first approved in 2012 and the last one upadacitinib uh 6 years ago 2018 I think um that there's no better data there's no systematic studies so again the bottom line is you shouldn't use it and then recommendations from the GI societies and Dr. Mahadevan who've looked at this basically say that you shouldn't use these uh unless there's no option and then use them with caution. Um the package insert basically says don't use them. The upadacitinib package insert says that pregnancy testing should be considered prior to the use of doesn't mandate it but it said it should be considered.
So I found um Dr. Maan's lecture really exciting and useful. Um, and then I think this data is a follow-up to that I think is instructive when managing patients who want to get pregnant or who are pregnant.
Uh, hope you found this interesting. Hope that you enjoyed RheumNow Live. If you weren't there, you can still actually sign up and get on demand access to all the lectures, the videos, the uh, podcasts, the downloads, and whatnot um, by going to rheumnow.live. And that's you can get that information secondarily. Anyway, we'll be back next week. Take care of yourself. Bye.
First, dermatomyositis and what we see and what we do. This is an interesting study. It's a combination of two different cohorts. Uh, 2,500 from claims data, almost 1,200 from a community-based electronic medical record claims data. And these are all dermatomyositis patients. And they found, as far as some basic benchmarks here, as far as what they observed, myositis panels were done in about half the patients, that 35% had testing for myositis specific associated autoantibodies. Not surprisingly, steroid use was common in roughly 70% between the two. But the most common drugs that were used in dermatomyositis — this was a head-scratcher for me. Hydroxychloroquine led the way, followed by methotrexate, mycophenolate, and then azathioprine. Number one, hydroxychloroquine. Really? What?
Now I have used it in a few people for the skin manifestations of dermatomyositis, but I don't know of any good data about its efficacy in muscle disease, and there's good evidence of hydroxychloroquine causing flares of dermatomyositis. So I find this one surprising. Again, this is observational data. Methotrexate we all kind of agree with, right? Mycophenolate though. Hm. We did report last year a cohort study from University of Pennsylvania about comparing mycophenolate to methotrexate outcomes as far as skin outcomes, and they were roughly the same. Okay, that makes sense. But mycophenolate — I don't have anybody on mycophenolate for dermatomyositis. Azathioprine — I think most of you are using methotrexate or azathioprine. I use a lot of leflunomide and there's only scant data to support that, but my experience says it works really, really well.
The outcomes as far as hospitalization and bad outcomes — these are expressed per 1,000 patient years. Not surprisingly, hospitalization leads the way at 92. Malignancy is next at 15. Malignancy is more common than — 15 versus six per 1,000 patient years — and myocarditis is really rare at only two events. So again, I think I like seeing these kinds of studies, although they are skewed by being observational data, but it sort of lets me think about what I do and how it compares to what's being done out there in the world.
A US biobank registry had lots and lots of patients. Looks at — and again really high numbers here — sought to evaluate the associations between osteoarthritis and osteoarthritis endpoints and sleep. And the osteoarthritis endpoints were knee OA, hip OA, knee replacement, hip replacement. Turns out that all of these were higher in people who had less than six hours of sleep per night. Hm. Moreover, night shift workers — people who worked that, you know, that graveyard shift and who were bouncing around between being night owls and trying to live daytime lives when they weren't working the night shift — these people had a 24% higher risk of knee OA and a 28% higher risk of knee replacement.
So why is that? What's the association here between sleep, bad sleep, and knee? I can't really put it together biologically. I can put it together from the standpoint of people with bad sleep have pain. People with pain seek attention. When you seek attention, you get a diagnosis, and then maybe something happens like a diagnosis or even surgery. But it still underscores the importance of sleep. If you as a rheumatologist are not an expert at sleep, you're really not doing a good job. I'm sorry to call you out on this, but I think it is so integral into what we do. It is such a big driver of pain and fatigue. If you do not assess for it and know what to do about it, you're missing a big chunk of the treatment options for your patient.
JRHEUM had a full read editorial on what HLA-B27 can and cannot tell us. I like this article because I like gene things. It basically tells you the prognostic and therapeutic implications behind B27. And they noted in this paper, B27 is associated with greater structural damage, higher inflammatory burden, better response to TNF inhibitors and IL-17 inhibitors. Now that latter part — that being B27 positive makes you more likely to respond to TNF and IL-17 targeted drugs — I'm not really that familiar with. I looked, and they just referenced one reference by doctors Diodar and Magra, and I couldn't really find much on that. I do know the converse is probably true. If you're B27 negative, you're probably not going to respond as well to those agents. Maybe because the diagnosis is less certain, but I certainly would like to know, and hopefully someone will tell me at some point, if I have a true advantage if you're B27 positive by giving you either a TNF inhibitor or an IL-17
inhibitor and which do I choose? Wouldn't that be a real advantage when it comes to prescribing? I think a real big move this week was the FDA changed its labeling on hormonal therapy. These are primarily estrogen based but sometimes combination estrogen progesterone based therapies. As you know when I was a fellow back in '84 I started — I think in the early '80s this whole issue of hormonal therapy posing risk to patients as far as cardiovascular disease, breast cancer etc was a big thing, became a black box warning and really it dramatically changed post-menopausal management and I got to say most of the women were not very happy about this and it's been shown that most of that data is probably not true and now you're going to see — now you see these box warnings being removed on six products, most of them being estrogen but then there were some progesterone only I think, and there are some topicals, but that's an important move because in the post-menopausal period estrogen and hormonal therapy proved to be very effective at symptom management and as long as it didn't pose a risk, why not do it.
Genentech announced the results of a phase two study of obexelimab, their anti-CD20 monoclonal antibody that we know was approved for lupus in October. This study, the Majesty study, is an open label study comparing obexelimab versus tacrolimus in 142 patients with primary membranous nephropathy and found more complete remissions at 2 years with the anti-CD20 drug. Now again, we know it's approved for lupus. This is going to be a big thing in lupus management. I thought you should know about this. Lupus patients get membranous nephropathy but I don't think there were lupus patients in this study because this was primary membranous nephropathy, but the good news is that it worked and it worked with an important outcome — complete remission at 2 years.
When we were doing in September, I believe it was, our campaign on — there was this argument going around by the experts about the utility of ultrasound in diagnosing ILD. And I thought that was kind of goofy because I thought you needed — I knew the chest X-rays were good, but high-res CTs were much better and really were the gold standard. And there were some reports of this. So I came across a recent study that looked at 73 patients with RA who had mild to moderate disease activity and they did both lung ultrasound and high-res CTs in these patients. Using high-res CT they found ILD in 29% of them, but when they used lung ultrasound it was found in 22%. That would make the sensitivity of lung ultrasound to be 59% and a specificity of 49%. It's noninvasive. There's no X-ray exposure. The ROC on this was good. You know, I think that maybe this could be an early screening procedure. But I must say that both ACR guidelines and the recent EULAR European Respiratory Society guidelines do state that if you're doing screening, the screening procedure of choice is high-res CT. But the lung ultrasound — who'd have thought?
Rotator cuff injuries we know are something that we commonly see. The prevalence of them goes up with age significantly. And this study that I put up this week, it was a study of 602 individuals with shoulder pain who underwent MRI. The average age was 58. Rotator cuff abnormalities were seen in 99% of people. I again was surprised by that number. 25% it was pure tendinopathy. 62% it was a partial tear of the rotator cuff. And 11% — only 11% — were full thickness tears. The point is, as we look at an elderly population with shoulder pain, is it really worth doing a rotator cuff MRI? Maybe if you're going to do surgery, and if that's the case, why should you be doing it? Send it to the shoulder guy and let him decide because he's going to do the surgery. In the meantime, all you can do is rotator cuff exercises, physical therapy, maybe local injections. But I think that this finding that with a mean age of 58, 99% having rotator cuff abnormalities makes me think twice about ordering MRI in the future before I refer or as a reason to refer.
Speaking of referral, someone said in the last two weeks, yeah, this person has this problem and I didn't know whether I should go to orthopedics or rheumatology. So I sort of looked that up. You know, what are the rules here? What's going on in the real world? Obviously, the decisions are either made by patients or by referring doctors, most of whom are either primary care or urgent care, emergency care. And you know what? There's no rules. And most of what's out there is kind of idiotic. You know, it says orthopedics, they get fractures, sprains, strains, and that kind of thing. And that rheumatologists only see autoimmune disease for immunosuppression. Obviously, there's a very big gray area in between. And there's a few papers that look at cohorts that were referred for
evaluation. And you know the ones that went to orthopedics — you know up to 25% or more — they said they should have gone to rheumatology, and that maybe 15% could have gone to rheumatology or orthopedics. And of the ones that went to rheumatology it looked like 90 plus percent should have been rheumatology with only a few percent going either way. So I don't think there are any rules on this. So I came up with my own, and it's for you to argue with me.
Number one, and again, this is something I would say to patients. This is something I would say to my primary care docs who want some instruction. Number one, anyone with a history of trauma, fall, you know, that sort of thing should go to the orthopedist or to emergency medicine, meaning the emergency department at your local hospital. That makes sense — you need to rule out structural damage and serious surgically correctable conditions.
Two, people with nagging or chronic musculoskeletal symptoms — that would mean more than 6 weeks — I think they should first go to a primary care doctor and then let primary care doctors refer to either ortho or rheumatology. And you would say, wait, primary care doctors don't know who to refer to. Well, that's what these rules are for. I'm honoring them. And you know there's what, 59 million people in the United States with osteoarthritis, 10 million with gout, 7 million with fibromyalgia, and 1 million with RA and 1.4 million with psoriatic. Come on. We can't see these people. We need a gatekeeper and primary care should be doing that and doing that well.
Number three, large joints — that's where that's the primary complaint — shoulders, hips, or knees. I say it's a toss-up between ortho and rheum. But if there's a discernible deformity, you know, a genu — an actual deformity, a contracture, or an abnormally enlarged joint — I think orthopedics should be first.
And number four, if it's small joint musculoskeletal problems — hands, fingers, wrist, elbows, ankles, feet, and toes — the rheumatologist is the choice to go to, especially if there are signs of swelling, inflammation, and no history of trauma.
My last recommendation is spinal problems should go to a spinal specialist. Neck, low back, whole back — go to a spine specialist first, a rheumatologist second, or an orthopedist third. I think this one we might want to argue about, but I think rheumatologists are adept at sorting out what needs to go to orthopedics, what may need neurosurgery, and being a good gatekeeper for the system. So anyway, these are my recommendations. I'd like to know what you think about them.
I think another big report came out this week. This was a press release from Lilly about their TOGETHER PSO trial. This is a trial of 274 patients with plaque psoriasis — moderate to severe plaque psoriasis — with obesity, who were then treated either with the IL-17 inhibitor ixekizumab, or the GLP-1 drug tirzepatide, and the combination was compared to IL-17 alone — ixekizumab. This is a phase 3b study. The 32-week endpoint was read out, showing superiority of the combination over the single drug. The primary endpoint here was a combined endpoint of a PASI 100 plus greater than 10% weight loss. That was achieved with the combination drug by 27%. If you were just on ixekizumab, only 6% got better. If you just look at the PASI 100 alone, it's 41% versus 29% — combination versus ixekizumab alone.
This is just like what we reported previously — this is the TOGETHER PSO trial that I'm talking about. Previously reported was the TOGETHER PSA trial that showed the same results, where the combination therapy was 32% versus less than 1% for ixekizumab at 36 weeks. Both these trials are only out as press releases. They're going to be presented at a major medical meeting coming up in the future. We're also waiting on the primary — the full endpoint of the study, which is week 52. I think this is a major advance in therapy.
Lastly, there was a great lecture last week at RWCS by Uma Mahadevan from UCSF on information about pregnancies. I got up and asked her a question. It was interesting to me that the guidelines on drug use during pregnancy look to me like the guidelines for drug use during surgery. One: continue all the DMARDs. Two: maybe either continue or suspend for a brief period — one dosing interval — the biologics. And for surgery the JAK inhibitor question is that you have a brief suspension, but in pregnancy you don't use them, according to Dr. Mahadevan. The reasons — I researched and wrote about in an article — and the bottom line is that the ACR recommendations on reproductive health really didn't have a guideline on this, but they noted that there is no available evidence regarding the use or safety of the new small molecule agents, and they pointed out tofacitinib, baricitinib, and upadacitinib during
pregnancy really for a lack of data but they also point out that um these drugs do cross the placenta and will be in breast milk and the animal preclinical data shows in very high doses that there's teratogenicity and some ugly effects but there are sporadic reports in the literature about they can be successfully used and whatnot um but again I do find it surprising since tofacitinib was first approved in 2012 and the last one upadacitinib uh 6 years ago 2018 I think um that there's no better data there's no systematic studies so again the bottom line is you shouldn't use it and then recommendations from the GI societies and Dr. Mahadevan who've looked at this basically say that you shouldn't use these uh unless there's no option and then use them with caution. Um the package insert basically says don't use them. The upadacitinib package insert says that pregnancy testing should be considered prior to the use of doesn't mandate it but it said it should be considered.
So I found um Dr. Maan's lecture really exciting and useful. Um, and then I think this data is a follow-up to that I think is instructive when managing patients who want to get pregnant or who are pregnant.
Uh, hope you found this interesting. Hope that you enjoyed RheumNow Live. If you weren't there, you can still actually sign up and get on demand access to all the lectures, the videos, the uh, podcasts, the downloads, and whatnot um, by going to rheumnow.live. And that's you can get that information secondarily. Anyway, we'll be back next week. Take care of yourself. Bye.
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