RheumNow - RWCS 2018 - Day 3 Save

RheumNow is pleased to present the RWCS Daily podcast from the twenty eighteen meeting here in Maui. These podcasts are a compilation of each day's presentations by our featured faculty and presenters. We hope you enjoy these presentations from RWCS.

Thank you.

Hi, I'm Doctor. Rachel Tate presenting from Rheumatology Winter Clinical Symposium in Maui, Hawaii. And today I have the distinct pleasure of interviewing one of our fellows, Doctor. Sheetal Patel, who's coming to us all the way from Michigan. So I'm sure she's very happy to be in Hawaii today.

Sheetal, tell us about your poster.

Sure. Hi, everyone. My name is Sheetal. So I'm from I'm a first year rheumatology fellow from DMC Henry Ford University. And today I have a very interesting case on multicentric reticulostriocytosis.

It's a very rare disease and it very commonly gets mimicked with rheumatoid arthritis. So we'll talk about how we can distinguish both of these diseases today. We'll start off with our case who was a young, very young actually African American female who had a history of couple years of inflammatory seronegative arthritis and we were treating her with methotrexate. And eventually, she came to our clinic with worsening, very worsening joint pain and swelling for a year, followed by six to eight month history of, these skin nodules, which were papillonodular in character, started off on her forehead and gradually spread all the way down to her body. As our workup, we ended up doing more serology on her.

She was positive for ANA, SSA, and her inflammatory marker, CRP, was quite elevated. Followed by that, we ended up doing some hand x rays to try to compare her hand and wrist x rays from previous year, and we were very astonished with what we found. Within one year, this lady had very aggressive, destructive, symmetric arose of disease, not just around her wrists, but around her MTPs MCPs, sorry, PIPs, along with DIP involvement. So this led to us to work very closely with our dermatology colleagues. We went in and, I'm very grateful that they were able to get a good biopsy of the node.

And the biopsy basically was very helpful for our diagnosis. It basically showed a lot of plenty histiocytes here, multinucleated giant cells, very irregular looking nuclei with a prominent nucleoli. And as you can see, the picture is mostly pink. There's a lot of eosinophilic cytoplasm within the histiocytes. And together with the staining along with the palisading pattern of the histiocytes, we were confident to say that this was more consistent with reticular histiocytosis.

So it's such a rare disease, my attendings have even told me I will probably never come across another case like this, so it's once in a lifetime. And when I was doing more research on this, we found that there are no guidelines, there was no structured treatment guideline for this. So I saw a lot of case reports on the very commonly used drugs are methotrexate and prednisone, followed by a couple case reports of TNF inhibitors. And lastly, very sparsely, found some on Anakinra, tocilizumab, along with rituximab as well. So based on, of course, the patient's preference and her insurance and keeping the whole socioeconomic background in mind, we decided to start off with etanercept, which is a TNF inhibitor.

Since she was already on methotrexate and it was not really controlling her symptoms, so we were hoping the TNF inhibitor can help us control not just her aggressive arthritis, but also her skin lesions, because she is a young female after all. And a couple important points to keep in mind. Number one, MRH, a multicentric reticulosteocytosis, is one third of these cases are associated with malignancy. So we did a thorough malignancy work up on her including CT, chest, abdomen, pelvis, along with S PEP, U PEP, you name it. We found some abnormalities, but not consistent enough to go forward with the malignancy.

So we'll have to keep a very close eye on her and monitor her yearly or a couple, six months or so. Number two, this disease is quite commonly confused with rheumatoid arthritis. So I wanted to bring up at least three or four points how we can help differentiate the two. And even though it's a rare disease, it's good as a physician to keep this behind our mind so we know the next time we see some similar pattern. So number one, in rheumatoid arthritis, you'll have sparing of the DIP joints, whereas in MRH, you may have DIP involvement along with the other joints as well.

Number two, even though we know that with uncontrolled disease for years, rheumatoid arthritis can eventually lead to mutilating aggressive sort of destructive pattern, whereas in MRH, it's very aggressive in a very short period of time. So we're talking about months or even within a year, and we saw that in this patient. Now most of the case reports I went through said that after the first three years of having arthritis is when you present with skin lesions. In our case, this was a little unusual. She had arthritis for ten years followed by the skin lesion.

So something to keep in mind. And lastly, it's about the papillonodular skin lesion itself. In rheumatoid arthritis, the nodules are mostly around the joint areas whereas in MRH, it could be anywhere. Like in our patient it started off on her face and then gradually spread all over her body. And as you can see in our picture we have I just have pictures of her hands but she also has periangular involvement which is interesting to see.

So overall, I think those were the important points I took from this and I'm very grateful for RWCS to give me this opportunity to present this case and network. So thank you.

Well, Doctor. Patel, are you gonna be writing some of these new guidelines for the treatment of our I hope I MRH.

And the medicine. You did.

Thank you again for letting us talk to you today. Thank Great poster. As always, check out roomnow.com for further information and for this and other poster presentations from our amazing fellows.

Aloha from Maui. My name is Bernie Rubin. I'm the chief of rheumatology at Henry Ford Hospital in Detroit, and I'm here coordinating the fellowship program at RWCS two thousand eighteen. We have a very interesting poster. Natasha Zohuri is a first year fellow at UCLA, and she has a case that I wanted to discuss with her.

So this is rheumatoid arthritis and it's an imitator. So Natasha, tell me what is interesting about this case.

Okay. So, this is a, case about a 65 year old with a, history of diabetes, hypertension, hyperlipidemia, hypothyroidism. She came in with, polyarticular joint pain involving her bilateral wrist. She had MCP, PIP, joint pain, and classic symptoms of rheumatoid arthritis. On exam, she did have, synovitis, and tender joints.

So what was that?

And, so what happened is she we started treating her for a seronegative rheumatoid arthritis because her inflammatory markers were elevated. Rheumatoid factor Rheumatoid factor. Factor is negative. Exactly. And then she we started her on DMARR therapy, and, she wasn't getting better.

We escalated the therapy to biologics. We started her on Humira. Wasn't getting better. And then she came in with these yellow tender papules over her finger pads.

How long after Probably after you started the diagnosis

of treatment did that happen?

So probably a year later.

Oh.

Yes. And then we we aspirated the TOFI, and it came at back as, these monosodium urate crystals. So then we gave her the diagnosis of gout, and then we later checked her uric acid level, and it came back high at eleven. So the learning points from this is that when you have a polyarticular joint pain, you should consider gout in the differential diagnosis because gout can present as a polyarticular manifestation. And whenever you have a seronegative rheumatoid arthritis and they're not getting better on traditional therapy, you have to reconsider the diagnosis.

Well, that's a very interesting case and a very interesting point. Have you seen any more since, this first case?

This is the first one I've seen, but I'm sure I will see more. And now I know that whenever I see patients with polyarticular joint pain, I should consider gout in the differential and check a uric acid level.

Well, thank you very much. That's a very interesting case, and I'm sure a good learning point for you. We appreciate your thoughts on it.

All all of you at UCLA,

so I just want to add that in.

Hello. I'm Bernie Rubin. I'm the chief of rheumatology at Henry Ford Hospital in Detroit, and I'm here at RWCS two thousand eighteen to talk to some of our fellows about their poster presentations. Today, I'm talking to Laura Howe. She's a second year fellow at UC Irvine, and she has a case of Kikuchi's disease, which I think I remember from fellowship.

But Laura, tell me about why we should be concerned about this condition now.

Yeah. Well, in our patients, she's a 29 year female from India who came in with shortness of breath, fevers, that were pretty persistent. We ended up finding out that she had some diffuse alveolar hemorrhage. She did have a biopsy of a cervical lymph node that showed the Kikuchi disease, that's a very, typical biopsy that we look for. So with her case, we have to kind of look back to Kikuchi's and recognize that it's typically associated with infections.

Viral infections, tuberculosis, it's a very T cell mediated response. So if you can kind of imagine how, you know, lupus and things like that, react to some infections like viruses, tuberculosis. This does a similar thing actually, but it's

more Wait. Wait. So tell me. So that might not be the first thing I think of when I see a 29 year old woman come in with Alvear or hemorrhage. So what led you to think that it might be something other than one of our normal vasculitides or connective tissue diseases?

Yeah. Well, so her past medical history, everything was totally clear. Really, she had no other signs of anything systemically. We you know, obviously, she comes in from Indians. We're really concerned about tuberculosis at that point with the diffuse or the the hemoptysis initially and the the fever she was having.

And then, I mean, we did a full evaluation because they when people come in like this, obviously, they want us to be on board to see if there's underlying connective tissue disease. And really, for her, there was nothing. ANA was negative. Everything was negative.

Got it.

So and that's the big differentiating thing between lupus too and Kikuchi's is with Kikuchi's, you know, we have our typical necrotizing, histiocytosis, which can also be seen in lupus, But then we actually have that staining of the, the nuclei, the hemotoxin staining of the lupus patients that differentiates.

Got it. So how did you, is there a treatment? Did you treat her? And how did she do?

Yeah. Well, so Kikuchi is probably more common than we think. Unfortunately, there's not too much in terms of treatment because it's fairly self limited, fairly benign. Typically, it goes away within four months or so. With our patient, obviously, with diffuse alveolar hemorrhage, we definitely had to you know, treat.

So we did give her, pulse steroids, one gram a day for three days of the Solu Medrol, and then we kind of tapered her down with the steroids. We eventually did find out, about thirty days after the culture that she was positive for tuberculosis. So, you know, at that point, she kept having recurrent fevers even though they're coming down on the steroids, and we ended up having to treat her with RIPE and the prednisone as well.

So do you think that it was the tuberculosis that maybe triggered the Kikuchis or we'll never know for sure?

Well, so I think it's pretty pretty to me after reading the papers, it just seems like a very, almost obvious thing, like, because Kikuchi is so reactive, so T cell reactive that it would make a lot of sense She probably had maybe latent tuberculosis, and then, you know, we're we're not entirely sure whether or not the the hemorrhage itself was from tuberculosis or the cucoochie, but, you know, it it is definite. I I I'd say it's probably very likely that the cucoochie was reactive from the tuberculosis.

Well, sounds like a very interesting case. I really appreciate it. Something we'll have to think about when we see these people who come in with what looks like a connective tissue disease. Now we'll keep cucoochies back, in our differential from now on.

Yeah. And always with the the big thing for us too that I forgot to mention is because it looks so much like lupus. That's one of the biggest things we have to remember. When we have patients with Kukuchi's, you always evaluate for lupus. You always get the ANA, and they do have a tendency, and it might be just the way their T cells are kind of hyper reactive, they do have a tendency to actually, some of them end up getting lupus later.

And the lymph node biopsy is key, right?

Always key, yeah, absolutely. Biopsying for sure.

So that's the take home message. Thanks again. Okay. Bye bye. Hello.

My name is Bernie Rubin. I'm the chief of rheumatology at Henry Ford Hospital in Detroit. I'm here at Beautiful Maui at RWCS 2018, and we're talking to some of our fellows who have amazingly interesting posters and cases to present. So this morning, I'm here with Kyle Mayer who's from the University of Colorado Medical School. He's a first year fellow.

Kyle, tell me a little bit about this case.

Sure thing. So we saw this guy, a gentleman with a history of GPA, been treated about two years before he came in to see us, sudden loss of vision in his right eye, saw an ophthalmologist kind of way out in the boonies in Nebraska and they told him they think this is the GPA so you need to get seen by Rheum right away. Sent him over to see us and we started evaluating him, took a couple pictures of the back of his retina and things didn't look awesome. Started treating and eventually got a vitriol.

What did you treat him with? Were you treating him for a recurrence of his GPA?

We didn't know exactly what was causing it so we started on treating him for a number of A couple things can do this CMV as was the case in this patient, GPA can look a little bit like this when it's reactivated in the eye, also worried a little bit about herpes zoster but kind of just started them on every treatment right out the gate and then figured out what it was later on.

So what was it?

In his case it looks like it was CMV retinitis which is why this is a little bit interesting. CMV retinitis is pretty common in folks who have HIV. In fact, something like twenty to thirty percent of people who have HIV AIDS will develop CMV retinitis.

So he had HIV and GPA?

He did not. He did not have HIV, which is a very rare thing to see. In fact, we did a literature review. CMV retinitis is reported in non HIV patients. Very rarely.

We saw two zero eight cases when we're look looking for information on it typically associated with transplantation and the meds you have be on for that but around twenty percent of those two zero eight that were reviewed had some autoimmune illness they're being treated for.

So for his GPA was he on maintenance therapy was he immunosuppressed?

Really he wasn't he wasn't terribly immunosuppressed. He'd received rituximab after a few cycles of cytotoxin back in the day when his renal disease was more active. His last rituximab was maybe a year before this whole thing happened but really wasn't terribly immunosuppressed at the time. Probably some residual effects of the rituximab which we discovered later on in some labs showed some hypogammaglobulinemia. We don't know if that was pre existing to the rituximab or not but possibly associated which is another little interesting tidbit about this case.

And how did he end up doing?

So at first, we started him on a a number of different treatments that are are usually used in CMV retinitis. Ganciclovir and Fosconet, he had to go to intravitreal injections of both of them and eventually both of them at the same time. This guy was driving in an hour and a half from Nebraska to get injected in his eye twice a week or something like that, and he just wasn't it was still progressing even on that therapy. So for that reason, we actually ended up adding leflunomide or Arava to that regimen, which as we go into a little bit more detail on the poster, is not a very common thing we do, but it does actually treat the virus. And in this case, it's uniquely fitting because of his autoimmune condition because it can treat both the autoimmune condition and the virus at the same time.

Did it work?

Actually, very, very well. He's completely stable on that therapy. He's on Arava monotherapy. He's had occasional steroid drops here and there, but really doing quite well on the leflunomide.

Well, that sounds like a very interesting case and a great outcome. And I'm sure, all of us will enjoy, seeing it when you publish it, hopefully, in the near future.

We'll be working

on it. Yes, sir. You very much.

Hi, I'm Doctor. Rachel Tate from Rheumatology Winter Clinical Symposium twenty eighteen in beautiful Maui, Hawaii. And I am here today with Doctor. Crystal Choi, who's here to tell us about her research. Crystal, thank you for joining us.

Thank you for having me.

And tell me about your poster, of course.

Yeah. So my poster is on consensus building on developing a curriculum on musculoskeletal ultrasound for rheumatology fellowship programs. So in 2011, there was an original document on this that was performed. And basically, we just wanted to update this given the increasing popularity of musculoskeletal ultrasound and its increasing use in rheumatology. So back in 2011, there were three tier designations, basically tier one, two, and three.

Tier one being something that was very important that we felt that all rheumatology sonographers needed to know, and tier three being less important. We looked at three things overall, region specific scans, documentation, and also scanning conventions. And we asked a bunch of experts in rheumatology ultrasound, basically, opinions on these three things and whether or not they agreed with the original tier designation from 2011. And so in regards to region specific scans, you can see here the original 2011 tier designation. And over here, whether or not the experts agreed on what was done in 2011.

And overall, we found that there was pretty good agreement, especially in regards to documentation and scanning conventions. However, in regards to the region specific scans, there was a little bit less agreement. So in less than half of them, the experts stated that they would advocate a change to a more basic tier. So for example, tier three to tier two or tier two to tier one. Meaning that, region specific scans that previously they said, well, maybe sonographers don't need to know.

They now felt that they should know and should be a basic part of the curriculum. And overall, we just felt that this probably just reflects changing views on ultrasound in the rheumatology community as we use it more. And as a result, the experts are saying that we should include more views, in any curriculum that we were to develop.

Doctor Choi, thank you. It sounds like this was a hot topic at ACR twenty seventeen and it sounds like it will continue to be. The better training that we have for musculoskeletal ultrasound, I think the better we will all be. So thank you so much for joining us and check us out on roomnow.com for this and for more information. Thank you.

Hello. I'm Bernie Rubin. I'm the chief of rheumatology at Henry Ford Hospital, and I'm here in beautiful Maui at RWCS two thousand eighteen. We have several fellows who have presented cases and abstracts, and I'm here to discuss this case with Jeff

Chua.

Chua, who is a fellow at Scripps, and he and I are gonna talk about his case. Jeff, I see you have a case here of granulomatosis with polyangiitis. I mean, lot of us in practice have seen GPA. Tell me a few things about your case that makes it unusual.

Yeah. So aloha. Large case, but small poster. This was a 22 year old younger patient that we saw in the hospital for consultation. Come in with pretty straightforward, seemed like a GPA case, had upper respiratory symptoms, came in with alveolar hemorrhage, a pretty thorough workup and had the C ANCA positivity, PR3 positive.

So it seemed pretty straightforward, everything was done and we were consulted.

So what was unusual about the

case? So

patient

was, I guess the unusual part of it was he was found to have bilateral lower extremity DVTs, which okay, and he had an IVC filter placed for that. And he was treated with pulse steroids and rituximab and was doing fine. And on his way out, on the last day, he he came in or he was found to have a a painful left foot. It was cyanotic. It was cool.

And that kinda kinda threw us off a little bit.

What did it turn out to be?

So it it it turned out to be, bilateral arterial clots as well for for him. And

So you think that he had evidence of both arterial and venous disease as related to his GPA?

Exactly. And that kind of caught us obviously off guard and just given his history of the alveolar hemorrhage, made it very difficult clinically to kind of figure out what the next step.

And what was the next step?

So we kind of went back and forth in terms of what to do. It's gonna be difficult to anticoagulate him, to treat the clots with his hemorrhage. So we had Vassar come by and unfortunately he ended up having bilateral amputations of of of his of his lower extremities. But

Oh, wow. Well, that's a terrible that's a terrible outcome. But I think, do you think that this might be something that we have to look at more often in our people with GPA?

No. Definitely. I think it's something that, you know, definitely caught us kind of off guard and, you know, something new that, you know, the faculty at Scripps, we we've never seen this before. So just kind of something you you you take away from from fellowship and definitely into your career. Yeah.

Something that.

Well, thank you very much. That's a very that's a very interesting and certainly a very morbid outcome for somebody with GPA. So I think all of us that take care of these patients will have to be aware of this kind of a problem in the future. Thanks again. That was a great case.

Thank you. Thank you so much.

Hi, I'm George Martin. I'm a practicing dermatologist here in Maui, and we're here at the Rheumatology Winter Clinical Symposia of twenty eighteen, and my lecture covered three major topics. Covered psoriasis and what's new in psoriasis, what's new in atopic dermatitis, and the current therapies in melanoma that pertain to rheumatology. In psoriasis, we've had a blockbuster year in 2017, which brought us the first of the IL twenty three blockers. We have gazelkumab, also known as the brand name Tremfya, was brought to market.

This is a zero four and then every eight week injection. In the pivotal trials, it was compared to adalimumab, and across the board outperformed adalimumab. PASI 100 scores of roughly fifty percent, were recorded with the use of giselkumab. And what's most interesting is that when you discontinue giselkumab, the median time for a PASI 90 score to drop was almost four months. So this is a very durable long acting molecule that works upstream to block the 23 pathway.

And it's an amazing, amazing new drug whose sort of grandfather was ustekinumab. It was figured out that ustekinumab blocked both IL 12 and IL 23, but the real power of the blockade was through the IL 23 pathway, which blocks downstream cytokines such as IL 17, TNF, IL 22, IL six. So we have just witnessed the, launch of the first pure IL twenty three blocker. There are two other blockers to come, tildrakizumab and risankizumab, both of which have amazing performance. Both will come out on the market as zero, four, and every twelve week injections, and these are new high performing drugs.

So look for, tildrakizumab to come out a little later in 2018 and then probably by early nineteen, the advent of risankizumab. The new news is that cerdulizumab, well known to rheumatologists in rheumatoid arthritis and, psoriatic arthritis, has now been the phase three studies are in. We're expecting an FDA approval soon, and it will be soon launched in dermatology for the treatment of psoriasis. This molecule, is, been submitted as a two hundred milligram and four hundred milligram, every two week dose. It was non inferior in the two hundred milligram dose to etanercept high dose, and the four hundred milligram dose outperformed etanercept as far as PASI 75 scores.

Atopic dermatitis, what's new? Well, dupilumab has now been on the market for a year. It's a selective IL-four alpha monoclonal antibody fully humanized, and it really blocks IL-four and IL-thirteen, two very important TH2 cytokines. It is dosed at six hundred milligrams loading dose followed by three hundred milligrams every two weeks. Our EC scores, which are the equivalent of your ACR scores or PASI scores, showed a 70% improvement across the two pivotal trials, and the ISH scores dropped by about 50%.

So this is the first of what hopes to be many therapies, systemic therapies, for atopic dermatitis that will be FDA approved. Heretofore, we've had cyclosporine, methotrexate, mycofemylate, and azathioprine, all non approved and all with their own toxicities. Dupilumab has an amazing safety profile. There might be some conjunctivitis in a few percent of patients and maybe some injection site reactions, but it's a very, very safe drug. And for those severe patients with atopic dermatitis, and we're talking about fifty percent body service area, this drug is a real game changer and an incredible safety profile.

Hi. I'm George Martin, practicing dermatologist here on Maui, and I am speaking at Rheumatology Winter Clinical Symposia twenty eighteen. One of my topics was new molecular therapies in metastatic melanoma. Prior to 2011, patients with stage four melanoma had basically a clinical trial as their only hope. If you're fortunate enough to have an isolated metastasis, maybe your cure rate was twenty percent.

But the median survival in metastatic disease prior to 2011 was six months. Very sad situation. So we've had now have the, advent of two important, categories of melanoma therapies. What I discussed was the immune checkpoint modulators, both the CTLA four blockers and the PD one blockers, both which demonstrate remarkable efficacy as far as halting disease progression and improving overall survival. Ipilimumab, which is an anti CTLA four antibody, prolongs the activated lifetime of T cells.

And in the pivotal trials and long term extension out at ten years, ipilimumab was shown to increase overall survival to twenty one percent lifetime survival. And if you were alive at three years on ipilimumab, the chances were you're pretty much a cure. So that's very exciting news. We also see the use of ipilimumab in stage three disease, which is nodal metastasis, and we show an overall survival benefit of about twenty eight percent in nodal disease. However, should be cautioned that there were some deaths in the study due to, the adverse effects, which are immune related, and they are usually colitis.

And that's a big thing to watch for when you have patients on if you live in that. Flip side of the coin, we have two p d one blockers, and p d one, blockers affect the T cell's ability to to kill tumor cells. Once a T cell arrives at a tumor cell, we understand that there's an immune evasion that involves a p d one and p d one ligand. When we effectively block the p d one surface protein, it allows the T cell to kill the tumor cell. The p d one blockers are safer and appear to be more effective and are used in combination with the CTLA four antibody.

However, one must be cautious about the immune related adverse events, most of which are severe colitis, and that's the big one to watch for. On the rheumatology slide, there's some arthralgias and such, but, really not much on the rheumatoid arthritis activation. The flip side of the point is if you have a patient with RA who has metastatic disease, particularly metastatic melanoma, and you decide that that patient is going to need an immune checkpoint modulator, we recommend taking them off TNFs, going to DMARDs, but expect that about three quarters of these patients will develop an immune related adverse event. Usually, those can be controlled with systemic steroids. In about fifteen percent of patients, you can use another immunosuppressive to get them through a reactive phase.

But as it turns out, the more adverse events you have when you're on these drugs, the more likely you are to survive. And the use of corticosteroids does not appear to impact overall survival. So, that's it from Rheumatology Winter Clinical Symposia two thousand eighteen. George Martin signing off.

Good morning. My name is Bernie Rubin. I'm the chief rheumatology at Henry Ford Hospital in Detroit, Michigan, and I'm here coordinating our fellowship program at in beautiful Maui at RWCS two thousand eighteen. And with me, I have Elaine Alexander, and she and I are gonna discuss her poster. Elaine, I think I remember hearing about Kikuchi syndrome when I was a fellow a million years ago.

Could you tell me a little bit about your case that makes it interesting?

Yeah. So Kikuchi syndrome is is histiocytic necrotizing lymphadenitis, and, it's usually very self limited. We usually don't see it, actually. And, what's interesting about this case is actually she developed macrophage activating syndrome and was very sick in the ICU. And we think that it has been reported before, but we think that there could be an underlying spectrum of this this lymphadenitis that could be occurring with or prior to lupus diagnosis.

And we do think that this patient this was her initial presentation of lupus as well as the Kikuchi syndrome.

Okay. So and you're at Ohio State? Am. And are you a first or second year fellow?

I'm a second year fellow.

And was this woman in the pediatric department, is she an adult?

She was treated as an adult. She was in the adult ICU.

Okay. And is cucoochie more common in children or in adults?

It's actually more common in young women. It can span anywhere from the teenage years to 20 upper twenties.

Perfect. I understand. And have you seen any other cases after this woman?

So, actually, we are thinking about publishing a case series because there was one other lady who had Kikuchi Fujimoto and also and she already had a presentation of lupus. So

So it sounds like something that we all should read up on and be aware of. If you have seen more than one case in your fellowship, we all might need to be boned up on it.

Maybe. Maybe they're they're just looking for it a little bit more with the pathology. Our pathologists saw it these two times, and so now they're actually staining for it a little bit more commonly.

Alright. Well, thank you very much. Appreciate the update. I'm Bernie Rubin. I'm the Chief of Rheumatology at Henry Ford Hospital and a Clinical Professor of Medicine at Wayne State University in Detroit.

And I'm honored to be here to coordinate our fellows program at RWCS twenty eighteen. Through the generosity of Drs. Cavanaugh and Martin and their generous supporters, over the last several years we've been able to bring up to 12 rheumatology fellows from across The United States to this amazing clinical meeting in Maui every February. A few years ago, Doctor. Cavanaugh asked me to help coordinate the fellows program to make sure they had an excellent educational opportunity and got to meet the faculty and some of the clinical rheumatologists who were attending the meeting.

We found it to be a great program. It's been universally well received. The fellows really are engaged. And for me personally, I think it's been a great opportunity to let these young rheumatologists of the future see what a great profession we have and what great opportunities lie ahead for them in the future as they look to make their careers either in academics, private practice, or industry.

That's it for today's podcast from RWCS. Be sure to check out the other podcasts from RWCS and RheumNow on our websites. And while you're at it, sure to rate us highly. And while you're there, it'd a good idea to subscribe to our syndicated channels. That would include iTunes, iPhones, SoundCloud, Google Play, and Stitcher for those of you on Android.