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This is QD clinic. Hi. I'm doctor Jack Cush with RheumNow. Today's QD clinic is brought to you by RheumNow's virtual ACR twenty twenty coverage. You give us two hours, we'll give you the ACR.

Today's case is a discussion of which IL one inhibitor should I use. I treat a lot of patients with auto inflammatory disease. I'm a self declared king expert of Still's disease. That's because no one will fight me for the title. And, and I use a lot of IL-one inhibitors.

You know, there's three on the market. There's rilanacept, which is given every eight weeks. There's canakinumab, which is given generally every four weeks. And then there's anakinra, which is given, every day. So when I'm treating someone either with Still's disease or FMF or Schnitzler syndrome or, you know, hyper IgD syndrome that you know, these are all IL-one responsive disorders.

The question is, which one do I use? Heretofore, I almost always use Anakinra first. One, because it's cheaper than the other ones. They're all really expensive these days because these drugs are indicated for very rare disorder, so that jacks up the price quite a bit. But I tend to use anakinra because it's very short acting and has a half life of six hours.

Works pretty quick, and it also is dissolved pretty quick, meaning when you stop it, its effect goes away and people will flare within one to three days on anakinra. The other ones are antibodies, monoclonal antibodies, which have a much longer half life. So, again, previously, I would use anakinra as my starting drug. And once the patient had gotten used to daily injections of anakinra and had done well, then I would switch them over to canakinumab, usually either when they complained of daily injections or, I was concerned about compliance or the insurance companies were giving me a hard time. The equation changes more recently with the FDA approval of canakinumab for, adult Still's disease.

It's actually the only drug that's approved for adult Still's disease. Now, there are, again, the other, IL-one inhibitors. Anakinra is approved, as you know, in, for use in RA and also for CAPS, the cryopyrin associated periodic syndromes. And then, canakinumab is also approved for systemic JIA. The CAPS, FMF, hyper IgD syndrome, and TRAPS.

And rilanosept is only approved for just CAP disorders. So when treating RA, you have an FDA approval for anakinra. When treating Still's disease in the kids, you really or adults, you really only have an FDA approval for, canakinumab or Ilaris. Again, the differences here are, the the half life. Six hours for anakinra, twenty six days for anakinra.

And so the dosing regimens are either daily for anakinra or every four weeks for anakinra. The doses are a hundred or two hundred milligrams given daily at night with anakinra. I use it at night because most of the fever occurs at night, and it's a very short half life drug. Some people will require two hundred, and that's higher than the prescribed dose. But when you're treating hot, red, inflammatory, systemic, autoinflammatory disease, you might need higher than normal doses that you would use in RA or other disorders.

When you're using canakinumab, the dose is either a hundred and fifty or three hundred milligrams given every four weeks. Now these are sub q administered drugs. The, you know, the they do have the problem of, of, ISRs, injection site reactions that usually go away after a month or so, and they're never serious adverse events where or hospitalizable, or the lesions are usually just red, elevated urticarial, but not itchy lesions and not mild discomfort that, again, will go away with repeated injections. So, which one do I use now? That's really the big question.

I think it depends on what the need for rapid control or chronic control is. I think the onset of anakinra is an advantage, but its disadvantages is a daily injection. And you have to rotate sites, and patients don't usually like to inject their abdomen that much, and they run out of sites on their legs, and God forbid, they're using their upper arms or buttocks. But if I'm looking for chronic control, maybe I can acutely control the condition with steroids. Often, if I'm using an IL one inhibitor, I'm usually using a background of methotrexate or another DMart.

And then you could use canakinumab as your first drug as well. If you're fighting the fight with insurance for FDA, you know, that this is not an approved drug, well, then your only option for Still's disease is going to be, canakinumab because it's not approved for, Still's in kids or in adults with anakinra. So that's my 2¢ on, IL-one inhibitors. Again, tune into RheumNow for expanded coverage of the ACR twenty twenty meeting. If you only had two hours or four hours to cut to review the ACR, and you can do it asynchronously, you can do it at night or during the meeting or in the morning before the meeting, It's all gonna be online.

How would you do this? I mean, you can go to the ACR website. It's gonna be good. Or you can go to our website, rheumnow.com, and see perspectives by key opinion leaders, see a lot of videos, a number of podcasts, panel discussions, takeaway message messages, all on video or audio, and then there's gonna be written content by our faculty of over 24 people covering the meeting. So tune in the room now starting November 1 all the way through the thirteenth.

We'll talk to you tomorrow on QD clinic. Welcome to QD clinic. Hi. I'm doctor Jack Cush with RheumNow. This episode is brought to you by RheumNow's virtual coverage of ACR twenty twenty reporting, analysis, and perspective.

That's what we're gonna do on the website. Be sure to check it out. Today's case, what to do when it's not RA? So, I saw this patient last week, 70 year old, gal, who had been diagnosed twenty years ago with rheumatoid arthritis. At the time, the patient had bilateral swollen wrists, sounds like RA, It was inflammatory.

It didn't respond to whatever treatment she got, she didn't remember, but she did get bilateral synovectomies, which were inconclusive, meaning that's kinda what you get when you do a synovial biopsy in RA. It's chronic inflammation and, you know, you don't usually see germinal centers or things that are truly diagnostic. So she was treated as someone who had rheumatoid arthritis. Oh, and her rheumatoid tests were supposedly positive. She says that early on she got, a TNF inhibitor that was infused and, boy, fabulous response.

She also got methotrexate, and when she could no longer afford the infusible TNF inhibitor, she was maintained on methotrexate, gee, that was almost good enough. And then six months ago, she, ran out of methotrexate. Her doc you know, why why do you stop drugs? Well, you know, the doctor retired, lost the prescription, COVID nineteen, you know, dog ate my homework, a million and one reasons why people stopped their medicine. She stopped her medicines, and she thinks that since then she's gotten worse.

The thing is, when you examine the patient, she's got fairly normal looking hands, except she's got scars over both wrists and limitation of motion where she really can't flex and extend as she should, suggesting there's damage there. What from? I don't know. But the rest of the exam, pretty much normal. Tender a few tender points, and that's really the source of her pain.

She does sleep blousy, but RA synovitis, no. RA deformities, no. MTP possibilities, not a chance. Nodules don't exist. It's not RA, at least not now.

So, that's sort of the first discussion. Patient comes in with a firm belief that it's rheumatoid arthritis, and it no longer is. I think I always take the tact, I wasn't there twenty years ago when you had all this going on, and gee, it sure sounded like rheumatoid arthritis. The good news is that it's no longer a problem. You don't have to have rheumatoid arthritis for the rest for your whole life.

RA does burn out after twenty or thirty years, seldom after five years, and maybe this is a case of burnt out RA. Well, she had lab tests done, and she is in fact zero negative for rheumatoid factor, CCP, ANA. Uric acid was normal. Got a fairly normal looking lab. No signs of chronic inflammation or hypoalbuminemia or hyper, anything or l o LFT elevation.

They're all normal. So, again, the good news is RA is not in play, but you do have pain. We do know that it's myofascial. You may have some degenerative damage and or mechanical damage to whatever you did in your wrist. So first question is explaining how RA can go away, and RA does burn out.

The second question is, what is going on? And I think that the longer someone has a history like this, the more you're calling it maybe now difficult or refractory disease, or you maybe you've gone through and tried a number of DMARDs, and tried a number of biologics, or tried a number of small molecule targeted synthetic DMARDs, and you're not getting better, you should now start to rethink that this is no longer immune mediated or inflammatory. And you should be thinking that, number one, the problem could be structural. And I think if that's the case, then imaging usually is, going to give you the most, telltale answers on what to do and how to proceed. Next, that the problem could be periarticular.

That's really evident in cases of shoulder and knee where you can quite commonly have in these burnt out patients, you know, rotator cuff disease and or meniscal tears and other periarticular damage. The same could, exist also in the feet and in the hands, and you may need to involve specialists. You need to exclude weakness as the cause for pain, especially as people burn out and get older. So I tend to rely in such patients on imaging, orthopedic and physical medicine referrals, and PT when necessary when dealing with the issue of, weakness. If you're not strong, you're gonna hurt.

If you hurt, you're gonna get weak. If you weak get weak, you're gonna hurt more. Again, there's a spiral of weakness and pain. And, of course, people can have, as this patient did, myofascial pain or fibromyalgia related to poor sleep. Interestingly, a colleague of mine had a similar question at a recent grand rounds that I did on, changing paradigms, where I, was saying that, you know, what I do in managing people, and the question that she put forward to me is, in someone who think has burnt out RA, what do you do?

When do you use a DMARD? Well, I do what I just said. I think structural, I think weakness, I think periarticular, ortho imaging, PM and R as my solutions rather than DMARDs. When would I use a DMARD? I use a DMARD when I can prove by exam or by imaging that synovitis, tenosynovitis, synovial flu synovial fluid effusions is something that a DMARD might be indicated.

I don't use DMARDs for pain. I don't use DMARDs for elevated sed rate and CRP. I don't use DMARDs for X rays. X rays are gonna change. X rays are what you have X-ray findings of erosions and damage is damaged.

The damage is already done. I'm again again, you have to be clear about what the goal of DMAR therapy and DMAR initiation is going to be. So what do you do when it's not RA? Well, number one, make the decision it's not RA, and number two, move on to these other options. Again, reporting, analysis, perspectives.

Follow us at RheumNow during ACR twenty twenty. Take care. This is QD clinic. Hi. I'm doctor Jack Cush with RheumNow.

QD clinic is brought to you by RheumNow's coverage of virtual ACR twenty twenty coming up in November. We've got the speakers, teachers, faculty. We need the interactors. That's you. Today's case is the trigger finger.

The patient's about 65 years old, well managed with knee OA, hand OA, history of diabetes, male, doing very well, and all of a sudden comes in with a new urgent appointment, and turns out my finger keeps getting stuck, doc. And they show you their finger that looks like this, although it's not stuck at this time. And, of course, it's trigger finger. They thought it was a Dupuytren's contracture, and in fact, it's just the trigger finger. Intermittent pain, clicking, catching, when it gets stuck, it hurts.

When it they try to open, it hurts, you know, trigger finger is not uncommon. Who gets it? As you get older, although it starts usually around age 50, peaks around age 60, and is not uncommon in the elderly. Diabetics, women, people with osteoarthritis, even inflammatory arthritis, sometimes trauma, you can get a nodule on that, that tendon, and that gets stuck in the pulley as the tendon goes through the pulley, and that is basically the pathophysiology of the trigger finger. The objective would be to reduce the size of the nodular change that occurs.

What fingers are most affected by this? As you might imagine, it's the ring finger first, then the middle finger next, and then the index finger. It's seldom or less frequent on the thumb. It's pretty infrequent on the pinky. So the question is, how do you manage this?

I thought this was really humorous. I actually looked it up. I have my management of it, and I'm wondering if it sort of jives with your management of it. But if you look up the treatment of trigger finger, the literature is really bad, and it's the literature is all very self serving. Meaning that if you're a surgeon, the literature is all about the success of surgery, you know, surgery on the A1 pulley, and then, you know, it's fifty to eighty percent effective.

If you're not a surgeon, you're talking about you know, actually, there's an interesting article from the Mayo Clinic this year, called, just shoot it. Trigger finger, just shoot. Meaning, obviously, they're a big advocate for local injections. There's three approaches. There's conservative, there's local injections, and then there's surgery.

By the way, in my opinion, half the patients work with conservative management. That's meaning you don't do surgery, you don't inject, you tell the patient rest. I like the idea of using a, ice cube. An ice cube is about the size of this RheumNow chip. I tell a patient, take the ice cube, put it in a paper towel, put it right there on the on that trigger finger three times a day for ten days.

You're trying to shrink the size of the nodule. It's kind of the same as basically putting a splint on the hand, not using the hand, using some reminder to reduce the activity. That's conservative management, with or without, an analgesic drug or non steroidal if that's tolerated. But basically, immobilization, ice, usual principles, and for the most part, time is taking care of the problem. That works in half the patients.

These are my numbers. The other half get steroid injections, and I often ask patients, what do you want? I can give you a steroid injection right there, or, and I can we do the ice, you know, three times a day for and you'll leave it on for, what, again, ten to fifteen minutes until it melts. Or we can do the steroid injection, and in my experience, they both work about half the time. The point being, conservative management works in fifty percent.

Of those that in whom it doesn't work, you do a steroid injection, and that works in fifty percent. The literature on steroid injections, by the way, is somewhere between fifty and seventy percent effective when you use local infiltrated steroids, not into the tendon, but peritendinous around the nodule, usually going in right at the crease here and going proximal to the nodule, or just distal to the nodule, proximal to the crease. And then surgery. And I don't know what the success of those guys are, but the hand surgeons say, oh, yeah, we fix these all the time. So very few of my patients have progressed to surgery with trigger finger.

Most time can take care of it, and getting to that time point that they're going to get better, you can either use an injection, or you can use, again, conservative management. Systemic therapies don't work here. I mean, I would not use systemic steroids, I would not use disease modifying drugs, nonsteroidals I don't think really make much of a difference other than taking care of local pain. That's trigger finger. It happens a lot.

I thought you'd wanna know my perspective. Check out RheumNow's coverage of the meeting. Again, we need interactors, people to learn and to basically teach us what they think about what we're saying about the meeting. Hopefully, it's gonna be you. We'll see you then.

Hi. This is QD clinic. I'm Jack Cush with RheumNow. QD clinic is brought to you by RheumNow and where you spend your time smartly when going to a virtual meeting like the ACR, Consider it. This case is the diagnosis and treatment of peripheral spondyloarthritis.

The patient is a 25 year old, African American female who is b twenty seven positive. She presented to me a few years ago with recurrent uveitis and hip pain. Turns out she would have intermittent niacinnovitis and effusions that would need to be drained, occasionally injected. She was on nonsteroidals. She's been through the ringer, meaning she's had recurrent uveitis.

She's without damage, thankfully. She's had, recurrent knee effusions and oligoarthritis. She's had severe progressive hip disease and damage requiring a total hip replacement. All the while, a few years of this while taking etanercept, and then adalimumab, and then cerdulizumab, and then IV golimumab. And, you know, they kinda worked.

They might have been better at controlling her uveitis than her arthritis, but, boy, it never really worked. So what happened next? We put her on an IL-seventeen inhibitor. We put her on secukinumab thinking this will work. This will be great.

Wrong. Four months of that was horrendous, like, really, a few of the TNF inhibitors she took. I mean, it's really unusual why she doesn't seem to respond to anything. And then we put her on afliximab, and now she's had a miraculous response. I mean, five milligrams per kilogram has been just fabulous.

So where are the pitfalls here? Number one, the diagnosis. Peripheral spondyloarthritis means no axial disease. Her diagnosis is established by her uveitis. She had some early inflammatory like back pain, but I wasn't convinced.

Her X rays of her SI joint multiple times have been negative. She's had hip damage and hip replacements. She's had Achilles tendonitis, and she's had an oligosynovitis in the knees. So she meets the ASAS classification criteria. Look.

This is what they show. You can see on the right, if you have peripheral arthritis, you can have enthesitis and have the diagnosis, or you can have arthritis, enthesitis, and inflammatory low back pain. Again, she's been cinched by having her recurrent uveitis and her peripheral inflammatory disease. She happens to be b twenty seven negative, but yet she responds very well to drugs that would work just as well in b twenty seven positive individuals. So the diagnosis needs to be established and a little more difficult in people who have peripheral disease.

The next is going to be treatment, and she's been difficult. Nosteroidals, no effect, steroids, intra articulately some effect, but really oral, no effect at all. And then she's been through the Ringer. Three and a half, four years, four biologics, TNF inhibitors, no effect. Another less than half year with an IL seventeen inhibitor, really no effect there.

And it wasn't till she got afliximab. So the point is maybe sometimes you do have to go through five TNF inhibitors. My goodness. That's so far against what I have said in the past. But, you know, live and learn.

Trial and error is sometimes the best way to learn. I'm glad she's doing very well on this, but you have to be persistent. The question is, what would happen if she didn't respond to the moderate to high dose of infliximab? She's on five milligrams per kilogram. Well, number one, IL twenty three inhibitors don't seem to have much effects in axial disease.

Not not sure what they would do with peripheral spondyloarthropathy. Not been tested. Next, your option could be another IL seventeen inhibitor like ixekizumab or any of the others coming up in the future. Would she do well with an IL twelve twenty three inhibitor like, ustekinumab? I probably would not try her on aprimilast because I'm not sure it really would work in something like this.

But those are the remaining options when really frustrated, and, thankfully, I'm not really frustrated on this case. That's it for this episode of QD Clinic. Tune in for more. This is QD Clinic, and I'm doctor Jack Cush with RheumNow. QD Clinic is brought to you by the ACR meeting.

ACR twenty twenty has gone virtual. You need to go to RheumNow. Our case today is gout goes chronic. Gout certainly can be an acute and even a chronic disorder. What about this case?

66 year old African American female comes in with a history of gout that's going back to about six, seven years. She says the onset of gout was left toe swelling with pain, redness, swelling, swelling so bad that it, you know, it was it was red and hot and couldn't step on it. Classic. She went to her family doctor, was given, colchicine, got better, had another attack, and then was started on allopurinol. Initially, a hundred milligrams, then later, three hundred.

Yet, on three hundred milligrams a day, she has about five attacks in the last year. This is what she says. She says her attacks last seven to ten days, and they're usually only relieved by Medrol dose packs or, five day courses of steroids. But those work really, really well. So it's not clear that her gout is well controlled.

Although she says that she hasn't had an attack in the last three months when she comes in to see me, but she's coming in now because she has gout. She's had all these attacks, but she's got one problematic joint, and that is the ankle. Says the ankle's been a problem for like two or three years. Tender, swollen, wears uses uses crutches. It's always a problem.

She's gone to orthopedist. They've really not done much. They haven't done any imaging. It's not sure what orthopedics she went to who's not doing any imaging. But nonetheless, she's doing badly in that joint.

Her current medicines are allopurinol, and she also takes a a PRN nonsteroidals, but her ankle is again, a real problem. So I'm willing to give her the diagnosis of gout, acute recurrent gout. Not sure what to do with chronic one ankle monarteritis. A little suspicious, and especially in that it's not really swollen. When you, palpate the the foot, the MTPs, the toes, they're all normal.

Midfoot, all normal. The ankle, talocurl, true ankle joint, all normal. No Achilles tendon problems. But she does have peroneal and posterior tibial tendonitis that is really exquisite, and worse, she says, when she stands on it. So she's got a periarticular problem, and then when we do testing, her uric acid's normal.

Her uric acid is like five something. Her labs don't show any inflammation. X rays were done previously, didn't show anything. I ordered an MRI, and she's got a tear of the posterior tibial and just edema about both those tendons. So this now becomes an orthopedic problem.

But is it really? Could this be monosodium urate and uric acid deposition, in a peritendinous way? Could this be a gouty problem in addition to a traumatic problem? This is gonna have to be decided by the orthopedist. Of course, it may be better decided if we did dual energy CT scanning to show that she, in fact, does have urate deposits there, and we might do that.

I find that it's not easy to order. It's often not easy to interpret, and it hasn't been quite the gold mine in my experience diagnostically and clinically in management as it seems like it is in all the journal reports that I reviewed on this. So, again, this person has acute gout that's kind of controlled right now. As long as her SUA is under five, I think we're good. She has no nodules or TOFI, but and that's where she is.

She's right around five right now. But the question is, she's got this chronic ankle problem. So I think the takeaway lesson on this was, you know, if you, are not, buying the presentation, if the behavior is not quite what you expect out of gout. If it doesn't smell like gout under these parameters, it's probably not going to be gout, and that's what her current biggest problem, the right ankle, is. It's not a gout problem.

I don't believe. I think it's a traumatic issue. I mean, she's overweight, and, and that along with whatever led to the the the tendon, let's is giving her reinjury of that ankle. Again, if it doesn't respond, then maybe we'll consider it deck scanning. This is what I think about when gout goes chronic.

Tune in again for our coverage of ACR twenty twenty. It's coming up soon.