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This is QD clinic brought to you by RheumNow live. I'm doctor Jack Cush from rheumnow.com. This week, we have an interesting case. A 59 year old Latin male shows up with a swollen left fourth PIP. This one here, swollen contracted going on for about three months.

He's previously diagnosed with seronegative RA, but he never quite responded to Enbrel, methotrexate, Plaquenil, or nonsteroidals. Turns out he's been best controlled in the last year with low dose steroids, two point five of prednisone, and nonsteroidal anti inflammatory drugs. He is rheumatoid factor, CCP negative, and on b a b twenty seven negative. He did have x rays of his hand showing no evidence of erosions, but did show evidence of chondrocalcinosis in the wrist. So we had previously diagnosed him as having CPPD or chronic calcium pyrophosphate deposition disease, no episodes of acute pseudo gout, but nonetheless, he's been managed really quite well with low dose prednisone and nonsteroidals.

Now he presents with a new swollen joint that hasn't gone down, and it's been going on three months. So the question is how can we best treat him and is this going to be in fact pseudogout or CPPD chronic arthropathy? As you know, these patients with the chronic arthropathy are a little bit higher to diagnose. Acute pseudogout, not difficult, you know, attacks in the knees, wrists, are very common, feet, not uncommon, slightly different distribution than what you see with gout, where it's mainly MTP, MTP, MTP, ankle, tarsus, and then it ascends with multiple attacks. Whereas in pseudogout, you might have them first attack in the wrist.

So this gentleman has an attack in in he's never had a wrist attack, but he's had two attacks in PIPs in the past. And the question is, what is the, findings in pseudogout? Well, number one finding in pseudogout and CPPD is chondrocalcinosis. They tend to have normal mineralization unless they have, chronic inflammatory arthropathy. They have uniform joint space loss.

They can have subchondral new bone formation. They tend to have more osteo, some osteophytes, but more subchondral cyst than what you see in osteoarthritis, and they can occasionally have neuropathic changes. They tend to be bilateral in their findings, and the joints that are usually involved, as you know, are the wrist MCP two and three are not uncommon. PIPs are can occur. In decreasing order, it's the knees, hands, hips, and then unlike osteoarthritis, you can get shoulder and elbow involvement with CPPD.

So we were gonna treat this gentleman as if he had CPPD and recheck his x rays to see if anything has changed in that left fourth PIP, which means that he stays on the low dose prednisone two point five. Actually, we increased it to five for two weeks, and then we'll put him back at two point five. We're going to splint the finger, and hope that that gets better. We put him on colchicine zero point six milligrams QD. That's basically a treatment and then when they get into a chronic arthropathy, you can treat them like RA.

When they have acute arthropathy and you can't use the drugs we already mentioned, there's good research that we talked about here about using Anakinra injections, daily Anakinra injections, one usually two, three or four of them to control the acute attack. Again, a good case, an interesting case of CPPD that's not so well controlled here in the clinic. Make sure you check out roomnow.live, roomnow.live, which is where you would go to register for our meeting. I think what you'll like about the meeting is the fellowship. It begins on the first day on Friday.

We end at 05:15, and we go right to the roof where we have a nice reception called room now distilled, where we have Kraft Lemonade. I love Kraft Lemonade. You may love Kraft beer or Kraft Whiskey. We've got great food. We hang out under the stars for a few hours, and then people drift off into the streets of Fort Worth where you can dine at, like, one of 25 different great restaurants in the area.

So check it out. We'll see you in Fort Worth in a few weeks. Tune in for more QD video QD clinics. This is QD clinic brought to you by RheumNow live. I'm doctor Jack Cush from roomnow.com.

Today we're gonna talk about weighing decisions in rheumatoid arthritis. We did this today in clinic. We sort of said, what do you do? This or that? Here's some examples.

Drug one versus drug two. We don't really need two drugs. Which one do we stop? How do you make that decision? Usually this is in the context of being on multiple DMARDs and trying to stop one.

It could be, on the other hand, which analgesic to stop, or it could be prednisone versus nonsteroidals. But let's just say this is two DMARDs, conventional DMARDs, biologic DMARDs, it doesn't really matter. The decision is really quite simple. Number one, ask the patient which drug do you want to go off of? And this is of course assuming that you can go off of therapy and cone down to what is needed.

I mean the patient's doing well in remission, has no swollen joints. But ask the patient, which drug would you like to stay on, which drug would you like to go off? That drives the boat, least as far as I'm concerned. The next rung as far as treatment decisions might be cost, and that's cost to patient or cost to society. Third might be complexity of therapy.

Go with the easier regimen. Patients are already having a hard enough time keeping up with all your prescriptions and all the things that you want them to do. And then lastly, polypharmacy, though a drug that's going to take them out of polypharmacy and into some sort of simple regimen. So ask the patient, keep it simple, stupid. Kiss.

Second issue, do I wean the biologic DMARD or the DMARD or do I discontinue? What should I do? Well, here it's a different decision. It's actually quite simple. You spend most of your life trying to control rheumatoid arthritis, a deadly, dastardly, progressive, never ending condition, and yet someone wants to take monotherapy, less therapy, it ain't that simple.

So, one, you should discourage people who want to go off of therapy when they're doing great. Now that is assuming they've shown you active synovitis and clear cut evidence of rheumatoid arthritis. The odds of people going to drug free remission off of therapy are very low, ten percent. So do you wean or just do you discontinue when they're doing great? Well, ACR guidelines on this were actually quite intelligent, I think the best out there.

They say that if you're in LDAS, low disease activity state, you don't change nothing. The only way you can change is if you're in remission. EULAR guidelines, as we reviewed last week, said that if you're in deep remission, sustained remission, then you can consider changing the interval and taking less drug as opposed to going off of it. And then if you're on two drugs, you know, EULAR said you should go off of the biologic or targeted synthetic DMARD first because if you do go off and they flare, you can recapture response in eighty percent of patients. However, if you stop the DMARD, which is what I prefer to do, chances of recapture is less.

It might be only fifty percent. But staying on the biologic keeps the patient out of FLAIR, in my opinion, and, actually preserves radiographic, integrity, meaning they're less likely to progress. Do you increase therapy or add on therapy? Someone is on methotrexate, or a monotherapy DMARDs and they're not doing well. Do you swap it out because that drug wasn't working, or you just add on top of it?

The bottom line if this is that if it was methotrexate, add on top of it, keep them on methotrexate unless they do not tolerate it. If they do not tolerate it, then you can either go to monotherapy, but really you're gonna need two drugs. So you need another DMARDs like leflunomide, and then you add on top of that either other conventional DMARDs or a tar targeted synthetic or, another MOA non TNF or TNF. And then lastly, what do you do like this when the patient's got a lot of complaints but they got nothing to show for it? Meaning they have no synovitis and their sed rate and CRP are normal and you don't suspect that synovitis and inflammation are out of control, but yet they're not under control.

Number one, analgesics. Most patients tend to underdose their analgesics. Go with safe agents. Number two, modify lifestyle. And number three, fix their sleep and identify fibromyalgia and tell them they're doing great.

Because when they know they're doing great maybe they won't worry so much. Speaking of worry so much, if you went to RoomNow live, your life would be great. Let me tell you about our very first session, pod one, Rheumatoid Arthritis. Management of Infections in TB by Kevin Winthrop from Oregon. He is the master of disaster.

Your disaster is being infectious. Kevin's got the answers. Fabulous speaker. Followed up by Roy Fleishman, who is encyclopedic as far as his knowledge of new therapies and drugs that are just now new on the market. He's the guy that does all the trials.

He's the first author on all the major drugs. Hear what he has to say. And then John Giles from Columbia in New York is gonna give the best lecture you've ever heard on cardiovascular risk assessment and prevention. That's just the first session of many sessions. Room now live.

Register now. There's still a few seats. Talk to you tomorrow on QD Clinic. Hi. This is QD Clinic brought to you by RheumNow Live coming up 03/13/1415.

I'm doctor Jack Cush of RheumNow, and I'm gonna talk about dosing rituximab versus infliximab. Now, these drugs are fabulous drugs. They are mainstays in our therapy. There probably are declining numbers of people taking these drugs in current times or current years because we have so many options. I think at last count, I think in rheumatology, for the management of RA, I think we have 23 new drugs since 1999, and that's not counting the old conventional DMARDs.

That includes, I think, 11 or 13 biosimilars. There's two rituximab biosimilars, one neither of them are actually approved for use in rheumatoid arthritis. One is approved for GPA, the other one is not. And then there's FDA approved Rituxan. And we're going to talk about how to dose that drug.

I think many rheumatologists don't use a lot of Rituxan when they probably should. It's a fabulous drug, it's easy to give. It's got long lasting responses. It's the best drug to give your patients who are non compliant. They can get two doses per year and have fabulous control.

It works about 10% better or more in patients who are strongly seropositive for RF or CCP. And my regimen in dosing rituximab is the drug dosing that was used in the clinical trials. Thousand milligrams done twice or two weeks apart and then repeated every twelve months. There seems to be some concern about when you give the next round, a round being two infusions two weeks apart. I do it every twelve months because I have found that when patients respond great to rituximab, they drop their B cell counts, their CD19 B cell counts, and they go to zero for six months, and then they creep up between month six 12, and then they're gonna need it again at month twelve as far as clinical efficacy.

They don't change their immunoglobulin levels in general, until you've done many repeated infusions. The question is what do you give next year or the second go around? There are some rheumatologists that do this every six months. I think if you've to give rituximab every six months, you shouldn't be given rituximab. It's a drug that's designed to work longer than six months.

If you're giving it less than every six months, you definitely need to use another drug because there are better drugs with better responses. I had a patient yesterday who was on rituximab who felt fabulous after she got her rituximab infusions. Well that's because she got a hundred or two hundred milligrams of IV hydrocortisone. Rituximab doesn't work that fast. Rituximab really starts to work about four to six to eight weeks after they've got their their first or second infusion.

So my second go around, I'm either gonna do five hundred milligrams two weeks apart or one thousand milligrams and leave it at that because the dosing studies show that five hundred done twice is equal to a thousand done twice. My extrapolation of that is a thousand once every year is good enough. Should you use or be monitoring CD19 cell counts in these patients? I don't, unless I'm into like the third or fourth year. I don't do serum immunoglobulin levels prior to infusions.

I know they're gonna go to zero after the infusions. If you ask a number of rheumatologists and leading rheumatologists and those who've done the studies, the vast majority don't. You know who does recommend it? The allergists. Our friends who are board certified in allergy, Arti Kavanaugh, Ding Bingham, Anna Postalova, who gave a great lecture on this at RWCS last week.

They all measure it, be figuring that it's gonna help them make some decisions about whether they need to worry about those immunoglobulin levels as far as infectious risk going forward. Turns out that's a low frequency event. It's only seen with many, infusions. It's not it's not a bad thing to measure them. I just don't think I do them all the time.

Have my friends changed my mind? Not quite yet. What about Remicade? My starting dose on Remicade, whether it's infliximab or a biosimilar, I believe they both work fabulously well, is three to five milligrams per kilogram. I might amp it up a little bit if I think they're more aggressive disease.

But my starting dose is three to five, and I often do three, but I'm not afraid to use five. Turns out the more you use, the less immunogenic the drug is. Right? But nonetheless, three to five milligrams. If patient hasn't responded sufficiently well, I'll increase from three to five after the zero to and then six weeks later at eight weeks, I'll increase after that infusion, at my next infusion to five to six milligrams, and do it two more times.

If they don't respond, I'm not going to ten milligrams. I'm sorry. If you need to use more than six milligrams per kilogram to use Remicade to treat rheumatoid arthritis, you need to be moving on. Because there's one thing clear to me as someone who monitors safety data and all the safety reports, turns out all the biologics are similar as far as their efficacy and as far as their safety, especially with regard to serious infectious events, TB events, opportunistic events. You know what stands out?

Remicade. All the time, Remicade stands out as the bad player with the worst event rates, and that's because of people who are escalating the dose. It's not people on three milligrams per kilogram who get in trouble with Remicade, it's the ten milligrams per kilogram who get in trouble. So I don't need to go there. Now, again, occasional refractory patients who failed everything else and are only controlled by ten milligrams, yes.

But they're the exception and not the rule. You've got another enough choices running around that you don't necessarily have to use a ten milligram dose. That's it for this week, for this day. Tune in tomorrow for another great QD video. Let me tell you about our step or TED talks that we're going to have.

We have this fabulous session on Saturday morning, masters of the EU, our international experts, the future of rheumatology by Gerd Burmester. Ten, fifteen minutes crisp. Lord knows what he's gonna say. Are we doing this right? Robert Landaway, a real thought leader in the EU on RA and the master of T2T, treat the target, Joseph Smolin's gonna say, after ten years of t two t, is this still a good idea, and are we getting it right?

You really need to tune in and be there for this. Tune in tomorrow for QD Clinic. Hi. This is QD Clinic. I'm doctor Jack Cush, executive editor of roomnow.com.

QD Clinic is brought to you by roomnow.live. You know, there's a quote that I put up recently. It basically says, people don't care what you do. They do care why you do it. Let me tell you why I've done RheumNow Live for the second year in conjunction with my partner, doctor Arty Cavanaugh.

The reason we've done it is because we wanted to have high impact education. We're a little tired of a lot of the usual meetings that are out there. You know where they are. They're big, thousands or five, six hundred people. And and basically, you know, they you get lost in the crowd.

There's hour after hour after hour of lectures that are then not really backed up by any q and a time. So what we wanted was to have lectures that were different. Different in that there was a lot more q and a time, that there was going to be this face to face time between you and a small number of participants and the faculty. We want to have this face to face sort of coupled with a large Internet spread to anybody that wants to watch it from home. We have the flip classroom where you learn before you watch or come.

And then, again, more than 25, 30% of the time is devoted to interaction, polling, questions, q and a. It's really quite astounding. And then, of course, we're doing it in Fort Worth, which is truly novel. And I don't know how to describe why Fort Worth is different, but it's one of those cities that actually is different. It's not cowboy.

It's kinda cool Texan. But if you wanna find cowboys, we can show you where they are. They're down at the stockyards, and there's a big honky tonk that you can listen to country music, or you can just do one of a million things that you'll see in in in Fort Worth, is uniquely Texan, uniquely American. Anyway, today's case for, QD video, QD clinic. It's a 49 year old white man who comes to see me because he saw me about a year and a half ago with a trigger finger.

Specifically, a trigger finger in his left fourth finger. This one here. And it would get stuck and it would snap open, and it was now at the point of not snapping open and being very painful. He was back for a repeat injection. Now we do see trigger fingers.

I just wanted to review what trigger finger is and maybe what you should be doing about it. Can happen in almost any age, although it's more common with the elderly. It is said to be part and parcel OA and RA, but it's a fibrotic nodular change to the flexor tendon usually near the a one pulley, which is right near the crease of the MCP joint, and that's what gets stuck, that fibrotic tendon. Which fingers are most common? It turns out actually the fourth one, the the ring finger, followed by the middle finger, followed by the index finger, and then pinky and thumb being in the middle or being last on the list.

Risk factors for getting this would not just be RA and OA, but also those who are doing repetitive movements. That's a key feature in a lot of people. Said to be a little higher in diabetics and those with hyperlipidemia, but is really high more so in women, than men, maybe two to threefold higher in women more so than men. Treatment is a challenge. You know, avoiding it is the best problem.

Not many people need surgery. I tell my patients, number one, change whatever is that you're doing, stop doing it. If you do a lot of this all day long, stop doing this all day long, change your job and get a different kind of mouse or whatever is driving that problem. I use ice. I tell patients I can inject it here and now, and it'll probably get better in about two thirds of cases, or half the cases will get better if you just take an ice cube and put it right on that tendon, at the crease, put it in a paper towel, let it melt over fifteen minutes, do that two or three times a day for the next ten days.

If it doesn't get better, then come back and see me. A lot of people opt for the ice, and most don't come back for an injection. When you do an injection, just obviously, it's a touch here. I mean, a fine touch is needed. You don't inject the tendon.

That will damage the tendon. That will cause a tendon snap. You don't inject the trigger finger more than two or three times because then you'll cause fibrotic tendon changes and the tendon rupture. So once or twice makes sense, but after that, you gotta send to the hand surgeon. Injection needs to be near the nodular change, in a perinodular fashion.

So I use an anesthetic, and then I kinda squirt a little bit here, little bit there. I try to put in a diluted amount of ten milligrams of Depo Medrol in and about the nodule. Tell patients to immobilize the joint, not use the joint, the finger, put a, an ice cream stick in there with some tape so they can't flex it for a day or two, and then tell them modify their their activity, and many get better. The ones that don't, the ones that come back for a re early repeat injection or repeated injections, you gotta send them to the surgeon. They'll go in and do an open surgical, excavation and sort of try to, make that tendon slimmer and more functional for the future.

That's it for trigger finger on QD video. We'll talk to you tomorrow. Don't call me seronegative. This is a QD clinic brought to you by RheumNow live. I'm doctor Jack Cush from RheumNow, and our case today is called don't call me seronegative.

A 42 year old guy comes to see me transferring his care from another city where he was diagnosed by a major university with a big name. Like this university a lot. Don't know the doc there, but, you know, if they're good enough to work there, they're good enough to work anywhere. Right. That's New York, New York.

Anyway, and they diagnosed this gentleman with acute onset of polyarthritis in hands, knees, feet, whatever, as seronegative arthritis. And then, he gets treated strangely with one round of nonsteroidals, and then he gets a TNF inhibitor that doesn't work, and then he gets another TNF inhibitor that does work. Never methotrexate, never prednisone, and he's had a little bit of back pain, but really not really. And so the next four years ensue. He's taken care of by three rheumatologists, and he's called seronegative arthritis, seronegative RA, and seronegative spondyloarthritis.

What? These are actually three divergently different conditions that aren't even close to each other, but the term gets thrown around not like manhole covers, but like nickels. I like that analogy. And I don't think we should be using the term at all. So let's be clear.

There is no such thing ever again in this world as seronegative spondyloarthritis. It's just spondyloarthritis or axial spondyloarthritis or nonradiographic axial spondyloarthritis or ankylosing spondylitis, but never is it seronegative. It's supposed to be knucklehead talking to me if I've ever used that term, and you if you've ever used that term. Spondyloarthritis, spondyloarthritis. There should never be another chapter written.

And when when you do a search looking for as I did, I was writing chapters and pieces and lectures on seronegative RA. I could only find things written about seronegative arthritis, seronegative spondyloarthritis, and it's all talk talking about SPA related disease, not about RA and inflammatory arthritis, peripheral arthritis related disease. So there is no more seronegative spondyloarthritis. Do not use that term. You can use seronegative RA because you diagnose rheumatoid, the tests come back positive, boom.

It's one of the twenty percent, fifteen percent who are, in fact, seronegative for rheumatoid factor NCCP. We don't care about b 27. That's talking about that other condition we just spoke about, spondyloarthritis. And then, you know, seronegative arthritis is like the most noncommittal, label and shame on any of us who use that. Call it what it is.

Inflammatory arthritis. I don't know arthritis. Wish it were arthritis. I hope it ain't arthritis. Whatever.

But don't call it something that doesn't say anything like seronegative arthritis. I'm not even sure you're it really is arthritis when you call it that. But it is important, I think, to maybe use the term seronegative RA. It's fifteen to twenty percent of patients. It actually denotes a condition that's severe, more severe than seropositive at the outset because you gotta have more criteria to be called RA because you can't have the seropositivity.

And over time, they may respond as well. They may have less X-ray progression, and they may respond less well to at least rituximab and abetacept. Seronegative RA is an important subset. It's just not a subset of RA. It's probably another disease.

But, again, the big point of this whole schlameal is let's drop the seronegative spondyloarthritis term. It's so archaic, so confusing. Three really good rheumatologists in the last four years have used it inappropriately in this patient who, by the way, doesn't have any of those conditions. Seems like it's a lot of arthralgia related to bad sleep, if you know what I mean. Anyway, that's it.

Check out our rheumnow. Live site for more information on registration. Tune in tomorrow for another QD clinic.