QD Clinic - Week 4 Save

Welcome to Cudi Clinic brought to you by roomnow.live. Roomnowlive, the little big meeting. Little in that we're expecting a crowd that will be small enough to be intimate, big in that we're gonna broadcast over the Internet so that everybody can watch it even if you don't attend. Check it out, roomnow.live. Today's case is called recurrent infections in a patient on a biologic.

This is a 66 year old woman with rheumatoid arthritis for a number of years. She's got a lot of comorbidities, recurrent UTI, renal insufficiency creatinine about 1.5. She has myofascial pain, OA of the hands and low back, osteoporosis of vertebral compression fracture. She's been treated with a number of different DMARDs and biologics including methotrexate, Enbrel, Humira, Cimzia. Last visit in October, she was, started on Arencia and like so many of the biologics before that it was never started or it was delayed or she's largely not been on the drug because she's had recurrent infections.

Now she has, in her history recurrent UTIs which I think have resulted in hospitalization and hence she may or may not have pyelonephritis associated with that. Sick and been in the hospital with pneumonias in the past as well. The problem is every time she gets sick everybody stops her biologics her arthritis goes to hell in a handbasket. And then I'm left to clean up the mess. The question is, what do you do?

Well, the problem here is a misunderstanding on one, who's prescribing and managing rheumatoid arthritis therapy, specifically the biologic, that would be me. And number two, who has the power to stop the drug? And that would be, again, me and only me. So here's some rules on how to manage patients with recurrent infections and who go off of therapy and then get worse because of it. Rule number one, I own the drug.

I'm letting the patient borrow it. If I let you borrow my Mustang, you wouldn't gas it or not gas it, paint it or not paint it. It's my Mustang. You drive it like I tell you to drive it. And that's the way it's supposed to work.

Here, I'm letting you use my medicine and I'm in charge of it. Nobody knows more about the biologic or rheumatoid arthritis therapies than I So again, that has to be instilled upon the patient. Other people who mean well are voicing their opinions, the patient stopping medicines, that's a bad idea. Nurses, pharmacists, psychiatrists, next door the hospitalists, they don't get a vote. Why?

Because they get their education from the television and TV ads. I know about the biologics. So number one, I own it, only I can stop it. And the only other rule is if you're the hospital and on IV antibiotics, you can stop the drug. Rule number two is you never stop a biologic.

If you get a cold, a sniffle, a URI, a flu, unless you had a temperature of a greater than 102, I don't care. It doesn't matter. URIs never progress to pneumonia and death. Okay? And stopping the biologic, holding the biologic makes everyone think that the biologic causes the infection when clearly it doesn't.

The evidence is very clear. Biologics rarely, rarely augment infection risk. That's actually proven by this case. This woman has been on therapy and not been on therapy and yet she continues to have recurrent UTIs. So if she's on a biologic, she has UTIs.

If she's off the biologic, she has UTIs. Everybody thinks it's a biologic. It's not the biologic, it's her rheumatoid arthritis and her plumbing and her mechanical issues regarding her genital urinary tract, she's having addressed by urologists and surgeons, etc. So again, only when the patient has multiple comorbidities, is on high dose steroids, has lots of stuff going wrong, does the addition of a biologic significantly augment the risk? And you know what, it augments the annual risk of an SIE, serious infectious event, from thirty percent to forty percent.

The patient's already in a bad way. So again, never stop the biologic, understand the true risks of infection associated with the biologic. And then when you have to prescribe something, what's the safest regimen you can use as far as rheumatic therapy? Well, DMARDs and then above DMARDs, I would say the lowest dose of a TNF inhibitor that especially is adjustable with Remicade or another infusible possibly, but, it's also with etanercept. You can lower the dose and once you get someone established and doing well, you could change it to twenty five once a week or fifty every two or three weeks.

Lowering the dose probably is, a way of reducing risk, although it's a marginal reduction in risk. The next way is actually probably use abatacep. Abatacep, when it comes to infection numbers, looks like it's better than the other biologics including TNF inhibitors. Not in all studies, but a lot of studies enough that it would be my go to drug. And then if you're really strapped in all biologics, all drugs cause this, then I would use a conventional DMart.

In this woman, she hasn't been on hydroxychloroquine a long time, started her on hydroxychloroquine, guess what? She's gonna have the same number of UTIs on hydroxychloroquine as opposed to when she was on Cimzia as opposed to when she was on nothing. But at least hydroxychloroquine is going to be a safer drug that she's told not to stop and that they won't stop in the emergency room. So again, those really hard and fast rules are very important in managing the patient. Of course, in this patient, she's going for a GU evaluation as to why she has recurrent infections.

That's another lecture, actually, another blog called the difficult RA patient. Look that up. Tune in for more QD videos. Take care. This is QD clinic brought to you by RheumNow Live, a great meeting in Fort Worth.

Check out the faculty list. It's on the website, roomnow.live. And this is the last week of discounted registration, so you have until the end of the week to save a lot of money and come to Fort Worth and enjoy the meeting. My case I'm going to discuss today is called the ToFi guy. This is a 68 year old gentleman who comes to me with an acute attack of gout that had been going on for almost two weeks.

This was in 2017. When I saw him, was impressed by his tophi, which to say the least were voluminous gobs and gobs of lumps and bumps over the back of his hand, on his Achilles tendon, on his elbows, on his knees. The tophi were grapefruit size. On his elbows, they were easily pool table, pool ball size, if you will. They were just gigantic.

And he had a long history of gout, not treated for many years and tried to treat it in the last few years. The problem is he's got all the comorbidities. He's got really bad hypertension, AFib, multiple hospitalizations for CHF. He's had a defibrillator. He's had a bypass.

He not only has had hyperuricemia, he has COPD, sleep apnea, and a number of other things that are probably not germane to the discussion today. So we treated the acute gout attack. At the time he was already on three hundred of allopurinol. I raised him to four fifty at the same time I gave him some steroids and he came back in a few weeks, he was better. Interestingly, his labs showed he had a creatinine of about two and a half.

He had uric acid that was around three. It was actually really low. His CRP was very high. His sed rate was also very high. Yet he clearly had gout.

We did an ultrasound that showed a double contour sign with stippling and beaded urate deposits being seen. Synovial fluid aspiration was chock full of MSU crystals. The aspirate was milky, clumpy, kind of unlike anything you'd ever seen before. So the question was how to treat him. We talked for a long time about aggressive urate lowering therapy, maybe combination therapy.

We talked to him about the use of peglodecase, which may be the drug that was designed for him. Ultimately, he went on pegilodecase. He was on pegilodecase for about eight weeks, took eight milligrams as an IV infusion, a two hour infusion, every two weeks, during which time he would do well and then flare and then have to go on prednisone for the really bad flares. Just when he was coming down off the prednisone and managing the flares, he would have to go back for another infusion. It was a little bit like the story you have with chemotherapy patients in that they are okay when they go in for therapy but then therapy induces a storm of activity that is hard to tolerate.

And in his case, had more and more attacks that can only be managed with steroids. So over time, the issue with him was, Doc, how long do I need to take this? And what became apparent was that with each month, his urate deposits got sizably, noticeably smaller. His wife noticed, he noticed, he had greater mobility. So on one hand, he was delighted.

On the other hand, he was dismayed with how long this therapy was going on. It was at six months, I told him I needed six months more. At nine months, I told him I needed six months more. And then, you know, at some point when we made a gigantic reduction, like a 90% reduction in his urate, visible urate deposits, then we could consider going on oral urate lowering therapy. Well, he only took therapy for an eight months and then he was lost to follow-up.

And then he died seven months later. And such is the case of people with really, really bad gout. Patients who I have considered for severe urinary lowering therapy and pegyloticase therapy and being very aggressive often don't want to take the therapy and when they don't, their outcomes are horrible. Kidney outcomes are bad, heart outcomes are bad, sometimes they die. And that just shows you how complex this total body urate deposition disorder really is.

So it takes, a long short term plan, a long term plan. It takes a lot of coaching to get someone through who has TOFI and needs them to be reduced because uric acid is a bad marker. It's a bad biomarker And it's a, know, urine, of course, you give them a drug like pegilodecase, their uric acid levels just go down to zero, they become undetectable. In his case, we put him on a background azathioprine to suppress an immune response to the peg, the pegylated part of pegyloticase, which is often immunogenic and when they develop an anti drug antibody, makes the drug ineffective and their uric acid levels shoot up suggesting one, inefficacy and two, toxicity. So we suppressed that with, one hundred milligrams azathioprine and did very, very well, with the exception of his long term outcome and his in his, intermittent flares based on, uric acid lowering or depletion of his uric acid, deposits.

So a difficult case. What I learned from this I think is that again it takes a short term and a long term plan. What do you think? More QD videos tomorrow. Welcome to QD Video brought to you by roomnow.live where every seat is a good seat, where all the rheumatologists are above average.

It's sort of like the Lake Wobegon meeting for rheumatologists. Today's case is PSA versus EOA. 59 year old female with psoriasis since 2006, taken care of and diagnosed by Major League psoriatic navy in Dallas, has been largely managed with methotrexate, weekly methotrexate for a number of years with a good skin response, but a lot of joint pain, some back pain, a lot of pain and problems in her hands. She'd been treated with secukinumab in the past with a great response to her skin, not to her joints. She never took a TNF inhibitor cyclosporine.

She had a past history of back pain. She had a DIP arthrodesis a few years ago, and she really has had no response to her joints for, the therapy she received that included methotrexate, NSAIDs, Tylenol, and secukinumab. At one point, she took prednisone, she doesn't remember how that responded. When you look at her X-ray, she has a pin in her DIP three. She has some reactive, central bony erosions.

And in the DIP three, she has a sclerotic scooped out erosion medially. So is this PSA or is this ELA, erosive inflammatory osteoarthritis? Clearly the treatments would be different. PSA would respond really well to many of the therapies we would use and maybe methotrexate recent data with PSA SEEM study, look for that, suggests methotrexate would work. You know, we know that IL-seventeen inhibitors do work in PSA.

We do also know that, TNF inhibitors work very well. So there are a lot of things that would work really well. However, all those drugs would really have no effect, have been proven to have no effect in patients with inflammatory osteoarthritis. So the distinguishing features here could be the distribution. Joints, DIPs and PIPs are present for both.

Other joints might help to sway, your decision. So in a rosuvial way you can have CMC and MTPs involved, But in PSA you can have other joints but more importantly you should look for obviously dactylitis and enthesitis that would help you think psoriatic arthritis. The erosions in OA are central erosions, the gullwing erosions where there's a central erosion and an outer lip of reactive bone, as opposed to PSA where they're mouse here or marginal erosions that like what we see here. But this patient had both central erosions and a scooped out, well actually your scooped out erosion was medial, not necessarily on the lateral edge. So it looks like more of a central erosion of erosive OA.

Serology should be negative for OA and less than fifteen percent being seropositive for PSA. The proof is unfortunately, I think often based in a response or non response to your best therapies. Erosive OA doesn't respond to anything. PSA has synovitis and tends to respond to the drugs I mentioned earlier. There are lots of effective trials and therapies for PSA but not so much for erosive inflammatory OA and the progression is very slow in both, almost not able to tell just from progression.

I think this patient had more erosive inflammatory OA and since I have no effective therapy, the plan in my best therapy in patients like that is not a biologic, not a DMARR, they don't work, not plaque, but a waste of time. Methotrexate did that a long time ago, didn't do that. Tried every biologic, actually, none of them work. My best therapy for erosive inflammatory always small dose of steroids, two point five milligrams of prednisone, plus somewhere between thirteen hundred, nineteen fifty of acetaminophen, the long acting form, Tylenol arthritis or extended release acetaminophen, given as a once a day dose, two or three pills once a day, sometimes twice a day with that little dose of prednisone is often very good. Then problematic joints, manage by using CoBan cohesive tape.

Wait, I have some in the drawer here. For those of you who are listening at home, you need to look at the video, but the same kind of tape that you use when you're getting your blood drawn and they wrap the gauze with this clingy stretchy tape. Two inch cohesive or Koban tape wrapped around a PIP and DIP for fourteen days is a great way of controlling their pain and making them better. That's it for this QD clinic. Soon as tomorrow's.

Hi, this is QD video brought to you by rheumnow.live. We're down to the last few days of discounted registration. Check it out at rheumnow.live. Today's case from the clinic is entitled how many days of fever? And this goes to the diagnosis of an auto inflammatory syndrome.

I'm fortunate enough to see a lot of patients with Still's disease and auto inflammatory disease and a lot of patients who don't have those diagnoses. There are lot of mistakes often made in diagnosing such patients and many of you throw around a diagnosis of Still's disease like they're Nichols when in fact they really should be manhole covers. But you really need to be very, very rigid about the criteria used to make these diagnoses. So this fellow came to me with a history of periodic fevers. They weren't every day.

They'd be bouts of a few days and they would kind of recur at uneven intervals. He's treated with steroids and he does very, very well. His fevers would be 103 to 104, last three to five days. And the question is what kind of auto inflammatory syndrome does he have? Well, we have a final diagnosis because we've done gene testing showing that he has an MEFV gene rearrangement.

He's heterozygous for that gene that says that he has familial Mediterranean fever or FMF. So the very clear and easy way of looking at these febrile syndromes is how many days do you have the fever? And we're gonna talk in real fever here. We're not talking a hundred ninety nine nine one zero zero point seven. Tell them I'm in the shower.

So how many days of such fever do you need? Again, it needs to be at those high levels, usually greater than 102. And if it's three to five days, and usually closer to three days of fever, then you want to consider the diagnosis of FMF, also Muckle Wells. The diagnosis of FMF is important because it doesn't have to be in someone who has a Mediterranean heritage. You should not, exclude the diagnosis on the basis of ancestry because we often don't know our ancestry.

This fellow actually, his family, comes from, Korea and he was surprised that he has a Mediterranean disorder but clearly he does because he has the following symptoms. He has recurrent bouts of fever lasting usually three, last one was five days. There's not a typical periodicity. These are not quotidian daily fevers. He's heterozygous for the MEFV gene mutation that's sometimes associated.

He doesn't have one of the five top genes that are often tested for. He's seronegative for everything. His last CRP was two sixty seven milligrams per liter. His white count 26,000. His ferritin, 500.

He's had evanescent rashes. He's young. He's 20 30 years old. He has had a prodromal sore throat, lymphadenopathy, pericarditis, and itchy urticarial rash. Again, all these are short, very short lived.

Again, three to five days you think FMF. Two weeks of fever, you think of what? Traps. The TNF receptor one associated disorder responds well to etanercept. And if you have daily fevers, daily quotidian, quotidian means they occur at the same time every day, almost like a circadian syndrome occurring at the exact same hour or minute every day.

Still's disease tends to be late at night, sometimes late afternoon, never at seven a. M. It's a quotidian disease. So if you have a daily high fever spikes up to 100, 300, 400, you would consider a diagnosis of systemic JIA in the adult or in the kid. And if it's an adult, you might also consider the diagnosis of Schnitzler syndrome and you should do an SPEP and look for a monoclonal or polyclonal gamopathy that would be sort of the marker for that disease.

So that's how you know how many days of fever can lead to a diagnosis. Tune in for more QD videos. Enjoy. This is QD video brought to you by rheumnow.live, where the goal is to inspire, inform, educate, and interact. More on that later.

Our case from the clinic is the normal SED rate PMR patient. So I have this gentleman. He's 57. He comes to see me. He's been around the block with a few orthopedists.

He's had neck injections. He's had shoulder injections. He feels horrible. Occasionally, someone's given him a Medrol dose pack and he feels wonderful. And when I see him, he's got, you know, pain up in here from his neck down to his shoulders.

You know, he's sore. He can hardly move. He can hardly raise his arms. His hips and thighs and low back are killing him. He has one to two hours of morning stiffness.

He does not have any fever. He does not have any jaw claudication, anemia, LFTs or weight loss. It's this stiffness and soreness, morning stiffness, and soreness that is overtaken him and changed him dramatically since, about three months ago. So, of course, I see him and say, you're a little young for PMR. Most of my PMRs are, you know, about the average age of PMR, is about 67 to 70 years of age.

I don't diagnose many at, you know, at 90. I don't diagnose many at 50, but it's still possible. The criteria says over the age of 50. So when you look at his labs, no anemia, no white count, set rate is one. Oh.

But his CRP is marginally elevated at nine milligrams per liter, and his platelet count is unexplainable 490,000. Of course, he goes on ten milligrams of prednisone, is now a champion, and there's no other other evaluations that have been done on him have been negative, and this has been curative. So it's really to go over the case that's not the usual, meaning you like them to have a really sky high set rate and CRP, but that's not always the case. It turns out actually somewhere around seven to twenty two percent of patients with PMR will have a normal sed rate. If you look at other acute phase reactants, they'll occasionally be elevated, but they don't need to be.

These kind of patients tend to be younger, tend not to have the other inflammatory I just mentioned, that being anemia, fever, high white count, LFTs, weight loss, those are not usually common. They tend to have a delay in diagnosis, they tend to be a little less female than do the very high sed rate PMR patients. And they tend to respond maybe a little better and get away with a little bit less steroids in the long run. So it happens, it happened to me, it could happen to you. Look out for such cases.

Cases. Let me give you a reminder about the faculty we have for RheumNow Live. It's incredible, it's on the website. It starts on Friday, March 22 with Mike Hollars, John O'Shea, Mike Hollars on preclinical RA, John O'Shea talking about JAK inhibitors, he invented them or he discovered them. Mike Weinblack giving you a history of methotrexate unlike anything you've ever heard.

Eric Madison on the history of steroids. Ted Pincus, Fred Wolf, a safety session with Lisa Samaritano. You know, on a previous recording, I said Lisa Sammartino. Don't know where I got that from. Know Lisa well.

Maybe it has to do with my growing up idolizing Bruno Sammartino, another story. Len Calibre is talking about checkpoint inhibitors. I'll be talking about infections and how to manage them and prevent them. The next day, we're gonna have a talk on the price of drugs, from Matti Feldman, Ron Van Hull Boenhoven, Georg Chet, and Philip Conigan, the masters of the EU doing TED like talks. A session on psoriatic arthritis that features Arti Kavanaugh, Philip Conigan and Craig Lianardi, they'll blow your socks off.

A session on lupus with Ken Kalunian, Richie Fury, and Dorian Erkan talking about the antiphospholipid and catastrophic antiphospholipid syndrome. We have an orthopedic session, a vasculitis session session, and a spondylitis session. We're gonna end with Carol Langford, Philip Sio, Paul Monarch from the Brigham, and then spondylitis, John Ravelle, Eric Ruderman, and Elaine Husney. It's a killer lineup. I don't roomnow.live.

Check it out.