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This is QD Clinic, and I'm doctor Jack Cush. QD Clinic is brought to you by RheumNow Live, a next generation medical meeting. Our case this week begins with the reluctant rheumatologist and peg Lodicase. Saw a 60 year old white male who had a lot of comorbidities and a history of gout. Not surprising this patient had hypertension, diabetes, chronic renal disease, was on many different medicines.

He had been diagnosed with gout ten years ago, has had many attacks over the years, of sort of incomplete, control with, the attacks going from acute and intermittent to chronic and additive, and now he's at the point of having chronic to aphasia gout, involves the hands, the feet, the elbows, occasionally the knees. And when we saw him recently, he was on four hundred milligrams of allopurinol. His uric acid level was 6.8, and he was still having intermittent attacks and a lot of pain. And a lot of his pain, as you might imagine, is related to inflammatory damage and secondary pain and periarticular pain. But then he seems to have warmth and inflammation in some joints as well.

The question is how do you manage him? He's at the stage of having a chronic inflammatory polyarthritis because of his his urate deposition disease evidenced by some big bulky, you know, walnut to pear size, not pear size, almost pear size, collections of of tophi, elbows, feet, hands, knees. It's, you know, obviously, deforming and, and hard for him. The issue is, in discussion with the other rheumatologists managing this case, is that there's a reluctance to start this man on Peglodecase. Yes, you could step up his allopurinol, and yes, you could be one of the few rheumatologists out there that, you know, would use a dose higher than four hundred or three hundred.

But the facts are that rheumatologists aren't as great as we think we are at managing gout. We just like podiatrists and renal docs and internists largely only use three hundred milligrams a day. We seldom have ever used combination therapy. Very few of you have actually used peglodecase, although the numbers of peglodecase use in the last ten years that it's been approved has actually gone steadily up. But many of you have never used it for fear of side effects, anaphylaxis, tales told around the campfire or clinic fire, whatever.

And, and I'm here to tell you that I'm not afraid to use it. I've tried to use it a number of times and had problems either with the patient or the insurance or the patient being really sick and thinking they're too sick to get this infusion. And then, and I have used it. And it's really, I think a very effective way. The issue here is the argument that was presented to me by the other rheumatologists in discussion was, well, if we increase his dose up to six hundred, even up to eight hundred milligrams, we can start to get him to a hypouricemic state where he can lower his levels enough that he can dissolve some of those, tophi.

The problem is the tophi are the tip of the iceberg. He has a tremendous total body rate load. When you see tophi at all, what you're not seeing can be magnified 10 times fold, a 100 fold. And if you want to prove it, then do do do the dual energy CT scans, the deck scans that show urate deposits lighting up. The problem with, I think, the use of this therapy is an overestimation of anaphylaxis.

You know, infusion reactions, I think it's like six, seven percent. And very few of those, you know, less than one in ten of those actually meet the NIH definition for anaphylaxis. So while reactions do occur, the main reaction is because you're mobilizing all this urate, you get more gout attacks and patients feel sick. So the drug was approved ten years ago, done in studies where you give eight milligrams every two weeks or every four weeks. The response rates are basically forty to fifty percent of patients.

There's a dramatic lowering of serum uric acid levels from whatever they were down to undetectable on this drug. The real issue is whether or not you can fight the problem of anti drug antibodies and their anti PEG antibodies, which can get in the way in a long term success, could contribute to some of the toxicity. And I think that this trend right now is to use a background of either methotrexate, azathioprine, or mycophenolate. There's a study going on right now with mycophenolate being done at UAB by Ken Sagg. I've used azathioprine.

We have a recent report in room now about the use, a published report about the use of methotrexate in people going on this. Why would they use these DMAR drugs? Not to treat the chronic synovitis, but to suppress the development of an anti drug, anti PEG antibody that can get in the way of, of long term success. Patients need to be infused. It's not a slow infusion.

It's a fairly easy infusion though. They get premedicated with antihistamines and Solu Medrol more so than hydrocortisone. It's done every two weeks. You have to get a uric acid level prior to the next infusion because you wanna see uric acid levels declining, going down, and staying down. But then if uric acid starts coming back up, well, that's basically anti PEG antibodies getting in the way, and now you're gonna have a rise in uric acid.

And that means, oops, we shouldn't use the drug. You can prevent that anti drug antibodies, anti peg antibodies by using, again, azathioprine, methotrexate, probably mycophenolate, and patients will have long term success. How long do you go? As long as it takes to make them disease free, and to, reduce their total body urate load, which adds to their risk of renal toxicity, cardiovascular toxicity, etcetera. I am fairly liberal with the use of steroids when we're starting out therapy because infusion reactions are very common and, patients should either be on a low dose of steroids or be very quick to use twenty milligrams of steroids at the first hint of a gout flare.

Again, rheumatologists, the experts in all tough diseases are somewhat reluctant to use, peglodecase, and I don't think that's really necessary. Look for your next patient. I want to tell you about RheumNow live and a session I'm going to be in that's going to be on Saturday. It's the second step session on, rheumatoid arthritis. In my session, we have the opening lecture being done by Bruce Cronstein from NYU, famous for his work in adenosine.

Bruce is gonna talk about the mechanisms involved in the efficacy and benefits and toxicities of methotrexate. Should be a fabulous lecture. Alvin Wells is gonna be talking about updates in imaging and new guidelines for imaging in rheumatoid arthritis, including ultrasound. And then I'll be talking about the differences in seronegative and seropositive and telling you things you didn't know about seronegative RA that will scare you to death. RheumNow live, you can still register at rheumnow.live.

Talk to you tomorrow. This is QD clinic, and I'm doctor Jack Cush of RheumNow. QD clinic is brought to you by rheumnow.live. Keen minds need great meetings like this, roomnow.live. Today's case, seronegative room rheumatoid arthritis.

45 year old woman presents with a six month history of polyarthralgias, morning stiffness, and said to have some abnormal labs. On exam, she has 12 tender joints, symmetric polyarthritis. Five of them are swollen, two plus so even warm, and she's unable to close her hands. She has a C. Dye score of 25.

We put her on ten milligrams of prednisone and hydroxychloroquine, we get labs. Labs come back somewhat disappointing. Normal sed rate, sorry, CRP was elevated. Sed rate was not. CRP was like 12 milligrams per liter.

ASO, ACE levels, other labs, ANA, rheumatoid factor, CCP fourteen three three eta, all negative. Upon further questioning, she has had carpal tunnel in the past. She has not responded to the therapies we gave her. She comes in a month later, and she's doing really poor. The only thing we did find on lab tests besides somewhat elevated CRP was that she had marginal elevations of LFTs.

She herself is a little overweight. Someone told her she's had LFTs in the past. Fatty liver, I don't know. But nonetheless, the question is, what does this gal have? She has a seronegative, but nonetheless, polyarthritis not responding to conventional medicines at four or six weeks.

And so what do we do? We well, we put her on etanercept in addition to hydroxychloroquine and ten to fifteen milligrams of prednisone. We manage her pain with QHS analgesics, and we labeled her a seronegative RA. The question is, is that the right label? And I think it's a label that's the right one for now.

You bear that label when you meet the criteria for rheumatoid arthritis, and she does having both small and large joints, by having an acute phase reactant, having synovitis for a long enough period of time. Obviously, you get there a lot faster as far as criteria if you have a CCP antibody and a rheumatoid factor sheath is not. I think the designation of seronegative RA is important. To have that diagnosis, you actually have to have a lot of features of RA and still be seronegative to qualify as having RA. Two, it's borne out over time, so chronicity sort of verifies and solidifies the diagnosis.

However, there is no proof that over time that you're safer in that diagnosis. In fact, over time, a significant minority of these patients will evolve into another well identified syndrome, Whipple's disease or IBD or psoriatic arthritis or Lord knows what. What we do know is that chronicity of swelling and pain, meaning more than twelve weeks of swelling and pain, makes you likely to have an inflammatory arthritis. You're never fully going to be called rheumatoid for certain while you're seronegative, and I think the point that I want to stress is that being seronegative is your opportunity to rethink the diagnosis at every visit. I'm a little concerned about this particular patient's LFT elevations, so we are ordering things like an ANCA and anti mitochondrial antibodies, anti smooth muscle antibodies, and getting a liver consult for them to look at her, because if she has persistent liver enzyme elevations, they may want to do more than just ultrasound to see the size of her liver and whether it's echogenic and has signs of steatosis.

So, again, surrogate is a big challenge because you never quite know and will she respond? Well, didn't respond to Plaquenil and prednisone pretty high dose. We'll see if she responds to etanercept and then over time, non response further questions the diagnosis of seronegative RA. That's it for this edition of QD video. Tune in tomorrow.

This is QD clinic. I'm doctor Jack Cush, RheumNow. QD clinic is brought to you by RheumNow live. Great rheumatologists like you go to great meetings like this. QD Clinic is coming to you from RWCS in Maui where we discussed some cases yesterday.

I'm going give you one of them. Twenty nineteen October, a patient goes in for a hip replacement. You, the rheumatologist, get a letter from the orthopedist saying, Guess what? The gentleman was treated with a spinal block and IV sedation. He had physical therapy immediately post operatively.

He was sent home the same day on analgesic medicines and meds to prevent deep vein thrombosis. That's right. Same day outpatient hip replacement. We've heard about this at our meeting here several times. Just heard a great lecture from Doctor.

William Bugbee, a great orthopedist from UCSD in San Diego, where this has become commonplace. He says outpatient surgery is being driven by number one Medicare, two economics, and three entrepreneurialism. It's also being driven by new techniques, new anesthesia, and I think the idea that you can do a lot better, a lot faster. There's also some recent guidelines that are published in the CMAJ, the Canadian Medical Journal, about who basically shouldn't get these same day outpatient procedures, largely being done on hips, often being done on knees. Who shouldn't get them?

Individuals over the age of 80. Those with a bleeding disorder. Those who have chronic renal disease, greater than stage two CKD. Those with liver disease, those who have sleep apnea that's severe, those who had recent cardiac events, diabetics, those who are overly obese, morbidly obese. These are all non candidates for same day outpatient surgery.

Otherwise, patients who are otherwise mentally able to consent and adapt and who have the support system in place for transportation and home care can go home the same day they have their hip or knee replacement. Things are changing in rheumatology. That's it for Cutie Clinic. Tune in tomorrow for another. I'm Jack Cush.