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Good day, mate. This is QD Clinic, and I'm Jack Cush. QD Clinic is brought to you by Rheumatology Roundup twenty twenty, only on RheumNow. It's gonna be a week from today, next Monday night, the ninth at 7PM. If you're a rheumatologist, sign up.

We're gonna send you a webinar invite on Zoom. Everyone else can watch it on our webpage or watch it streamed live on YouTube. Today's case is HIV and joint pain. 27 year old man presents to the clinic. He has a history of HIV.

He's currently on HRT therapy. He's got a problem of iron deficiency anemia that's not yet resolved and, hasn't been fully worked up. A year ago, he presented with acute knee swelling that took a number of weeks to go away, and then he, for a while, developed an oligoarticular migratory arthritis, mainly large and medium sized joints, kind of moved around, ultimately responded to, nonsteroidals, and now he's doing fine, although he has lingering wrist pain. Happens that his wrist was a place where he previously had damage from an injury, but now it hurts. It was previously swollen, is it the old injury, is it the new thing?

The wrist isn't really the issue. The issue here is what's the cause of his joint pain, and what's the role of the anemia? So, I think there's several things that should jump out at you at this kind of story that helps you to formulate a differential diagnosis. Number one, HIV. What are the possibilities there?

Two, joint pain, and remember, said it was migratory. And then lastly, we have this sort of GI issue on the table. Let's go through these bit by bit. First, HIV. The first thing you should think of is, well, actually, HIV people get the same kind of arthritis that everybody gets at the same rate.

So there's you know, they're allowed to get gout and rheumatoid arthritis and polymyositis just like anybody else. There are a few things that the HIV positive population may get that the regular population does not. Number one would be HIV agents, meaning the protease inhibitors and his current HRT therapy. These actually are quite notorious for causing arthralgias, myalgias, autoimmune disease, inflammatory arthritis. Again, drug induced rheumatic syndromes, you should certainly be thinking of HIV drugs.

This gentleman's on Biktarvy, which is a new combination one, and and this is one of the warnings in there. If you continue to have joint pains and problems on this drug, then like all other drug induced syndromes, you should stop the drug. Next, HIV. Those of you who've been around long enough know that, HIV patients, are notorious for getting reactive arthritis, something we don't see much of anymore, but they also get psoriasis and psoriatic arthritis. They can also get IBD.

They can also get inflammatory arthritis directly related to HIV. They get, this DILS, diffuse, infiltrative lymphocytosis or lymphadenopathy syndrome. They basically look like Sjogren's syndrome, and, that's kinda odd. They can get myopathy, myositis, hypersensitivity vasculitis, and, obviously, other infections. So there's quite a differential diagnosis.

I mean, right now, this gentleman, the way he's behaved is more like a reactive arthritis than anything else, and maybe, he has IBD for reasons we'll talk discuss next. Why IBD? Well, again, it's in the differential. There is a dependency on CD8 positive T cells like there is with reactive arthritis and psoriatic arthritis. So there might be a little bit more IBD going on here.

He does have a history, one episode of proctitis, and he has this unexplained iron deficiency anemia for which he's needs to go and get further GI workup. I mean, he has a very, very low MCV, and he is anemic right now. And he's 27 and healthy and really not taking nonsteroidals right now. He takes nonsteroidals intermittently if and when he does get joint pain. So, yes, he could have GERD and upper GI bleed or gastritis or esophagitis, but he could also have occult IBD.

So they're probably gonna start with an upper and then maybe go to lower endoscopy to further assess this gentleman. And then lastly, you know, migratory migratory disease, disease, you you should certainly think the classic one, rheumatic fever, he does not have. Gynecoccal arthritis and chlamydia arthritis, notorious for migratory arthropathy in a young male. Other viral arthritities, probably the leading one these days would be hepatitis B. So, you know, he's had hepatitis testing, those were negative.

He hasn't been tested for rheumatic fever, it doesn't seem appropriate at this point, but you should certainly use that migratory label as, something that you formulate. So, the next steps are a GI workup to understand this both his anemia and whether it could be some IBD. He's now a symptomatic management person, meaning he gets nonsteroidals, and that's about it. Steroids generally don't work in reactive arthritis or in this kind of arthritis unless you wanna inject a a joint or two. Patients with bad recalcitrant polyarthritis, you can go on and use the same drugs you would use in RA, methotrexate, you know, cyclosporine, TNF inhibitors.

There's really, no, hazard, of using more aggressive therapy if aggressive therapy were warranted, although it's not warranted here. That's it for this episode of QD Clinic. Tune in for more. Hi. This is QD Clinic.

I'm doctor Jack Cush with rheumnow.com. QD Clinic is brought to you by the morning report and the evening digest, twice daily news during ACR twenty twenty. RheumNow is gonna deliver you the meeting. You give us two hours. We'll give you the meeting.

Twice daily emails. Don't be bothered by it. Check them out. There's a lot of good stuff, and it changes twice daily. Our case today is hyperuricemia in psoriatic arthritis.

Our patient, a 49 year old male who has psoriatic arthritis with oligoarticular involvement, nail involvement, mild psoriasis, and he's had spondylitis in the past. He's he's b twenty seven positive, and he's done just fabulous on a TNF inhibitor. He's been on this TNF inhibitor for about four years, really had no complications. One time had, like, a cellulitis of the lip. That was very, very odd.

We think it was a a shaving accident gone awry, but, other than that, he's done really well on the TNF inhibitor. And because he has an elevated creatinine, his routine lab follow-up on this visit, which was totally normal, included a uric acid. So his labs come back totally normal. His creatinine is 1.3. No good explanation.

No hypertension. No renal insults in the past. Not really taking nonsteroidals. And his uric acid is nine. And so the question is, what's the deal with that?

Well, you do know that psoriasis patients and psoriatic arthritis patients can often have hyperuricemia. That if they are hyperuricemic, they're at a greater risk of developing gout. So if you have psoriasis, your odds of developing gout are about twofold higher than the population. If you have psoriatic arthritis, your odds of developing gout are about four point fivefold higher than the regular population. And if you have hyperuricemia and psoriasis or psoriatic arthritis, you're also at a higher risk.

This gentleman has never had nephrolithiasis. He's never had acute gouty attacks or lower extremity flare ups that might be construed as gout. He's really been a few joints, never the feet, some heel pain, and plantar fasciitis early on, and as I said, spondylitis. But now he's at risk. The question is, are we gonna do anything about this?

Can we do anything about this? Should we lower his uric acid? At first glance, I'm not going to, but I'm gonna watch it. I do think hyperuricemia is part of the metabolic syndrome, and we certainly know that the psoriatic patients have, greater comorbidities, including the metabolic syndrome, and and this could be part of it. He's also I'm gonna watch for gout and nephrolithiasis in him and have cautioned him about that.

If he continues to have, asymptomatic hyperuricemia above nine, I'm gonna treat it. You know, there's a controversy about whether you should treat that or not. I believe it should be treated because I think, systemic hyperuricemia is bad for the vasculature, bad for a lot of organs, and and there's a lot of evidence to support that. Historically, it's been thought though that you don't treat asymptomatic hyperuricemia unless the patient's at risk for either renal damage or kidney stones, and that's really high levels. Now, the renal story here is a totally different story.

This man, started out with a creatinine of about 1.1, and now it's 1.25, now 1.3. So, yes, he's gonna be evaluated by nephrology, to figure out could he possibly have uric acid nephropathy but not have evidence of gout or nephrolithiasis? It's actually been described. So interesting case, an interesting twist on psoriasis and hyperuricemia. Keep your eyes open for that.

I I think you should check that annually or periodically in your psoriatic patients. That's it for QD clinic. You give us two hours. We'll give you ACR. Tune in front of the QD clinic tomorrow.

It's QD clinic, and I'm Jack Cush with RheumNow. QD clinic is brought to you by the great and many panel discussions we're going to have this upcoming week from the ACR twenty twenty meeting. Panel discussions with the big leaders on RA, PSA, spondyloarthritis, gout, biologics, and auto inflammatory disease, and a whole bunch of others that my faculty are gonna come up with. I think if you watch our videos, you're really and you like those, you're gonna really like the panel discussions. Today's case is another kind of dermatomyositis.

A 40 year old male, presents with, digital ulcerations, weakness, and, and, of course, is found to have a CPK of about, I think it was around eight hundred. But it was these digital ulcerations which were really perplexing. It was also in the context of having really deep, violaceous Gatren's like lesions over the MCPs, PIPs, and even in the feet. But then he developed over those and near those these deep digital ulcerations that were secondarily infected with an atypical mycobacterial species. We call that nontuberculosis mycobacterial infection these days.

And and that was difficult to treat. Again, early on, his CPK was four ninety six, aldolase was 12.7. He had increased LFTs, and he had, negative a negative ANA and a negative panel of myositis specific autoantibodies, but he also was tested for TIF one gamma, and that was negative, and MDA five, and that was positive. As you know, MDA five, dermatomyositis are patients who often have dermatomyositis, synane myositis, and are at significant risk for interstitial lung disease, progressive severe interstitial lung disease that can kill even though their myositis ain't that bad at all or not even present at all. And they can also have these ulcerative lesions, can be very difficult to manage.

This gentleman had, you know, some wide pains, and whatnot. A biopsy was done showing evidence of inflammatory myositis and vasculopathic dermatomyositis. And he was treated initial initially with IVIG and high dose steroids, later on cyclosporine and azathioprine. When I took over his care actually, he also received Cellcept and, and azathioprine, as I I already said. When I took over his care, I left him on the azathioprine, and I switched him over to leflunomide.

Leflunomide is my second go to drug with dermatomyositis and polymyositis. I like methotrexate first. Leflunomide works really, really well in my experience. It's really another agent like CellCept and azathioprine. I think it's easier to manage.

And you just have to worry about patients who have LFTs. Are there LFTs from liver? Are there LFTs from muscle? And you gotta be clear about that before you start using a drug that will give you LFTs like methotrexate or leflinamide. Anyway, he's done fabulously well.

PFTs done on this man were totally normal, but we continue to watch him for this. He's now in his second year. His lesions have all healed up. He has, sort of persistent low grade Gottren's lesions, but no CPK or aldolase elevations as muscle strength is is normal. So MDA five dermatomyositis, a unique subset of dermatomyositis.

You give us two hours, we'll give you ACR twenty twenty. Tune in. This is QD clinic, and I'm Jack Cush with rheumnow.com. QD clinic is brought to you by ACR IQ, a daily quiz during the ACR twenty twenty meeting where you can check out how you stack up against others. This is our last clinic, our last video that we're gonna shoot, prior to the ACR.

So it's a good one. It's a brain thumper, stumper, it's called running out of options. My patient's a 67 year old man who has seropositive rheumatoid arthritis. I've taken care of him for about six years now. He also has some low back pain, degenerative disc disease, had knee OA that led to, two knee replacements.

And the sad ugly part of the story is that he's had multiple prosthetic infections. And of course, he had those while he was taking biologics. So what has he been treated with in the past? He's been treated with the following: methotrexate, adalimumab, Humira, prednisone, Cimzia, Symphony, Otezla, Orenzia, hydroxychloroquine. And we're now at a point where we don't know what else to use.

Oh, he also took rituximab. On, TNF inhibitors and methotrexate, he had two septic joints after he had his surgery, both were MRSA. On, I think, rituximab and another DMARD, he had a candida septic joint. So you can imagine the surgeons are worried, the patient's worried, the rheumatologist is worried about what to use next. And yes, the man has active synovitis with six or more swollen joints, a bunch of tender joints.

He's got a C. D. I. Score that's 21 today. He's currently taking leflunomide, gabapentin, trazodone at bedtime, PRN, Tylenol arthritis, don't know that because his pain level's an eight, but he just takes PRN, Tylenol arthritis.

He's not on steroids. So what do you do? What do you offer? At last visit, we talked about, let's add let's try to go after triple DMARR therapy when we can't use methotrexate. He won't take methotrexate.

We'll use leflinamide, hydroxychloroquine, and maybe we'll add sulfasalazine later. We gave him hydroxychloroquine, nausea, headache, didn't headache, couldn't take it, stopped it. He's generally not difficult when it comes to taking medicine. So if he says he has a side effect, I believe he truly has a side effect. So again, I'm stumped.

What am I going to use next? We really can't use TNF inhibitors. So I've written about treating a difficult RA patient and my solution is reboot, control alt delete. What does that mean? Delete number one, the medicines you can't take or the patient won't take.

That includes methotrexate, Humira, Symphony, TNF inhibitors, Otezla, Orencia and hydroxychloroquine. What controlled them in the past? Well, actually the TNF inhibitors and methotrexate controlled them, but he got these infections. He won't go there, so my control and delete list is the same. What's the alternative list?

The alt thing. Otezla, we tried that, didn't really do anything. Haven't used other drugs for which you might act be using an off label indication, something like tacrolimus or mycophenolate cyclosporine, which actually is an indication for. This is what I decided. I offered the man to take daily injections of Anakinra or every eight week injections of Canakinumab, an IL-one inhibitor.

They have been associated with, you know, joint infections or serious infections. We just don't use as much of that drug and I like Canakinra, it's a short half life drug given once a day. It is approved for use in rheumatoid arthritis. The Canakinumab, long acting IL-one inhibitor is not approved for use in rheumatoid arthritis. In fact, it didn't work in rheumatoid arthritis in clinical trials.

What else can we give him? We could also give him a JAK inhibitor. Do JAK inhibitors have a very high rate of serious infections? They generally don't. It's really what zoster infections were worried about most.

And so that was a choice, daily injection versus daily pill. He wanted the daily pill. Oh, and by the way, he only has Medicare and that's not, neither of those are covered. So we're gonna go with a JAK inhibitor and try to start out with some samples, try to get compassionate use or he has a secondary insurance that might cover it. If that doesn't work out, then we'll go with the daily Anakinra.

We're gonna have to apply for patient assistance through the foundation. Again, these are really difficult, but when you have difficult cases, you go to that control alt delete solution. I think that works for a lot of people, and he really does have swollen joints, so I'm forced to do it. The bottom line here is a man who's at high risk for infections with rheumatoid arthritis, what's your best choices therapeutically? Number one, get off steroids.

You shouldn't be on steroids. Number two, methotrexate, sulfasalazine, hydroxy chloroquine seems like you're doing something without really doing something bad like starting an expensive, possibly dangerous biologic. Iabotacet would be the first choice. I think it has the lowest infectious risk of all the biologics. However, that was tried, couldn't take it, won't take it.

Now we're just left with either a low dose of a biologic, that's why I went with a short acting Anakinra with a half life of six hours, and I don't know there's really appropriate risk, appropriate choice given the risk, but a JAK inhibitor might be the solution here, especially if you can get control and use less drug or half dose. But again, above all, avoid the steroid. That's it. Hope you enjoy the meeting. You give us two hours, we'll give you the ACR, should be fun.