QD Clinic - Week 2 Save

This is QD Video brought to you by roomnow.live, the next best meeting in rheumatology. Today's lesson is on psoriatic arthritis and an elevated creatinine. Interesting combination. 36 year old Indian male with psoriasis and psoriatic arthritis going on now for almost ten years, his psoriasis, psoriatic arthritis, maybe six years. And he's been on, mostly Humira or adalimumab during this time.

He started out, was treated with some other, agents including, I believe a brief trial with methotrexate and, maybe even etanercept. And he's been on adalimumab, forty milligrams every other week religiously going on now for five or six years. Really well controlled at one point had elevated LFTs, he lost weight, stopped taking nonsteroidals, did really well. Those mildly elevated LFTs went away. He's always been normotensive and always had a normal creatinine.

Normotensive meaning he's actually had high blood pressure taking a low dose of losartan at fifty milligrams once a day, fairly well controlled. At this visit, he has normal exam, no active skin disease, no swollen, no tender joints, taking his, adalimumab TNF inhibitor religiously. And all of sudden, boom, his creatinine is 1.44. Previously been 0.9, one point o, now it's jumped up to 1.44, and that's only in the last three months. So the question is why?

Well, does have high blood pressure and today's blood pressure is one forty three over 92, and he swears that that's unusual for him. His last visit with us, it was one forty over 85. All the other visits before that were one twenty over 70 something like that. So, there's no good reason why his blood pressure would be up and then maybe that's the cause of why he has an elevated creatinine. His weight has remained stable and he's on no other drugs.

He does not take nonsteroidals and has no other risk factors other than his psoriatic disease. Now you could go looking for, know, other forms of renal disease and do a renal ultrasound and CT abdomen. But I think at this point, let's just repeat the creatinine and see what it is. That's what we did today. But I think it bears discussion on what the possibilities could be.

He could have a totally new condition like amyloidosis or something like that. But I really think this is going to be a sporadic finding and we'll see where this goes. But I think that begs the question, is there an association between renal dysfunction and psoriatic disease, skin disease and psoriatic arthritis? Well, there are reports of both RA patients and psoriatic patients having a higher risk of CKD irrespective of the drugs they take, mainly irrespective of use of nonsteroidals. A recent report about six months ago showed that there was about a thirty percent increased risk of CKD in patients with psoriasis.

And it's not clear that it's related to the severity of the disease. So maybe you're thinking they have a lot of severe disease, a lot of skin turnover, They have, you know, they might have hyperuricemia and hyperuricemia might contribute to their renal disease. Well, that's, none of that's in play here. But I do think you need to worry about, a creatinine of 1.44 in a young man who should not have a creatinine one point four four but does have psoriasis, psoriatic arthritis. Could a TNF inhibitor be a cause or a factor here?

I can see no reason why it would be. Anyway, what do you think of a case like this and how would you manage it? We're just gonna repeat it, tell him to monitor his blood pressure at home, we'll see what it comes back next, next few days. I'm pretty sure it'll be normal. If not, then he'll get a bigger workup including probably starting with a renal ultrasound.

That's it for today. Tune in to the next QD video. This is QD video brought to you by RheumNow Live, the connected digital meeting. It's all about networking and interacting, and that's how we're gonna measure education at this meeting. Truly gonna be novel.

Check it out. Today's lesson, today's case is about a 14 year old who became a 23 year old all the while having enthesitis related arthritis. This interesting young gal presented to me at age 14 with bilateral heel pain. She had a year of pain and dysfunction. She was an athlete.

She was actually sort of a state level, world class kind of athlete trying to get a college scholarship. And, because of her enthesitis in her heels she was unable to perform and her future was in jeopardy. So she came and of course we did some testing and HLA B27 was positive. She had already tried a few non steroidal. She was put on a TNF inhibitor and boom, her life changed dramatically.

You know, she'd been called plantar fasciitis, she had some low back pain, but she had no other features of a spondyloarthritis and related condition. She had no iritis, no GI, no skin. Her back was back pain kind of inflammatory but not truly inflammatory and never developed over the many years I followed her sacroiliitis. And of course her heel pain which was largely Achilles tendonitis that and with some plantar fasciitis thrown in, was dramatically responsive to TNF inhibition. She resumed her athletic career, got a college scholarship, moved away, came to see me every six months.

I've been following her and she's now 23 years old. She's a wonderful young woman. She's in business. She's completed her education. She continues to take sort of a half dose.

She spaced out her dosing on her TNF inhibitor to take it, twice as infrequently. You do the math. But she's doing really, really well, not needing nonsteroidals, had a little back pain recently. I did a recheck of her back x rays and they were normal and she has no sacroiliitis and again she's never had eye disease, and really might have had some swollen ankles to begin with but honestly arthritis synovitis has not been a part of her picture. It's been largely enthesitis.

So this subset as we know, JIA subset has been reclassified several times. This includes, this is now called ERA or not early rheumatoid arthritis but instead enthesitis related arthritis occurring in a pediatric population. They like to present with enthesopathy. They may have oligoarthritis or polyarthritis. They tend to be older in that nine to sixteen age group.

They can get back pain, inflammatory back pain, they seldom have sacrolytes but they could have sacrolytes and this subset could make up as much as fifteen to twenty percent of children presenting with arthritis, before the age of 16. And guess what? It can continue to twice this young woman has discontinued her TNF inhibitor only to have her heel pain return. So we'll continue to test that over time. She seems to do well again on half dosing of her TNF inhibitor without any side effects or risks.

And again, she's now childbearing potential so I'll have to discuss that with her, at each visit coming up. But again, the, outcome of these young people can be really, really good with inhibitors and possibly with other agents like the IL-seventeen inhibitors as well should they be needed. So interesting case, tune in to QD Video for more like this. Welcome to QD Video brought to you by RheumNow live. Hi.

I'm Jack Cush from RheumNow. Today's case is entitled the nontraumatic hemarthrosis. This is a 73 year old white female who presented with right knee swelling, and recurrent hemarthrosis. Her story started about, I want to say now, four weeks ago. She woke up with acute onset of right knee swelling, couldn't stand on it, couldn't walk on it.

She wasn't sure if it was red or warm. She went to her orthopedist. The orthopedist drew out fluid and found a lot of blood. How much? I don't know, but, like, a few cup fulls.

Because of that, he did not inject it. He gave her a nonsteroidal, sent her home. She recurrent returned two weeks later, again, with a recurrent effusion, in this case, a bloody effusion, and sent it off for culture, unclear about what else he did. Tried her on nonsteroidals, and now she's seeing me after having consulted her with her primary care doctor. No history of trauma, no history of athletics, no history of potential industry.

She has no background of arthritis or problems in that knee. No prior surgeries. No prior, history of bleeding. So what's the deal? Well, an x-ray was supposedly fairly unremarkable.

I think the money lies in the MR results and the MR results showed that she had a complex tear of the lateral meniscus, the anterior and posterior horns. A lot of, you know, sort of fuzzy stuff described that doesn't mean anything. No displaced fragments. However, mild reactive edema seen in the tibial plateau adjacent to the insertion of the posterior cruciate ligament. I think that's where the money is.

Question is, could the meniscus, torn as it is, cause this amount of bleeding? Or is this due to that insertion point of the posterior cruciate on the tibial plateau that's the site of bleeding and recurrent bleeding? So again, the issue at hand here is what's the differential diagnosis of hemarthrosis and how do you manage it? In this case, you know, most cases of hemarthrosis are going to be in young people, going to be related to sports injuries, And, you know, in my experience, an acute onset hemarthrosis in someone who's young and athletic is going to be due to a anterior cruciate ligament tear, sometimes a posterior cruciate ligament tear, rarely due to, a meniscal tear, although that is in fact possible. Other cases I've seen, in older people included, chondral osteochondral tibial plateau fractures.

The differential diagnosis includes in getting young people patellar dislocations, hemarthrosis from neuropathic joints, pigmented villanodular synovitis, synovial tumors, rarely scurvy and of course people with bleeding disorders such as hemophilia and even sickle cell. So that's sort of a wide differential diagnosis and I think what we're going to do here is send the patient to the orthopedist with that MRI and see how he wants to proceed. Question is do you do arthroscopy in people who have recurrent hemarthrosis? Generally you don't have to, conservative management is the way to go. The question here is did she fracture her tibial plateau?

Did she damage her posterior cruciate at the point of insertion? And again management of that is the problem. We're going to look of course for evidence of other diseases that might contribute here, mainly inflammatory diseases, scurvy is something you could look for. Check her PT, INR and PTT to see if she has some sort of bleeding test. Look to see if she has, you know, paraproteinemia I guess, with an S PEP, but honestly the real money here is, in in looking at getting the orthopedist opinion.

So we're gonna send this to an orthopedist in our area who does bloody knees. If I was from The UK and I said send them to the bloody orthopedist, bloody knee orthopedist, you'd think well I don't know what you mean is that someone who's anyway, you get what I'm saying I think. Interesting case and I think that, she's gonna be best managed by an orthopedist who's used to seeing such trauma, and and hemarthrosis but also someone who has a non traumatic hemarthrosis. I guess there's always a possibility that, this could be pathologic fracture and this could be due to a tumor malignancy, etc. But that will all be worked up in time.

Check out roomnow.live. We have fabulous faculty. We're gonna post the faculty this week. Just in the rheumatoid arthritis session, we have Weinblatt on methotrexate. Mike Holers on preclinical RA and John O'Shea, the guy who discovered JAK is going to talk about JAK inhibitors.

And then you get to talk to them, all of them in a panel discussion for thirty minutes at the end of their short presentations. It's gonna be a cool meeting. Check out more QD videos. This is QD video brought to you by rheumnow.live, a great meeting to be held in Fort Worth. If you've never been to Fort Worth, it's one of those cities in The United States that truly has its own special feel.

It's kind of Texan. It's kind of cosmopolitan. It's got like a 130 things to do from downtown at the Worthington Hotel. Check it out. Roomnow.live.

Today's case is an interesting one in that it's a 74 year old woman who presents because she has a positive ANA and has aches and pains. The usual consult, I thought this was going to be an easy, you know, usual ANA consult. Turns out there's a little bit more to it than that. She has history of some back pain, some head trauma. She had an MI in CABG a number of years ago.

She's had a hip replacement. She doesn't sleep all that great. But it turns out that about two months ago, she had bilateral aching in her shoulders and couldn't move them. And then while that got a little bit better for Tylenol, it got worse again and then she started complaining of a pain in her hand. She went to her PCP, they gave her a Medrol dose pack.

She did better. Her lab showed that she had a sed rate of 31. She was negative for rheumatoid factor and CCP, but her ANA was positive at one to twelve eighty in a nucleolor pattern and that's like as high as they go. It was greater than one to twelve eighty in a nucleolor pattern. She had some wrist stiffness and swelling that lasted two weeks over the holidays, and now we're about two weeks later and she says her wrists are better.

She has some aching here and pains here and there in her wrist, in her big, in her thumb, in a few fingers and sometimes her neck. She doesn't sleep all that well. She's got no history of rainouts. She has no history of renal disease. She has no dysphasia, no signs of crest or limited systemic sclerosis.

She has no cutaneous features of telangiectasia or sclerodactyly, and she just has these aches and pains and a really high nuclear pattern ANA. So what's the deal? What do you do? You know, if this was a centromeric pattern in a high titer, you thought well maybe she could have something else, maybe this is from thyroiditis, maybe she has primary biliary cirrhosis, maybe she's going to develop CREST. Well, the exam is totally normal in her.

Nailfold capillaroscopy is normal. Her skin findings are zero. She has a few DIPs suggestive of osteoarthritis, just a CMC one that's a little tender. But again, this is not a centromeric pattern, it's a nucleolar pattern. We know that nucleolar patterns are most commonly seen in patients with diffuse systemic sclerosis, again, the systemic variety, and also seen in patients with lupus.

After that, the list gets really small and really rare. I mean, I even looked this up and I really couldn't find a lot else going on. You know, sometimes hepatitis, sometimes cancer, and no specific cancer has been associated with nuclear pattern ANAs. Patients who have atherosclerotic disease and coronary artery disease are thought to sometimes have nuclear pattern ANAs and not associated with an antiphospholipid antibody and oh yes, antiphospholipid antibodies will sometimes give you a nuclear pattern ANA. So I'm not treating the ANA, I did do some investigations, I ordered a smooth muscle antibody and a mitochondrial antibody.

I ordered hepatitis serologies. I ordered something else. What did I order? TFT as well as had an anti an anti phosphol panel with a RPR, DRVVT for a lupus anticoagulant and anticardiolipin antibodies. Again, think she will have nothing but I think you're obligated to, when a red herring shows up, you have to decide whether it's worth pursuing or not.

I think there's enough specificity to a nuclear pattern ANA and a high titer that I'm obliged to do some workup and follow the patients. That's it for this case. Tune in to more QD videos.