QD Clinic - Week 1 Save

Hi. I'm Jack Cush. This is QD Video brought to you by RheumNow Live, the next best meeting in rheumatology held the weekend of 03/22/2019 in Fort Worth. QD Video, what is this? Well, is a new thing.

We're gonna run this every day for the next month or two to see how this goes. Short videos on things that happen in clinic that I think are important that maybe you think are important too. So today's lesson has to do with a patient showing up with aches and pains, and she's on a statin. And I think I want this lesson to be about what's the likelihood of actually having a problem with statins and what you do about it. The story is repeated millions of times every day.

Patient usually older, middle aged older, goes on a statin, has aches and pains, and then the question is do we stop the statin to see if they get better? It's always tried. You need a few weeks off to know yes or no if it's worth stopping or not. It turns out that it almost never works, meaning patients with aches and pains usually have aches and pains not because of the statin. So what are the real numbers?

Statin related myalgias are quite common and usually quite mild. They do get better when the drug is stopped. The numbers I think are like ten, less than twenty percent, but again, they're mild. The stuff we really worry the damage stuff, the rhabdomyolysis, you know, the I think we recently published, that it's less than zero point one percent. Really, it's probably not one in a thousand, but more like one in ten to, one in a hundred thousand.

It's very, very uncommon. But if it happens, they get myoglobinuria, they can get renal failure, it's a disaster, but it's very, very rare. And then also very, very rare are the necrotizing myopathies associated with select autoantibodies. So again, what do you do? Stop it, it's worth a try, but then go back to the drug that they truly need which is the statin and then deal with the aches and pains.

A recent report we had showed that rosuvastatin and atorvastatin were maybe the more ones more likely to cause symptoms in patients receiving statins. Hi, I'm Jack Cush, and this is QD Video brought to you by RheumNow Live or rheumnow. Live, a weekend CME investment in a newer, smarter, better you. This lesson today is about a 50 year old with inflammatory oligoarthritis and carpal tunnel syndrome going on for three months. He's had bilateral carpal tunnel syndrome.

In fact, he was gonna come to me to have bilateral wrist surgery for his carpal tunnels. And he had swelling, he had one other swollen joint in a finger. And so I worked him up and treated him. Gave him some prednisone, gave him some Decadron, did some labs, brought him back. He was somewhat better.

He's had no response to nonsteroidals. He sort of had a so so response, good, to steroids and sort of big doses. And yet he still has carpal tunnel syndrome, wrist pain, his finger is better. So we're now like into week twelve of this. And the question is, what do you call this and how do you treat it?

When he first presented, he also had girdle soreness. He's had some shoulder problems in the past, rotator cuff damage from sports, but also had some hip sort of soreness. So morning stiffness was forty five minutes. He had girdle soreness and stiffness. He had one or two to three swollen joints, slightly elevated ESR and a CRP of two or one one to two milligrams per deciliter elevated.

And everything else negative. You imagine it, I did it, it was negative. X rays, didn't do. So initially we thought, know, this could be PMR, polymyalgia rheumatica, but he's only 50 years old. He's not had a big response to twenty milligrams of prednisone and he continues to have complaints despite prednisone.

So PMR is not on my list anymore. It was on the at the first visit, but not now. The question is again, do you call this inflammatory arthritis and just treat it as such? Or do you call this seronegative arthritis? Or do you keep searching despite having two rounds of more extensive testing?

And again, as uric acid, B27, ANA, QuantiFERON, hepatitis tests are all negative. So I'll tell you my approach to this. I prefer to call this at this point because it's twelve weeks the dividing line of chronicity. This is going to be a chronic inflammatory oligoarthritis. It's on its way to being a polyarthritis.

That's not for me, I hope. We're going to disregard the call. But the question is what do you call it? I call this seronegative arthritis and not inflammatory arthritis because I believe two joints can become three, become four if you're not paying attention and I don't want this to go untreated. So he's going to be treated with methotrexate.

He's started on drug and we'll see how he's doing in a few weeks. He's still on prednisone and we're going to continue to look as the great Owen Kavanaugh wrote about in one of our RheumNow blogs, he said, you know, someone with rheumatoid arthritis who's seronegative is really your invitation to reconsider the diagnosis at every visit, but also to reconsider the idea of withdrawing therapy at every visit should they be in sustained remission. So again, I prefer to call such patients seronegative RA, manage them aggressively, hopefully put them into remission, and then answer the question later on, a year from now, eighteen months from now, can we get off therapy? Until then, aggressive therapy is the way to go. That's it for QD Video.

Tune in tomorrow. Hi. This is QD Video brought to you by rheumnow. Live. Rooms like us go to great meetings like roomnow.live.

In today's lesson, we're gonna talk about a patient I recently saw, a 57 year old male who has a history of uveitis times two and has a sort of acute presentation about four months ago of sort of widespread pain starting in his hips, diagnosed as raging capsulitis seen in multiple major medical medical centers, in the Northern US and in the Northeastern US. He was found at B HLA B27 positive and, had tenosynovitis, ultimately later had trochanteric bursitis, gluteus minimus tendinopathy, polyarthralgias, a high CRP of 111 milligrams per liter. It's really high. Recurrent worsening diarrhea, and negative x rays of his shoulders, pelvis and hips. Again, the MRI showed raging capsulitis.

He was treated with nonsteroidals and steroids really to no avail. And in my seeing him, he's got a lot of tendinosis, a lot of periarticular pain, in and about the hands, elbows, shoulders, and greater trochanters. He does have synovitis in one wrist. He does have mild synovitis and a PIP two on the left hand. And his labs that I just did showed a CRP of 91, a normal calprotectin level, ASO, parvo, immunoglobulins all negative.

His CBC and chem profile were relatively normal. He's not anemic. His set rate is a little bit high. So he's only been effectively managed when given higher and higher doses steroids. Five milligrams doesn't cut it, fifteen to twenty milligrams is necessary, nonsteroidals provide some relief, but bottom line, nonsteroidals and steroids are somewhat effective here, but not completely effective.

What do you do? Where do you go? What are you going to call this? Clearly he has a B27 related syndrome, and but it's not spondylitis. It's going to be a peripheral arthritis.

And the real question is, is it related to this underlying as yet unevaluated diarrhea? So he's been sent to GI. He's going to get his tomorrow. His diarrhea is six times a day, watery, no blood, no mucus, no prior history of IBD. So we'll see, you know, it could be that that's where all the money is, but then that's where you go, Sutton's Law.

The money in this guy is acute phase reactants off the wall, tendinitis and severe GI symptoms. So you go where the money is, get the GI evaluation, but if positive or negative, he's gonna have a B27 related syndrome, either colitis or peripheral arthritis. He needs to be treated with more than nonsteroidals and or steroids. So I think the appropriate treatment for a patient like this would would be TNF inhibitor. That would be my first choice.

I think going with a DMARD would be an unwise choice because I'm not sure which one would work in his tendonitis, enthesitis, oligoarthritis, along with possibly colitis syndrome. The unifying best drug is going to be a TNF inhibitor. If not there, you can march on maybe to other therapies. So we'll see what happens when he gets his TNF inhibitor after he gets his colonoscopy. Maybe at a later date I'll give you an update and tell you what it was all about.

That's it for this episode of QD videos. Check out roomnow.live. This is RheumNow's QD video brought to you by roomnow.live. Today's lesson is going to be on Takayasu's arteritis. I just saw a patient, 43 years old Indian diagnosed ten, fifteen years ago with tachyasis and never treated.

Now she was treated with stenting and angioplasty, but her story was at age 31 she had hypertension, underwent evaluation, found to have renal vascular hypertension due to renal artery stenosis, had stenting done. And then the course of that evaluation was found to have occlusion of bilateral iliacs, which were angioplasty stented, but ultimately totally occluded and never reconstituted. And also bilateral carotid artery stenosis about sixty-seventy percent she said although she never had stents. She does not know about her lab. She said that they never treated her with steroids or any biologic or immunosuppressive agents.

And she comes to me now at age 43 probably having had this for at least twelve, thirteen years. Now with symptoms of numbness and tingling especially in her right lower extremity. On exam I find really nothing other than a woman with pulseless disease meaning she's got a carotid on one side but not on the other. She has a weak pulses in her right arm and almost no pulses in her left arm. She's got no femorals, no brachials, no dorsalis pedis, no posterior tibials.

That's on clinical exam in a very lengthy long clinical exam. These patients do take time and are complex in their evaluation and management, which is why I'm sort of presenting this to you today. My approach to this is number one, assess her clinically. Is her numbness related to vascular insufficiency or is it related to something else? We're getting a back x-ray.

I think we're going get an EMG nerve conduction studies, but I think it may well be due to vascular insufficiency. How do we assess that? Well, it's going to be by first symptoms. She doesn't have fever and nothing in the way of systemic features. And again, her main clinical abnormality is the lack of pulses.

We can further assess that with imaging and other testing. What about laboratory tests? Again, patients with active, inflammatory Tachyasis usually have elevated acute phase reactants, but not always so. On the other hand, other tests that we might normally do for inflammatory or autoimmune diseases are typically absent in such patients. ANCA, ANA, Rheumatoid Factor, complements, they're really not very helpful.

And there are no suitable biomarkers that are commercially available for routine use. So the question is how are you going to assess for vasculature? Well, one way would be with ultrasound. That would be cheap and easy. However, it's really only good for the carotids and vessels that can be easily assessed by ultrasound.

It's not too good at deeper vessels that branches off the aortic arch or the abdominal area or pelvic aorta. So that's not a good one. You know, systemic evaluation with FDG PET may be of some value but primarily in people who have fever and widespread systemic disease. Other things to do, CT angio or MR angiography, which is better? Well, for many years it looks like the literature says a lot of reports on CT angio, but of course there's a lot of radiation with that.

It's not suitable for repeated assessments. MRA may be in fact better. They seem to have the both the same degree of sensitivity and specificity. The CT angio is better at looking at abnormalities in vessel wall, whereas MRA is better at looking at widespread vasculature, luminal disease basically in stenotic disease. There are newer assays like three d MR and again FDG PET.

So this patient is first off getting just simple arterial Doppler studies to find out how her vessels are doing in the periphery. And then when we get those results back and her labs, which I don't have at this point, I'll make an assessment to what we're going to do as far as, a widespread, vascular assessment with MRA or focal assessment with MRA. And then we'll decide whether or she needs treatment. She's really asymptomatic. Not all patients with Tachyosis need to be treated with systemic corticosteroids, immunosuppressive or biologic agents.

Know, rituximab or in this case the IL-six inhibitor for a large vessel vascular disease. Not currently approved, but, a lot of our case reports using IL-six inhibition in patients with Takayasu's and large vessel vasculitis seems to work very well. But again, there we need studies in that area, double blind, randomized, placebo controlled trials. Anyway, that's it for today. Tune in tomorrow to QD Video.

This is QD Video brought to you by roomnow.live, the next best meeting in rheumatology, February 2019 at roomnow.live for more info. I'm Jack Cush. Today's lesson is about what to do with one joint. So I have a patient who I just saw who is 62 years old with seropositive rheumatoid arthritis, RA based on symmetric polyarthritis, high high titers of rheumatoid factor CCP antibodies, previously treated with sulfasalazine, methotrexate, Arava, Plaquenil, and most recently put on prednisone in low doses and Cimzia. She did really really well.

She's currently taking Cimzia PRN loading, little bit of gabapentin at bedtime, not taking prednisone. She's doing great, you know, on a scale of, you know, zero to 10. She's about a inactivity and about a in pain, so she's doing quite well. She only complains of some pain in her right hand on exam and the whole of her exam is totally normal with the exception of one joint. In her case, it's right MCP II.

It's swollen, it's two plus swollen. It's really tender when you palpate it or when you manipulate it or when she uses it too much. And the question is what to do about that. In the past, she's had x rays of her hands showing some erosions. I don't know if it's specifically at that joint but that was done two or three years ago.

And the question is what to do about it today. So again, patients well controlled, know, one time their C. Dye or I do a gas score, which is like the C. Dye, one time was, you know, 15 and then with therapy came down to ten, two, one, three, one, it's been really very low. Today it's a two.

What do you do with disease activity like that? Her labs are normal or acute phase reactants are normal. She's not anemic. There's nothing else going on metabolically or inflammatory wise. So again, you have certain treatment options.

But the first thing I think you have to do is think about one swollen joint. You need to assess that joint and the general rule in rheumatology is when someone presents with a chronic monoarthritis, you need to go after it. Biopsy it, aspirate it, culture it, look for crystals. Again, monoarthritis can be a crystal induced arthropathy, can be an infection, could even be a malignancy or something truly, totally unexpected. So when your best therapies are working in everything but one joint, don't think rheumatoid arthritis, think of it another disease.

Now, if it is rheumatoid arthritis, then I think you need to, not just jump in with more DMARDs or more escalated biologics. I think you can do some simple things to better manage the case. My first manipulation is immobilization. In the old days when there were no drugs and it was just gold and aspirin, ask the old guys, they'll tell you they actually used to hospitalize people with very active disease and that would quiet things down because they would put them at total bed rest. If you immobilize a joint totally, maybe you'll actually have a significant beneficial response.

The next approach of course would be to inject it locally, and that's based on how skillful you are at that and where the joint is. If it's in sternoclavicular joint or an SI joint, you may not be, so enthusiastic about injecting it. An MCP II, most of you should be able to do, especially those of you who do ultrasound. I think that, my next approach in someone like this would actually be to add back low dose prednisone, and I'm talking like one to two and a half milligrams of prednisone might be enough to make a big difference so that you can avoid either adding on nonsteroidals, which are gonna be probably much more toxic in the long run, or another DMARD, which the patient doesn't want, or changing biologics. That's my approach for one uncontrolled joint.

Tune in tomorrow for more QD videos. This is QD Video. I'm Jack Cush. QD Video is brought to you by rheumnow.live. More at the end about that.

Today's case is about a 70 year old with rheumatoid arthritis and thrombocytopenia. Kind of a difficult case I must say. This is a longstanding patient of mine who's been treated for many years for rheumatoid arthritis. In fact, she's been on gold, methotrexate, sulfasalazine, black quinil, obviously prednisone at low doses. She's tried TNF inhibitors, IL-six inhibitors, and more recently has been taking methotrexate and then was switched to Arava.

Her story is one that she was fairly well controlled on methotrexate and then was later switched, or actually had Arava added to methotrexate. Somewhere in and around there, which is around late twenty sixteen, she started dropping her platelet count. Her other blood counts, white blood cell counts, red blood cell series were all normal, but her platelets dropped from 200, two fifty down to around 100. And with the idea that maybe it was otrexate dropping this, methotrexate was stopped, although she continued to drop from 100 to 90 to 70 to 63 and more recently to 50 while taking a leflunomide, tramadol, atorvastatin, acetaminophen, metformin, and lisinopril. So really not taking very much to be implicated as a cause.

So she's been followed by and evaluated by the hematologist who call this chronic ITP because it's been going on now for over a year and, almost two years, really hovering around again sixty, seventy, 80 and more, but again recently now it's 50 and they've called chronic ITP, said it's not worth doing a bone marrow biopsy. But because she dropped, now there was a concern a bone marrow biopsy was done. The question is, what is this and how to manage it? Well, turns out that, number one, I don't think this is going to be methotrexate. It's not possible when you look at the chronology and when methotrexate was stopped and whatnot.

And we do know that methotrexate can cause a pancytopenia, but methotrexate is going to affect the marrow, it's going to affect the white blood cell series. It's notorious for leukopenia and leukopenia, leukopenia and then if you're really unlucky, you'll get pancytopenia. It doesn't in an isolated fashion knock out platelets or knock out the red cell series and not affect the white cells. It's always the white cells and then if you're unlucky you get the other ones and that's usually in the context of renal failure and you know the scenario there. So the next question is, is this Felty syndrome?

Spinalomegaly, leukopenia, recurrent infections, and chronic long standing severe seropositive RH. She's seropositive, long standing, not too bad, no deformities really, not much in the way of erosions because she's been treated by a great rheumatologist. But, you know, she doesn't fit the bill for, for Felty's because she has no enlarged spleen. That was checked by ultrasound and by exam. So the question is whether or she has a marrow disease like myelodysplasia or something along this line, some sort of infiltrative disease, we'll find that out on the biopsy.

But I'll tell you, I think this is due to Arava or leflinomide. She'll be the second patient I've had where this has occurred, where the consideration was either a marrow disorder like myelofibrosis or Felty syndrome and there was no resolution when those were either addressed, treated or considered. When you stopped the leflunomide, boom, the platelet counts resurged up to a normal limit. We just recently stopped her platelet count. I'm going to expect to see her platelet count rise.

And if I'm wrong about that, I'll correct myself in future videos. But that's the approach, my approach to someone with thrombocytopenia and rheumatoid arthritis. Right now her RA is well, but she did stop the Arava a few weeks ago, three weeks ago and put her back on methotrexate today. So I don't want her flaring because she's really a wreck as far as, worry about this. I don't want her to be a wreck with inflammatory synovitis coming back and taking over because she's prone to do this.

Anyway, tune in tomorrow for more cool cases from the clinic.