QD Clinic - Week 7 Save

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You can just watch it from home in your fuzzy slippers, and I think you'll enjoy it that way as well. Look for more information this week from RheumNow about how to sign up. Our case today is called new changes to gout guidelines. I have a 62 year old Moroccan male who I recently saw who's got a diagnosis of gout probably for about two years. He also has a past history of insulin dependent diabetes, hyperlipidemia, heart failure requiring treatment, V tach and a low ejection fraction of 30%.

So the gentleman who's on treatment for his hyperlipidemia, his heart failure, he's on two diuretics, was put on initially, febuxostat, and he took it for a month and stopped. And then he's been sort of self managing attacks, seems like they've been going on for a year or two, but not diagnosed until recently, not diagnosed with gout. So he's in because he had an attack eight weeks ago and now he's complaining of pain in his feet and his knees and he thinks he needs treatment for that. So what's the approach? Again, current medicines include Entresto, two diuretics, febuxostat at eighty milligrams and PRN over the counter naproxen, in low doses.

We know the gout guidelines, they changed how we manage gout and threw in a few new things for us to consider. I think the first thing of course is to manage acute gout. If he had evidence of acute gout, then you would treat that and my algorithm on acute gout management is steroids, steroids, steroids. Then if I can't do that I might use nonsteroidals. I seldom need to use colchicine to manage acute gout.

Steroids intramuscularly, intra articularly or systemically are safe and effective in the vast majority of people. He did not need that. He has sort of MTP pain, an MTP squeeze that's positive, but really no acute attack, but he does need some control of his pain and his risk of recurrent attacks with the use of urate lowering therapy. So starting urate lowering therapy is step number two. Again, you should start at Allopurinol one hundred milligrams and then escalate that to three hundred milligrams once it is tolerated and you should monitor urate levels periodically to know that you're achieving your target serum uric acid of less than six.

Now a guy who has TOFI, this guy has a lot of tophi on his elbows, none others that I could detect, you probably want to get your target SUA level down to below five and hopefully in a three to four range, that's how you're going to end up with a reduction in tophi size and amount. So you need not worry though about renal function. This guy this fellow has elevated creatinines of 1.5 to 2.1 related to his diabetes and his other risk factors. And again, you should not not use allopurinol when people have reductions in their GFR. It just means that you need to follow their GFR and their creatinine.

The real risk of renal complications as a result of allopurinol at very high doses, and at very low GFR's. Most patients, can have a creatinine of two to three and take whatever allopurinol dose you need to get that uric acid level down. They just need to be watched. And that's all often been a reason to maybe use febuxostat in people who you were otherwise concerned about. But there are new guidelines that say that may not be the right thing to do.

So what about gentleman has basically not been treated with because he really wasn't taking it correctly. He was given eighty milligrams right off the start, took it for about a month, stopped it, restarted a few weeks ago. But now there's this warning that came out last week of a boxed warning for an increased risk of cardiovascular death and overall increase in overall mortality rates in people on febuxostat compared to allopurinol. That's the CARE study. We've written about that in today's edition of RheumNow and it's in past editions as well.

So what is the new FDA guideline? It says number one is a box warning, meaning you should be aware of this risk. That's maybe more than that seen in patients on Secondly, they changed febuxostat from being a first line agent to being a second line agent, meaning you really need to try and must try allopurinol and other measures before you use febuxostat because of this cardiovascular risk. Now, at the FDA hearing that I was at back in January, we noted as a panel that there were higher rates and higher risk in gout patients who, in these gout patients were already had risk factors when they were on background aspirin. So that's not in the new FDA guideline, I personally would avoid, using febuxostat in patients also on, cardio protective doses of aspirin.

So again, this patient walks out the door with a new prescription for low dose allopurinol that's gonna be escalated to three hundred a day. I'm gonna follow his uric acid levels. He's gonna be put on initially, five milligrams of prednisone, and then I'm gonna transition him to what he wants which is low dose colchicine zero point six milligrams once a day. I've given him instructions on how to manage an acute gout attack should he develop one while initiating this new urate lowering therapy. That's it for QD clinic.

Tune in for more of these during the rest of the week. This is your next QD clinic brought to you by RheumNow Live where rheumatologists can connect, learn, and interact with your peers and the faculty for three days. And you can actually attend the meeting in Fort Worth or you can view it from the Internet by signing in and registering, and you'll see more information about that in the next few days. So our case today is a gal named Sue. She's 35.

She was seen by me about six weeks ago when I diagnosed her as having fibromyalgia. She presented with low back pain, fatigue, polyarthralgias, migratory arthralgias, and her evaluation has further, disclosed that she does have fibromyalgia. The diagnosis of fibromyalgia is based on, widespread pain, many tender points, a sleep disturbance, fatigue, headaches, irritable bowel, history of anxiety, paresthesias that are unexplained, back pain, TMJ pains, poor memory, and allergies to multiple drugs. So the plan on her was pretty straightforward. Give them something for pain, give them something for sleep, make them do the right exercise and they come back and they're better.

But guess what? Patient's not better because they didn't do what they were told to do. So the story of this case is basically less is not safer. And what do I mean by that? Well, the patient has basically taken less or not done the things that were required or prescribed at the last visit.

She was given acetaminophen six fifty, told take three pills a day. She did that. She says it does help her substantially. She was given Xanoflex, Tizanidine for bedtime sleep and, and pain relief from the spasm she would get in her back. She took one, she did it for a week or two and then stopped it because well she only slept for a few hours and then she was wide awake.

Well, sleep problem continues. She was given baclofen to take if her back pain got worse during the day, she never tried it. She was told that the tramadol prescription that she had, she could take on a PRN basis, never touched it thinking can't mix tramadol with acetaminophen. Where she got that from, I don't know. And she was referred for a sleep evaluation and sleep study, never did that.

So again, the patients, and I don't fault her for this, really was afraid of taking medicines, really afraid of taking more. She was afraid of doing the full regimen as was prescribed and explained to her. And in her mind, she's thinking taking less is going to be safer. So what happened here was, she's worse and we've had to reinforce, her plan and restart all over again. So why do patients want to take less and do less?

Number one, they don't like taking medicine. We can understand that, but mainly many of them are of the belief that taking less medicine is going to be safer. When in fact that's really not true. What the problem is they don't know what they don't know so they're left to guess that safer must be is going to be when they take less medicine. I think it's important to let the patient know that you really need to take the medicine as I'm prescribing it here at the outset and that taking less is not a good idea.

You know, for instance, I tell patients when they're on a medicine like methotrexate or even a biologic that the longer they're on it, the safer it is. And that's absolutely true because all the toxicity with most medicines we use is front loaded. It's gonna happen when they first take the drug, the first few doses, if not the first month. After that, it's more of those studies that show you, you know, the eight year follow-up of Enbrel, everybody looks the same and they're all doing great. That's because the drug continues to be safe and it continues to work and it's not surprising what the results are.

So again, you have to tell them that at the outset when you're starting a treatment plan, you're gonna often go in with more medicines than they want and admittedly, maybe even more medicines than you want because you're trying to one, get a better response right from the start. Two, find the drugs that work best and then cone down to the ones that they really need. So again, they have to buy into this and you have to sort of let them know that if they continue doing what they were doing and not taking medicines or taking the wrong medicines or vitamins or whatever, they're going to get more of what they already got, is pain and fatigue and dysfunction, etc. And that what you're all offering is a change and a change that has been time tested and shown to work in many patients. So again, the idea that less is not safer, and that you really need more medicines at the outside, you know what the right treatment is going to be is something that takes a lot of discussion, lot of note taking, you got to write things down and then maybe even follow-up on the patient to make sure you're not stuck with them coming back six weeks later and restarting all over again.

This is one of the challenge that happens frequently in the rheumatology clinic. Tune in tomorrow for more. Hi, this is QD Clinic brought to you by rheumnow.live. A great meeting twenty three days from now, and you can attend by just registering. You can watch it free on the Internet starting on the twenty second and the twenty third and the twenty fourth, all from home.

It's gonna be great. You can be a part of the audience and see great speakers, great presentations, and great interactivity all at roomnow.live. Our case today is called rheumatoid cachexia. It's a patient I saw recently who's an 86 year old white gentleman who I've taken care of for more than ten years. I diagnosed him as having rheumatoid arthritis in 2008.

At that time, he had polyarthritis, morning stiffness, a bunch of swollen joints, high sed rate, a strongly positive CCP, a positive rheumatoid factor. He started on methotrexate, did great, has done great for the last ten years. However, starting about ten, eleven months ago, he came in, he looked a little thin. He looked like he had lost about 20 pounds. I said, what's the deal?

He said, I don't know, I'm losing weight. My appetite's a little less, but I'm losing weight. I said, okay, well you gotta get that worked up. I've seen him now like this is the third time I'm seeing him with weight loss being the big ticket item on the table. He's now lost 80 pounds of weight.

And I don't know, nobody's grabbing the bull by the horns and taking care of this, so I am. So this is profound weight loss and a guy who's been seen by his primary care doctor and has had some workup but doesn't seem like there's been much workup. For instance, there's been no GI referral and the gentleman has never had a colonoscopy. There's been no chest X-ray. There's been lab tests done and recently he had a cardiac workup thinking this was cardiac cachexia.

He doesn't really have much of a cardiac history, I must say. So anyway, we're gonna take over and at eighty pounds, we're telling the primary care what needs to be done. This clearly is cachexia. You know, he's dropped his weight from two twenty one down to one hundred and forty two. This is not good.

So the question is, what's the cause? He has no other medical illnesses that would account for such a cause of extreme weight loss. His drug methotrexate is really his only rheumatoid arthritis drug, is really not associated with Cachexia. If you look it up, you'll find out there are a lot of reports, usually rheumatoid arthritis is being treated with methotrexate or methotrexate being used for another condition which is also the which is really the cause of their profound weight loss. You know, many of the drugs that we currently use like the TNF inhibitors can cause a little bit of weight loss, and that's because of why?

Well, inflammation makes people, lose their appetite and they can, actually lose weight as a result of inflammation and then when you correct their inflammation with an effective biologic or anti inflammatory, they get back their normal appetite and boom, they actually gain weight. So I might have said the TNF numbers cause you to lose weight. No, they actually cause you to gain weight. Of all the drugs that we take care of, in my experience, the only one that really can cause significant weight loss in patients is number one, leflunomide. They often have GI symptoms and yes, you stop the leflunomide and their 20 pound weight loss goes away.

And then two, a premilast, as you know, it's part of the package insert. About ten percent of patients will lose 10% of their body weight and that's sort of a nice side effect, but it may come at the risk of having GI side effects. But methotrexate, doesn't really cause weight loss and I've excluded that possibility. However, she's so sick or sick looking, I have to stop the methotrexate, we'll see what happens. The question is, could it be rheumatoid arthritis?

There is such a thing called rheumatoid cachexia. I've seen at least two good cases of rheumatoid cachexia. One was in the county hospital about twenty years ago. One was about twenty years ago in a third world country where patients had overwhelming, uncontrolled, severe inflammatory polyarticular rheumatoid arthritis and these people just shriveled up and you know they were like ninety pounds and when they should have been one hundred and forty or one hundred and sixty. And yes, effective therapy, helped them to regain their weight.

I came across a recent, article from the Brazilian literature where they did a meta analysis of the topic of rheumatoid cachexia, looked at 136 articles, narrowed it down to eight. They define rheumatoid cachexia, using usually dual energy, x-ray absorptiometry or where you can actually estimate total body mass, muscular lean mass and fat mass, and they defined it as free fat mass below the tenth percentile and full mass index above the twenty fifth percentile with this sort of liberal definition of cachexia, they say in their pay paper that it's seen up to thirty two percent of rheumatoid have rheumatoid cachexia. I don't think so. There are more, stringent measures says nineteen percent of rheumatoid have rheumatoid cachexia. I don't think so.

So again, it's out there. It tends to be in places where patients can be undertreated. The one thing about this paper says that rheumatoid cachexia, as they define it, unfortunately, maybe wrongly defined it, had no association or correlation with disease activity scores and that's really what it is. It's incredible cytokine and pro inflammatory cytokines that make you get cachectic which means that you must have lots of extreme activity going on for a long period of time. So it's a rare thing, you can see it, it's obviously a big call for action as far as therapy.

The workup on this gentleman is going to be a chest x-ray, usual blood tests, usual health maintenance. He's being sent to GI for endoscopy and colonoscopy, which he's never had. He has no GI symptoms, must say. He's getting a QuantiFER at this point because his Sedrate, CRP, CMP, usual CBCs are all looking pretty good, a marginal elevation of a CRP. And we're gonna do the QuantiFERON.

His LDH has been normal. His SPEP has been normal. We'll check his urinalysis. His PCP wants to do a PET scan. Let's do the smart things, easy things first, and then get a PET scan later on.

But obviously, this is a very challenging case and hopefully you don't see anything like this. Welcome to QD Video brought to you by roomnow.live. I'm Jack Cush, executive editor of roomnow.com. Our case today is a recent clinic case. A 50 year old, African American woman presents with knee problems.

And the question here is, is this a torn meniscus or not? So her story is pretty simple. No medical history, never took any medicines, no joint problems. At the end of last summer, about six, seven months ago, car accident, She jammed her knee into the dashboard ever since. She's kind of a little, little problem but not much but about two months ago, it started to hurt more, started to swell a little bit.

She went to her primary care doctor, did x rays, showed some mild degenerative changes in the medial compartment, patellofemoral, DJD, little, you know, sort of mild. She was treated with a non steroidal, did fairly well, but didn't want to continue that, taking over the counter non steroidal's doing fairly well, but she continues to have problems. She's a nurse, she's on her feet, she needs to, you know, get this over with. What are you going to do? So again, the question here is does she have simple osteoarthritis?

She's a little young to have it, but she's post traumatic. It's hard to imagine that you you get those DJD changes of sclerosis and some joint space narrowing in in about a few months, I guess it could happen. But does she really have another problem going on and could she have had some other internal derangement of the left knee? So my checklist here is pretty simple. You could go right ahead and not examine the patient, do an MRI, but that would not be smart medicine or good medicine.

You know, someone who has actually had a torn meniscus, I kind of know the symptoms. And the symptoms I look for, you should look for, are locking, unexplained locking, which means everything is good and all of a sudden the joint seizes up. Used to happen to me laying down while totally relaxed, it would seize up. Or while walking, the joint gives out or gives way and patient almost falls. And the question is, you don't know why this happened and it's a sort repeated event and because that happens, you need a medical evaluation.

The physical findings that are most predictive and helpful, number one, joint line tenderness. This assumes you know actually where the joint line is and have a good history on, and a good clinical skills that you can find it. But if they're not tender or mildly tender, but when you hit the joint line you accentuate the tenderness that could be an extruded meniscus that's tender. And then also, you know, the McMurray test which you have to look up to learn how to do but basically, know, you you flex the hip and the knee as far as you can and while extending it you torque the lower extremity to put pressure on one of those two meniscus to see if you can get a pop or pain. Another finding is also the, presence of an effusion.

This patient had about a one to two plus infusion cool, not really tender in itself, but clearly the joint was swollen. I think she had enough, evidence to go ahead and get an MRI and refer her to orthopedics. Again, the literature says some interesting things. One, the MRI is really good at ligamentous damage as opposed to meniscal damage. It can miss some things.

So MRIs are better at, you know, ACL collateral ligaments rather than, and they're pretty good at meniscal tears, it's interesting to note that it's better at ligamentous tears. When you look at the sensitivity and specificity, joint line tenderness is very sensitive 75% but not so specific at 27%. On the other hand, McMurray test is 97% specific but not so sensitive. And so the point being that if you can have either giving one ear locking along with a physical finding, that's a really good reason to go ahead and get an MRI or refer to the orthopedist for further evaluation. So that's my story of meniscal tears.

I ended up having surgery way too late, but nonetheless, that's another story. RheumNow Live, check it out. It's gonna be really interesting. You can still come to the meeting, 03/22/2324. It probably costs you about a thousand to $1,500 to fly in, register, spend a few nights, learn a whole lot, and enjoy the hell out of the meeting.

But then again, you don't have to spend that money. You can register and watch it all from home in your pajamas. Just it's gonna be streaming live on those days, twenty two, 2324 in March. Check it out. Hey.

This is QD video brought to you by RheumNow live. Can't get to Fort Worth on March 22? Well, you don't have to. We've reserved a virtual seat for you. You can register at rheumnow.live, and we'll stream the video to you and your desktop.

Today's case is called dysgeusia. Can you spell dysgeusia? Can you use it in a sentence? Well, let me tell you about dysgeusia. A 58 year old woman with rheumatoid arthritis comes to see me and, after making the diagnosis, we put her on methotrexate.

She does well, but she's got problems. She's got oral ulcers, she's got a little queasiness, she feels blah like for a day and a half afterwards. We put her on vitamin A and also on dextromethorphan. If you don't know that story, tune in for other videos and I'll talk about management of methotrexate toxicities. Actually, think I've already done that called optimizing methotrexate.

Anyway, she comes back a month later and she's doing well, she's doing better, she has no more side effects, but she has this problem of dysgeusia, an abnormal unpleasant taste in her mouth, seems to be accentuated after the methotrexate, but it's kind of there all week long. Dysgeusia, d y s g e u s I a. It's also called paragousia. It's another it's the word you would use for someone who has metallic taste due to a drug or a bad taste due to drugs. Is it due to the drug?

Is it due to a disease? What's the deal? Is it due to methotrexate? So again, not knowing what to do here, I was not aware that it would be due to methotrexate and I've looked it up and I really don't think it's due to methotrexate, but I had to look up dysgeusia and learn more about it. It's actually also called paragousia.

These are really bad names. It's really hard to spell. I used to live in Paragousia. I moved to dysgeusia, but that was displeasing and so now I'm back in Dallas. But Diskusea again is a problem for the patient and so this patient wants this abnormal taste to go away.

So what did I do? I told her hold the methotrexate, go back on a lower dose and her arthritis can survive, being off methotrexate and we can answer the question about whether it's methotrexate. I don't think it's methotrexate. You need to think of other problems, dental problems, upper respiratory tract infections, sinus infections can all be important causes. It's often associated with mental illness and that's a problem in distinguishing it from true organic disease.

It's often related to drugs, antibiotics, the metronidazole, clindamycin, fluoroquinolone, quinolones, thyroid therapies, methocarbamol, the drugs that we use in rheumatology, the ones that are most commonly associated with Dysgucia includes penicillin, levamisole, gold, levodopa, we don't use those. Methacarbamol, I think I mentioned, and then of course Lunesta, a common side effect of Lunesta is a metallic taste. Methotrexate, not so much, but let's see what happens with this patient over time. You also need to consider the patients who have dry mouth and poor saliva or abnormal disordered saliva flow often complain of dysgeusia and so it's not an uncommon feature in patients with Sjogren's syndrome. The differential diagnosis is also long, it involves neurologic disease, multiple sclerosis, GERD, hepatitis, even diabetics and think about deficiencies of either zinc, mercury or copper.

My partner's got a case of zinc deficiency with dysgeusia. Who'd have thought it? Anyway, it can be a problematic symptom, especially in managing RA. We'll see what happens with my patient. I don't think it's gonna be due to methotrexate, but then again, I'm not sure what it's due to.

Maybe you can tell me. We'll see you in Fort Worth.