Obesity QD Clinics Part Three Save

Welcome to Obesity QD Clinic. I'm Derek Mueller, PA from St. Clair Shores, Michigan. And today, my case is entitled rheumatoid arthritis, IBD, and Frank sign. Frank Sinatra, uncle Frank from Home Alone?

You'll you'll find out. So this is a this case is about a patient of mine, a 71 year old male who's rheumatoid factor CCP positive rheumatoid arthritis and ulcerative colitis that were diagnosed about two years prior. And and the gentleman is currently well managed on a combination of infliximab and sulfasalazine. He has a couple harrowing, comorbidities, including obesity with a BMI of thirty seven. His coronary artery disease, aortic root dilation, hyperlipidemia, hypertension, bilateral advanced knee osteoarthritis, and lumbar degenerative disc disease.

At this time, his rheumatoid arthritis and ulcerative colitis are well managed, and some of his major issues are more so related to degenerative and mechanical musculoskeletal disease. His most recent exam, he only had two gender tender joints, both of his knees, and he had a high sensitivity CRP that was technically elevated at five, milligrams per per liter. So really since his RA and ulcerative colitis were under good control, kind of opened the floor to him about what were his major concerns. And his big concern after multiple visits of discussing the cardiovascular risk associated with inflammatory disease was really his cardiovascular risk. He said, I want to focus on doing what I can do to prevent heart disease and prevent anything that's going to shorten my lifespan.

So that, opened up the floor to some interesting conversations. And one thing that I didn't note physically on his exam, something that I note noted the first time that I saw this gentleman was he had a very distinctive crease on his, on his on his earlobe in a diagonal, pattern. So this is known as the diagonal earlobe crease sign, also known as Frank's sign. So, if this is not something you're familiar with or if you've you heard it and it's kind of, something you may have forgotten about, we're just gonna go over some history and the significance of what the heck is Frank's sign or a diagonal earlobe crease and why do I care about it in my patients. So in 1973, an American pulmonologist named doctor Sanders T.

Frank, he wrote a short letter in the New England Journal of Medicine that he'd noticed that some of his patients who had this diagonal earlobe crease seemed to have, seemed to be associated with coronary artery disease. And then fun fact about this doctor, he also published, on the pulmonary manifestations of rheumatoid arthritis. So well well versed guy. So this was a observation in the nineteen seventies, but how has this panned out now in the in the modern era? Well, actually, the link is quite strong.

According to a 2025 systemic meta analyses from the Journal of Laryngology and Otology, people who have this CRE sign did have a four times higher likelihood of having coronary artery disease. And this actually holds up independent of age and other risk factors. It's also been shown that, a bilaterality of these creases may confer a higher coronary artery disease risk than one crease alone And also potentially the depth or the, really how profound these creases are. There may be a larger burden of atherosclerotic heart disease. And it's also a predictor of future events.

A longitudinal population based study, the Copenhagen City Heart Study, followed 11,000 people for over thirty five years and found that the earlobe crease sign independently predicted heart attacks, ischemic heart disease, strokes, carotid plaques and even cerebral small vessel disease. But here's really the, big time caveat with this fancy sign here is even though there is an association, as a standalone diagnostic test, it performs lousy. The sensitivities and specificities are all over the map. Sensitivity is ranging from 26 to 90%, specificities of 32 to 96. So it really on its own does not shift the probability disease one way or the other.

And there's also not really a standardized way to grade earlobe creases. So if it's observed, it should prompt the possibility of a cardiovascular workup or looking at other factors, not relying that on its own. And also interestingly, this is not incorporated in any kind of cardiovascular risk calculator, having these creases, so take it with a grain of salt. Why does this even happen anyway? What's the deal with this?

And the truth is nobody really knows. A few leading theories are, perhaps this is a sign of small vessel vasculopathy since ear the lobes are an end artery blood supply that may be an early warning site of cardiovascular disease. And there's also theories of endothelial dysfunction that lead to this physical finding. And then maybe this is also a result of accelerated biological aging. Aging.

So really at best it's free, visible marker that could suggest the possibility of coronary artery disease. It's not a diagnostic test, so just understand the limitations of that finding. So with our patient who had bilateral quite deep, diagonal earlobe crease signs or Frank's signs, we talked about starting a GLP-one agonist drug to manage his obesity and cardiovascular risk. And thankfully he was able to access this through the Medicare Bridge program and he is successfully tolerating the drug. So we're waiting to see how he responds and what hopefully his long term risk reduction will be.

So that's it for me. Thank you again for listening, and keep an eye out for more content just like this, all month for RheumNow's obesity campaign.

Hello, everyone. I'm Bella Mehta. I'm a rheumatologist in New York, and I, wanted to talk about a case, about a patient with rheumatoid arthritis and how weight loss dramatically changed some of her outcomes. So this is a woman in her early sixties. I diagnosed her with seropositive RA a few years ago with classic joint pain, synovitis, stiffness in the hands, wrist, and knees.

You know, we started her on methotrexate, achieved good control of her arthritis. However, you know, she had some GI side effects to the oral methotrexate, which we switched to subcutaneous. It did help somewhat, but symptoms persisted. And, ultimately, you know, we needed to add add a biologic again. She was initially very hesitant, then we, you know, we've we discussed a lot of options, and then we put her on weekly tocilizumab or Actemra.

At that time, it was the brand was available, and it experienced and she did have have good experience with it. Do pretty good response. Over the next two or three years, she was doing moderately well, mostly well controlled with some flares two to three times a year. And then some days, she would just wake up with a lot of pain and stiffness. But, again, she was not very keen on changing meds, but for the most part, she was in low disease activity.

Now a few years down after being on tocilizumab, she decided, to focus on her weight partly because, you know, she had aches and pains all over sometimes, and they didn't seem to be rheumatoid arthritis related. And and somehow she got very motivated. So she adopted a lot of lifestyle modifications and did help somewhat but couldn't sustainably lose weight. Ultimately, she was started on a GLP receptor agonist, semaglutide. And within three to four months, she started losing weight pretty obvious in terms of, like, whenever she'd walk in, I I could sense that she's losing weight.

And over the next few months, lost substantial amount of weight. But what happened next was very striking. As her weight decreased, her rheumatoid arthritis symptoms almost completely resolved. No morning stiffness. No joint pain.

She suddenly started being very, very active, which is exactly what she wanted. And she she said that she's feeling healthier than when she was in her twenties or thirties. And, eventually, you know, she didn't even need the tocilizumab. We discontinued it after a lot of counseling, and then we talked to her. You know, we were still we are still monitoring her, but she's not needed no any methotrexate also now and no atosilizumab.

Now just about six months ago, she also stopped her weight loss medication. But with lifestyle modification, you know, that she was doing it doing over a sustained period of time, she's been able to maintain the weight. Again, a lot of patients who are on these drugs, sometimes, you know, they'll bounce right back, but this is some this is a patient who got active and could stay active and kept and could keep her diet in check. So I think this this is sort of one of the stories that strikes me the most promising because, you know, was obesity in the first place contributing to her inflammatory burden? And, again, you know, especially for me, we often think about obesity as a comorbidity with rheumatoid arthritis, but we know that obesity itself is characterized by low grade inflammation.

So, you know, the the fat cells or the adipose tissue functions as an active organ essentially, but we don't think at least I don't I never used to think of it like that. I know it produces inflammatory mediators like TNFs, IL six, leptin, and other adipokines, which can influence immune pathways, which are known to be involved in inflammatory arthritis. So, you know, this is clinically relevant because patients with obesity and rheumatoid arthritis often report higher levels of pain, more disability, you know, more disease activity, and this is known in the literature. Right? You know, there was a recent retrospective study, I think, in ECR Open, which looked at patients with RA and obesity.

And, you know, these patients who were treated with semaglutide or tirzepatide were associated with significant reductions in all the measures that we sort of care about in RA, which is pain, ESR, CRP, and disease activity. So, again, sort of my key takeaway point is that weight loss should be viewed as complementary to disease modifying therapy. Obviously, not a replacement to it, but can make a huge difference in patients. And and, you know, instead of just focusing on one thing that we're treating, we have to sort of broaden our horizons too. And, again, weight reduction does reduce the mechanical burden of joints for her, like her knee joint, improve mobility, or, you know, decrease in systemic inflammation.

Because at the end of it, we care about the overall quality of life and better outcomes. Further, another big teaching point, I think, is that while weight loss itself likely contributed to the patient's improvement, there is a lot of new evidence coming up that GLP GLP one receptor agonist may also have direct anti inflammatory effects on the synovium itself. It suggests that patients with, you know, inflammatory arthritis like rheumatoid arthritis as well as obesity, they can you know, GLP one agonist can be treating inflammation irrespective of the weight loss that it's causing. So, again, there's there's a lot of studies coming on the way for this, including some basic science studies looking into this. And, again, because, you know, GLP one, if it can if if it's showing that it's suppressing TNF and IL six also, we know those are important in RA.

Again, I think GLP one therapies are also changing the conversations. I have patients who come to me and talk about this, so it's becoming an easier conversation because, historically, we treated obesity as a comorbidity. Again, that's something that I take away from this patient a lot more, and I feel like this was somebody who started taking these meds right when this whole surge of GLP one happened. And, again, this patient did not just lose weight. She experienced improved functions.

Symptoms are better. Overall quality of life is better. And as research is evolving, case cases like this along with new clinical data and, you know, sort of refocusing that obesity may represent more than just a cardiovascular risk factor or a metabolic condition, and especially our patients, might be important. So with that, I wanna leave you with the one liner, I would say, is that obesity may be a target for disease modification in rheumatoid arthritis. And if that's something that you start talking to a lot of your patients, you will start seeing better outcomes.

So with that, signing off. This is Bella Mehta, and follow me for more updates on Twitter.

Hello. Welcome to Acuity Clinic for RheumNow. This is the obesity month with RheumNow. And today, I'm gonna talk about actually two cases rolled into one as we talk about treat to target obesity. We are very familiar in rheumatology with treat to target approaches, and I'll talk about two of the cases in which we have treat to target autoimmune or rheumatic approaches for this.

And in what cases should we add obesity management to that algorithm and treat to target approaches for obesity as well. First case is a patient I saw last week for gout management. He had uric acid of 6.2, non turfaceous gout, our goal has been getting him below 6.0. He's had mild symptoms for which he had to colchicine intermittently about twice a month with some improvement. It's a little bit unclear exactly how controlled the gout symptomatically is because he's still requiring treatment for it.

We talked about what options would be. Six point two, pretty close to the goal of six point zero. We can increase the uric acid. He was only on two hundred milligrams, lots of room that we could safely go up. We talked about that being a very good approach, we can do that.

And again, our goal would be to bring him down below six. When I spoke with him, he said, can't, I've been on more and more medications, I can't do any more, it's been too much, I just feel unhealthy and increasing the dose makes me feel that way even more so. So I gave an opportunity to take a step back, look at the big picture, and we talked about his metabolic syndrome. He has prediabetes, he has hyperlipidemia, he has blood pressure issues, he has all these comorbidities and it all stems within the metabolic disease. We know, again, gout is part of metabolic syndrome as well.

His BMI was thirty three and we talked about his goal of coming down under thirty. We talked about medical pharmacologic approaches like the GLP-one inhibitors, but he wanted to decrease his medication list and he wanted to work on decreasing his weight and make himself overall healthier. So, we partnered together and we set treat his target goal of under six for uric acid and under 30 for his obesity. And he came back that next visit, he had gone to the gym, he had changed his diet, he had been feeling really well, and his BMI was right at twenty nine. His uric acid came down to 5.8.

So, these lifestyle interventions are a tool in our toolbox that we can go to when medication changes either aren't appropriate or aren't desired by the patient. Same patient, the next patient, same story, very different case though. This is a patient with rheumatoid arthritis on biologic treatment with adalimumab monotherapy, takes it every two weeks. CDAI score was 11, indicating moderate disease activity, just above the low disease activity. Overall feeling pretty well, but definitely had a couple swollen joints.

I talked about adding CS DMARD or changing the adalumab to weekly administration. Same reluctance of the patient to say, You know, I'm overall feeling well, but I really want to not go on more medications. So we discussed once again the weight, we also discussed in this patient the smoking contribution into RA. And so we set goals of decreasing their BMI, decreasing cigarette consumption or quitting the smoking, and overall improving the disease control. And I said, we don't need to go up on pharmacologic agents yet if we can partner together, work on these non pharmacologic contributors.

And again, the BMI is a huge contributor with RA, we definitely know smoking is as well, exercise, lifestyle interventions, all these play a big role and that patient is doing much better on follow-up. We will continue to follow, we'll continue to see, we'll see if that is enough to control the RA to keep them in that low disease activity. But, you know, the patient was able to cut down on smoking, has not been able to completely quit, but something we will continue to work on. But when it comes to obesity management, and a lot of the conversation I'm room now this week is about the pharmacologic treatments, but there's also the non pharmacologic approaches. There are some patients who wanna be aggressive with their treatment and there are others who do not want to be on more and more medication.

So, it's important to understand who what their goals are, partner with them and overall approach health in general, and not to be focused on uric acid number or CDI score, but see the patient as a larger individual and not focus just on treat to target by escalation, but in that health goal in general. So, these are two cases for me that nicely illustrated that point to me. Lots more information on RheumNow for all of obesity month, check out the other Acuity Clinics and the other lectures and great content on RheumNow all month long.