Obesity QD Clinics Part One Save

I'm Anthony Chen, rheumatologist from Reading, United Kingdom, and today I want to present to you a case entitled The Wait Behind the Delay. I have a patient who has ankylosing spondylitis or sometimes also known as axial spondyloarthritis. He's male. He's in his early thirties, and he had a body mass index, a BMI of thirty four. And in his history, he's had six years of low back pain.

Now, these had been repeatedly called mechanical back pain due to his weight, due to his raised BMI. He had seen quite a few health professionals, and clearly his scans showed there was some degenerative change in the discs in his back, and therefore, with time this was put down to being a mechanical cause. He also had slightly raised C reactive protein, or CRP, and this again was put down to his obesity. In this case, the obesity delayed the diagnosis itself, not just the treatment. He was then referred to the rheumatology clinic where I saw him having had six years of low back pain.

On taking the history again, he presents with inflammatory back pain symptoms in his 20s. So he had typical symptoms of pain at rest, early morning stiffness lasting up to an hour, the pain was better on movement and worse with rest, and there was also nighttime waking. One of the key features that he suffered from was fatigue. And again, this was often put down to his obesity. But he was never screened for sleep apnea, which can be quite common in patients with obesity.

The CRP, looking back, had been raised intermittently, not very high, but above normal. Again, this was put down to his high body mass index. On further investigation, he had a scan done, an MRI scan, but this time we included the sacroiliac joint and also the thoracic and cervical spine. Most of the musculoskeletal scans had only included the lumbar spine and the top part of the sacroiliac joint, not the whole sacroiliac joint. And these showed that there were inflammatory changes of axospondyloarthritis.

He subsequently had a HLAB27 test, and this was also positive. Having already failed multiple anti inflammatory drugs, NSAIDs, he was then screened and put on to a biologic treatment, TNF inhibitor, and on review, twelve weeks after treatment, he only had a partial response to treatment. And we know in this condition, exosporinyloarthritis, we use cores such as the Acetas, the Bastai, to interpret treatment response. Now because of his obesity, there were many other factors here that could have been affecting his SDES and best dye. As you know, these scores are very much patient reported, and therefore, there can be other factors, including pain, fatigue, mood disturbances that often go with obesity that can affect the outcome measures that we use to assess treatment response.

So at this point, I want to bring you to my clinic, where we see him now at six months after he's been commenced on a TNF inhibitor, and his best eye remains high. His SDAS also is high. His CRP is normalised, but he doesn't feel great. He still feels very tired, fatigued. He feels low in mood and still has a lot of pain.

So what would you do in this situation? Would you escalate his biologics or maybe consider switch to his biologics? Or would you address the issue of weight, sleep, and also deconditioning? Or would you do both in this situation? Now, we will come to what I did in a moment, but we wanted to go back and look at the information in regards to obesity.

Now, obesity is actually quite prevalent in axial spondyloarthritis. There are two studies, firstly the Eurospar study, which had 14 countries, and also the data from the Groningen cohort show that in up to sixty percent of patients with axial spondyloarthritis are either obese or overweight compared to sex match controls. And secondly, obesity predicts a poor TNF inhibitor response. In patients who are obese and on TNF inhibitor, only a third of them achieve ASUS 40 compared to those who are within the normal weight. So therefore, there is also the impact of the obesity on the treatment response to biologics such as TNF inhibitor.

Thirdly, the scores that we use, namely, are very much patient reported, and we know that in obesity, other factors such as chronic pain, fatigue, and mood disturbances travel together with obesity. Hence, we have to match these scores with the CRP and also what we see on the MRI to ensure that these are measuring inflammation rather than non inflammatory pain. Now, a lot of you would be familiar with the new now concept of difficult to manage Axial Spar, but some of these patients, I would say, more, rather than difficult to manage, they're harder to treat axial Spar patients when there is also obesity and other co morbidities coexisting with the axial spondyloarthritis. What we need to do here is at the start of the treatment consider addressing these conditions, referring them to weight management service, and also to assess these patients in clinic. What can we do in clinic?

Firstly, of course, measure their weight. You might want to measure their neck circumference or waist circumference. And there are scores that you can do in clinic to assess, firstly, for sleep apnea, there is something called a stop bang score. And also the Epworth sleepiness score, you can be used to look at daytime sleepiness. And then you can use the FACIT F score, which is a way of measuring fatigue.

And these should be considered on top of the typical scores that we use, namely BEST I or S test. And when we have a fuller appreciation of this, we may refer this patient to a sleep clinic for confirmation of sleep apnea, for they may benefit from other treatments, and also for weight management services to be involved in this patient, psychological services for their low mood, and we can often use scores again to measure this. And I think this is part of the whole holistic view that we have to have in patients who have obesity in the context of Axospondyloarthritis. So my take home from this patient is that while we are treating the inflammatory disease, we also need to consider some of the other non inflammatory features that feature highly in patients of obesity, namely chronic pain, fatigue, and mood disturbances. The challenge for us is to disentangle them and to use the appropriate measures to understand this in order for us to have the best outcome for our patients.

I'm Anthony Chen reporting here for RheumNow in this QD obesity clinic.

Hello, welcome to obesity QD clinics for RheumNow. My name is Doctor. Marinalini Day. I am a fellow in rheumatology and internal medicine working in King's College London in The UK. And today's case is entitled Obesity Escalate or Reassess.

So this is actually a composite case based on several clinical situations I have faced within the rheumatology clinic, that will be familiar to many rheumatologists. So our patient is, a lady in her early 50s with an eight year history of psoriatic arthritis. Her disease had previously involved peripheral joints, emphases and the skin, and she also had obesity with a BMI of thirty nine. She had initially received treatment with a TNF inhibitor with only a partial response and eventually had changed to an IL-seventeen inhibitor. After twelve months on that, her psoriasis was almost completely clear, and the swollen joints seen before her treatment with the IL-seventeen inhibitor had resolved.

However, despite this, she continued to report considerable pain, fatigue and difficulty with everyday activities. So, her walking was limited, she had stopped exercising and she was struggling at work as well. So, these symptoms were starting to affect almost all parts of her life. Her disease activity score remained high enough to suggest that there was inadequate treatment response. So, on that basis, it would have been easy to conclude that we need to go for another advanced therapy and that her second mode of action, biologic, had also not worked.

However, when we separated the components of the score, it was actually more complicated than all her symptoms being attributable to PSA alone. So, she had 12 tender joints, but no swollen joints. Her pain and patient global scores were both eight out of 10, while her CRP was only mildly elevated. There was no dactylitis. Her psoriasis that she previously had, a very active disease, remained well controlled, and her examination didn't show any convincing active enthesitis, which she's also previously had.

We then went on and did an ultrasound scan of the most symptomatic joints, and this found no significant power Doppler activity. So, no evidence of inflammatory process going on. Some knee radiographs were also done because she was complaining of significant knee pain, and those showed some osteoarthritis. She also, in addition to all of this, described unrefreshing sleep. Her partner, who's with her in clinic, also reported that she was snoring now.

And she herself said that she was getting quite sleepy during the day, so what you describe as daytime somnolence. When asked about her mood, which is, of course, very important in our patients with rheumatic diseases, she reported very low motivation, loss of enjoyment, and feelings of hopelessness. So quite depressive symptoms as well. Subsequent assessment identified obstructive sleep apnea and, of course, the clinically important depressive symptoms. So, there's several pathways by which to go now.

So, should we change her biologic because she appears not to have achieved the treatment target? Should we continue with the same treatment, and accept that nothing more can be done at this point? Or should we actually step back and reconsider what's driving her symptoms? And, of course, the third option is the key thing to do here. So rather than immediately changing her biologic, the absence of objective inflammatory activity should make you question whether or not another change in immunotherapy would address the outcomes that actually mattered to her.

So instead, we discussed the findings with her. Importantly, we didn't tell her that every symptom is caused by her weight because that's not true. We explained that her PSA appeared reasonably controlled, but that osteoarthritis, sleep disturbance, mood, reduced activity and obesity were probably all interacting to amplify her pain and her functional limitation. So, in these cases, it's quite important to discuss obesity as a chronic treatable health condition, which, as we've suggested, interacts with other symptoms and other comorbidities the patient may have in order to ultimately contribute to the symptoms the patient is experiencing. So, for our patient, she was referred for sleep assessment and subsequently began treatment for her OSA, obstructive sleep apnoea.

Her depressive symptoms were addressed through primary care, although we did also refer her to our liaison psychiatrist who works within the department as well for additional help and support. And she received physiotherapy focused initially on achievable low impact activity, so a graded exercise therapy programme, since there was also symptoms of fibromyalgia here as well. She was also referred to a specialist weight management service to discuss behavioural, nutritional and pharmacological treatment options. And of course, weight management services do vary in terms of accessibility and the type of support they can provide, depending on where you are, not just in The UK, but around the world as well, and the healthcare system you work in. At follow-up, she was not pain free.

However, her sleep energy and walking tolerance had improved, and she had begun to lose weight, and there was still no objective evidence of recurrent inflammatory arthritis. So, when we reflect on this case, it is firstly important to remember that disease activity score is a prompt for clinical assessment and should certainly not be a substitute for it. Clinical assessment is really key, particularly when people have multiple coexisting conditions as well that may be contributing to symptoms. Composite measures are obviously essential, but tender joint counts, pain, fatigue, and patient global assessment can be influenced by other conditions such as osteoarthritis, sleep disturbance, mental health conditions, central pain mechanisms, and obesity as well, of course. And a high score should make us ask what else could the person be experiencing that is contributing to these symptoms?

The relationship between obesity and psoriatic arthritis itself, if we just take those two aspects, is very complex. Obesity is associated with greater symptom burden, poorer physical function and lower probability of achieving some treatment targets. It may also influence response to biological therapy, particularly TNF inhibitors. This has been shown in multiple real world studies, including one that I was involved in within the International METEO cohort. It's been shown many, many times.

And specifically adipose related inflammation can contribute to modest elevations in CRP, while mechanical loading may worsen pain at the knees, feet and entheses, just to name a few. At the same time, though, obesity should not become an explanation for every symptom that a person is experiencing. So, people with obesity can still have genuinely active PSA, of course, and undertreating inflammation is just as problematic as unnecessary escalation of advanced therapy. So, the aim is to assess inflammation carefully while recognising the additional factors shaping the patient's experience. Obesity in itself is complex and the management involves shared decision making, potentially the involvement of many specialties, as we've seen in this case.

It is, of course, important to ask a person's permission before discussing weight, especially the relevance to their own priorities, whether those are pain, mobility, fatigue or cardiovascular health. So, in this case, for example, her symptoms were affecting her ability to work, and so that might be a priority for her. We should also ask about sleep, mood, eating behaviour, medication, and also barriers to physical activity as well. Rheumatologists don't need to be the ones providing every component of obesity care, but our role may be to recognise the problem given, of course, how frequently we also see our patients and monitor them. But the key is to avoid stigmatising language and connect the patient with the appropriate multidisciplinary support.

It's also worth mentioning here very briefly about difficult to manage psoriatic arthritis, which deserves a whole video in itself. But persistent symptoms after several advanced therapies may result from continuing inflammation, but they also may be driven by comorbidities, as we've discussed, as well as structural damage, psychological factors or persistent pain. The term treatment refractory disease should be reserved for patients with convincing objective inflammation despite appropriate therapies. So clearly, the coexistence of obesity and psoriatic arthritis is clinically complex, but does require careful assessment to ensure treatment is escalated when appropriate, but also management of coexisting conditions are also offered in a partnership with a person living with the condition. Thank you for listening to this case.

If you'd like to find out more about RheumNow's coverage on obesity QD clinics, then do continue to check out the website for more cases and more coverage. Thank you.

Hi everybody, I'm Mike Putman. I'm a rheumatologist at the Medical College of Wisconsin, And I'm coming to you today for RheumNow. I'm excited to talk about GLP-1s and a couple cases that I think illustrate how I have changed my practice to incorporate these new therapies. So I have two cases I wanna share. The first is a 74 year old female patient of mine who had giant arteritis with large vessel involvement.

We did the usual things, steroids, tocilizumab, and she responded beautifully, went into remission. Fourteen months into her taper, she came back to me and she said, I wish I could just go back and suffer the consequences. The steroids had caused horrible, horrible changes to her her body and her self image, she'd gained 45 pounds, and she just felt like it hadn't been worth it. And you know, for me, this is heartbreaking. I'm here to try and help people live longer, live better, and we stamped out the GCA, but she was definitively not living better.

So I said, You know, there's these new medicines, these GLP-1s. I'll refer you to your primary care doctor. Sent her to the PCP. They said, Here's some dietary changes. And she came back to me and said, You know, I tried and it's not working.

So I went back and forth and I said, You know, we need to try GLP-one. They said, Okay, well consult endocrinologist. So she went to endocrinology. Got referred, it was denied. She tried another round of diet and exercise, did not make progress.

Six months later, maybe nine months, I finally got her on a GLP-one. But at that point, she was going for a TKR, and the whole thing was so frustrating, and I just felt like I failed. I gave her all the steroids that caused the weight gain. I tried to make the right things and have the primary care doctors handle the GLP-1s and do all the things in the way that the healthcare system does that. And it didn't work, you know?

So let me tell you another vignette. It's a little bit later. I had a 58 year old gentleman with rheumatoid arthritis. He came in to me with knee swelling. I aspirated the joint.

He had 2,300 white cells in the joint, mostly inflammatory. I injected it, he got mostly better, but not all the way. Increased his methotrexate. He was also on a TNF and hydroxychloroquine. So, you know, three drugs, difficult to control RA.

Got an x-ray, he had moderate to severe DJD. So I referred him to orthopedics and said, hey, you know, this guy might need a knee replacement. They said, sure looks like it. Put him on the schedule for a little ways in the future after he tried some physical therapy. And they said, maybe he should lose some weight.

And I said, alright, that sounds great. But you know what? I've been down this road. I'm gonna try something different. And so I prescribed him a GLP-one myself.

Went through, got approved, he went on a GLP-one. Four months later he came back from my clinic, and I have never seen him this happy in my entire life. He about gave me a hug and, you know, for a couple different reasons. Number one, the knee replacement was canceled because he'd lost 45 pounds, and his knees felt great. He said, hey, I don't need a knee replacement.

I'm working, running better than I've run-in twenty years. He also self discontinued the methotrexate. He said, I felt great. Everything was going so well for me. I stopped the methotrexate.

Here's my hands. And he had a C diet of zero. He had no disease activity. His inflammatory markers had also completely normalized, which had never happened in my entire time of seeing His ESR had always been like forties, fifties, know, passive aggressive. CRP always like point nine.

You know, not high, but not normal, and completely normalized. His ESR was in the twenties, and his CRP was stone cold normal. And this is despite him stopping methotrexate, which is usually the kind of thing that would, you know, instigate a flare. So, a couple of take home points from these vignettes. The first one is that I think we own this.

If you give someone steroids and they gain a bunch of weight, you know, that is a problem that you caused. Maybe you had to cause it, but like, you should participate in the solution, right? You know, we give PPIs to prevent GI bleeds, we give calcium and vitamin D, which doesn't really work, to try and prevent fractures. I mean, GLP-1s work, and we cause the problem. The second thing is that, you know, I don't know why we wouldn't own this.

Like, we have the prior authorization pathways. We're always running prior authorizations for super expensive medicines already. Like, this is our thing. We know how to do this. And so, I think we should do it.

The third reason I think you should do this is that patients just love it. I mean, patients love this. I've had many, many patients that I prescribed a GLP-one to now, who lost a ton of weight, came back and said, You you really changed my life. And I'm like, Is it the methotrexate? They're like, No, no, no.

It's the GLP-one. And then the fourth thing is that, you know, this is on brand for us because we really do think there are probably some anti inflammatory effects of the GLP-one. So, you know, the Together PSA study was just published, you know, that showed that people with psoriatic arthritis had better disease control, independent, probably, of DMARDs with GLP-one. So I think that there's definitely something here. And I think that that probably crosses different disease areas, where giving GLP-1s, cutting weight, cleaning up diet really, really has some anti inflammatory effects and could help you get people on less DMARDs, I think.

That's still to be seen in a lot of diseases, areas, but boy, there's so many other benefits to these drugs that I think it's worth considering. So, that's my pitch for how rheumat why rheumatologists should be prescribing GLP-1s. Hope you thought that was interesting. If you want more information about this, please check out all of our great coverage at RheumNow. Thanks so much, have a great day everyone.