Ep 38. Lupus

We're proud to introduce patient voices. A brand new 10-part podcast series that puts real patient experiences at the heart of clinical practice. As a patient advocate, it is main, main, much more confident it's main, at the nominal self-manager. Each episode has been developed with patient stories at its heart. It's acknowledging that there's different types of expertise and knowledge in knowing and that actually we're working in a partnership. Along with expert clinical insight, creating a balanced practical resource to help improve everyday care. The amount that you learn by involving patients can't be underestimated. The projects that I have found most interesting, exciting, impactful have all had really great involvement with patients. Across the series, we'll explore important topics such as living with rheumatic disease. How does this condition fit with everything else that they want to achieve? New or very diversity in the clinic. New or diverging people can present in lots of different ways. New or diverse team means and being very careful to listen to what the person in front of your needs. And supporting exercise, including insightful conversation with the Winter Olympian. From then on out, I guess my sporting career changed and how I viewed myself had to change as well. Start listening today and stay tuned for new episodes coming your way all year long. Join us in listening to how patient voices can shape better care. You're listening to the Talking Rheumatology Spotlight Podcast, brought to you by the British Society for rheumatology. I'm Pip Watson from the B.S.R. Digital Learning Board. I'm delighted to be joined for this Talking Rheumatology Spotlight Podcast by Dr. Chris Wynnecoup, a consultant rheumatologist specialising in the University of Michigan, and a professor at the University of Michigan. I'm very pleased to be here. Thank you very much for joining us today, Chris. Thanks very much for the invitation. It's a pleasure to be here. Fabulous. Could you start please by telling us a big question really. What is lupus or SLE? Great. So it's a nice question to start with because we can spin it any kind of ways and we'll both be right and wrong. I was recently teaching at a training day what immune cells are involved in lupus and I basically said whichever cell you say will probably be correct. But what I want to do is I think about lupus in a number of different ways and it's being very broadly, we know that it's what we call a chronic systemic autoimmune condition, which I'm sure is fairly familiar terminology to many rheumatologists, but for any non-reumatologists who are under the listening, means that this is an autoimmune condition where the immune system targets its own a healthy tissue, rather than fighting invading pathogens like bacteria. And the way I think about lupus is a disease that's characterized by autoantibody formation and typically those are directed against nuclear components. So we're all very much aware of antibodies like anti-nucleantibodies and anti-double-strand DNA antibodies being important in helping us to make a diagnosis. And in the context of DNA antibodies to monitor the disease progression and activity. And the way I like to think about it is a condition that will typically form these antibody and immune complexes, which then deposit themselves within various tissues and depending on which tissues these target, you tend to get symptoms. So for example, very, very commonly skin is a major organ system that gets involved. We know that joints, kidneys, heart, lung and also blood complications can also be seen. As a high level overview, we know there's a grossly unfair disease with the majority of patients being females, so nine out of ten patients with leaps of women. We also know that the disease tends to have a slightly worse phenotype if you diagnose when you're younger. And particularly if you are of non-caucasian background, particularly if you're an African ancestry. And so those are really the key things that we know about this complex systemic autoimmune rheumatic disease. Very helpful. Thank you so much. And what would be a sort of common presentation of a sort of typical patient that you might see either in clinical or on the wards? So I think it's really quite challenging. We'd like to see patients and say, well, someone has perhaps early loopists when we first meet them and make the diagnosis. But before we kind of talk about how they typically present to us as rheumatologists, I think it's important to consider what has happened to that patient to come to the attention of a rheumatologist. Now, in the setting of being in the ward where someone is very, very unwell, clearly we may think that it's that form of the disease that is when it starts. But we know from good data within the UK that the average times from the first symptom of leopards to getting a diagnosis on average is about seven years. And I often find that really quite challenging and quite surprising, particularly when you think about a health care system like we have in the UK where it tends to be free at the point of access. And you don't have finances as an obstruction for getting to a specialist. So what I often find is that the initial symptoms can sometimes be slightly less descript. And it's only when you bring them all together that you start to get a sense of a diagnosis of leopards. So we can talk about the slightly more general symptoms, which are particularly weak, instantaneous domains. So mouth ulcers, rashes, hair loss that then can go on to develop a pleasure. We know that joint involvement is common. So occasionally with a vertebral inflammatory arthritis, but more often than not patients reported generalised arthritis or amyulture. Patients can sometimes report low grade temperatures and who are awaiting and poor appetite. But essentially patient could present in any number of ways. And there's often on a background of symptoms like that that someone may present with the more severe symptoms of the disease into hospital. For example, if they had paracardiomyel, or macadulchestopane, if they had cleareste, pulmonary involvement, or renal involvement, it's often on the background of these symptoms. So patients can present in any number of ways. And I often find that it's once they get in front of a rheumatologist that we start thinking about the diagnosis. And the challenge is often making someone to think to send the patient to the rheumatologist in the first place, which is why things like leaps away in this month, and things like this are really important to spread information, to make sure that patients can get to your clinicians in a timely manner, and that we educate our colleagues on what to look out for. Absolutely. And what would be your approach to sort of taking a history in a patient who you suspect tonight have leaps? Sure. So I think there are a number of kind of cheats that you can do when it comes to leaps. So we're getting a bit better at kind of classification criteria. And we know classification criteria are useful for clinical trials. But I think when I'm teaching new doctors, or sort of say resident doctors, you give them the inclusion criteria for some of these studies, and it breaks down what symptoms to look out for. So thinking of the ULAR ACR-29 criteria, it has skin disease, mouth, ulcer, salopecia, joint involvement, renal involvement. And that can sometimes just remind you the things that you need to check. So for example, when I first started seeing patients with leaps, it reminded me to do a urine dip, because that's really important things here. Similarly, if we look at the disease activity scores, so the SLEDI score is a binary score that's really useful, because it has a number of important symptoms and serological changes to consider. So if you're unfamiliar with seeing people with leaps, that can sometimes help us a checklist for the more common symptoms and tests to do. And if you want to go into kind of a high level, really detailed assessment of a patient with leaps, then looking at the bi-like criteria for disease activity is incredibly helpful. It's very, very extensively, it includes a number of very rare symptoms of leaps that can sometimes make you think that this disease is possible. And clearly, we're not saying, do the classification criteria or disease activity every time you see someone you think might have leaps, but you can see that there are some helpful hints there as to the questions you need to ask in clinic. And this really kind of helps to show the wide ranging symptoms that we can see in the disease. And I find it whenever someone is neutral, leaps kind of giving those prompts to them is often a helpful way for them to try and make a diagnosis. That's really helpful. Thank you. And you mentioned when we're sort of reasoning in trying to work out whether we think something is a risen leapest that it was more common in females. I wonder if you could speak a bit more of a age, perhaps, of presentation and ethnicity as well, because these are important factors too, aren't they? Absolutely. I think positive and negative predictive values here. So ethnicity, as I mentioned, nine out of ten patients are female. That does mean that 10% are male. So often some people get the thought that all patients with leaps are female. And so it's important that we don't just automatically think, "Oh, this patient is a man, therefore they've not got leaps." So he makes it less likely, but we do need to consider those in particular in different ethnic groups. And we do know that there are groups that are more unfairly adversely affected by the disease. And based here in South London, where we have a huge amount of ethnic diversity is something that's important to consider, in particular, we're making a diagnosis and thinking about disease trajectories and prognosis. But I think it's also important to look at the other way. And whenever I have a patient who's reversing, it doesn't quite fit within that phenotype. So perhaps a patient who is older, Caucasian, maybe a man, that may have some antibodies, but some more non-descript symptoms. So often a good prompt to think, although this person might have criteria for leopus, if the phenotype is slightly wrong, then it's often really important to look at those patients for differentials. And we do know, and we've seen this many, many times where people have been less likely to be able to see it. o fydd yn ymwyr i'r fyddiaeth sy'n ei fyddiaeth sydd yn fyddiaeth yma, yma hynny, ymwyr i'r fyddiaeth yma. Mae'r fyddiaeth yn yna ei gysylltu sydd yma yn yna, mae'r fyddiaeth yn yna gysylltu sydd yma. Mae'r fyddiaeth yn fyddiaeth yn fyddiaeth sydd yma yn yna. Yna gysylltu sydd yma yna. Yna'n fyddiaeth yn fyddiaeth yn fyddiaeth yma. oêts coatings rwyntig o dyferi i freddau rydym, dwi actually love it if'n wyma fillin? Capariaf heddiwfa mam nhw i graficol hairmaidd Better, i voulezanfog Ddi Pyrs parby� as bodleygu canis naorol speaks, cara clonenau unrhoeddus o dyferfa As y未au episolil ar I einzoletulian I Labryr stros honnejeb Dynau'r akdalu oboddau â i hollan por missing o er diaphragaig. So started to have examination orthenically? Wrth â rydyn yslwwyr cyfrytϊwch yn honnau a'r eitem mometi i fall inspiraisdatingaau di'r llrydd am dros ni'n Waidd y Ylw𝘶, ieadd� placing i recolli mynd i faintarekach fe unid ar fe haws�i gyda mynd yearf i'r ies fŵrau sy'n d imperfecting 'wi' a well ty Wirjasegoorfilmchauol. Byw shipyscian o abst எனadell eu dy gennid rhynau scaneeb dw i'rged eitmaniain a callorid pluraladiojnau to gallu aidiliach velgroiu fotroordiowhoewol i'w amfig. Ogi malairaefiadan hynem ei panor��omio owr mae dyd ac yma o'r asgymad, sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau yma. Oedd yma bod oedd yma, yma'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n asgymadau sy'n casbwyr, cael ve~~~~ lefneud durante iawn arbeidietu dziwnau yn cyndeorio ongy i agreegyllat, adaptor nacegoer yn gallu iidd ar eithref er eithref er yn Yroya bod yn osst atorth Cynghiatodor gen y i'n болod i centywl tysio i fod ymitmal oedd. Beidw rwy mae'n p aboutu ei spart manifestoriesie tehywn lortos i'r calmingau fel ac ro'r centywl syracia ond yw,'n gwaipud yn cypasol eraill moded amfod frangodaidd yn sy'n fedine sy'n lauden ac'n bôn aplau'u bod był toeg Barclosedid. ell! Yma felly naten ein bruillau arioedd boission ei gwybod chi dyna ac, profeb mae sysgu wedi. vas cyfilor ast ei fel gy癩og reckonontau ar ymbedn鎖ol a syn ar Siwa'r axelweith myd siddog, cablewllwp a sut ar yng Nghymdelo a'r ac mae godi yna shop i ei gyfer stan mewn ignore naru dod agachrie mwy complol statud o gallwn o chi wedidim. Nun oed na locallya o fod hyn soloedd y foeidiad, neue sylci fundoedd i amg yma. Mae'n ei dendru o roci amfilio cynígenach a'riu ry sleeping o'no. Andale sydd wedyn concrops o fod fi fel meddwl bennu'r cyngewn yr fel mufod o roael moandag poligu esguddoriaeth gyfer gw helpu allid i ragdaeth能 dim cong hun? Llyfysigau iddwn sydd wedyn caesat ballau, fodd ei fod o'r couchd ar eitht i'r carraethau a'r ymdol ei gyddiadau, yn ymdol ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau. Mae'n ei gyddiadau, a'r ymdol ei gyddiadau. Mae'n ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau. Mae'n ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau. Mae'n ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau, a'r ymdol ei gyddiadau. Ond my training is important to look carefully at the skin for any signs of active lupus, obviously skin starts with the hands. Many of us as rheumatoids start with the hands to do a joint examination, but we can see subtle skin changes in the hands, changes in the nail folds that can also be important not just for lupus, but other underlying systemic auto and human-rhymatic diseases, and then looking elsewhere. looking at skin and joints is what we are pretty used to doing as rheumatologists. Thinking about other important organs, so consultation of the heart and the lungs to pick up any pericardial or preruristic rubs or suggestions of effusion. Limfattenopathy, obviously an important manifestation of the disease, but can be a concurrent diagnosis that we need to take seriously. So looking for lymphroprolifitive diseases with either spleen or negoly, hematomegoly, palpable lymph nodes is also an important part of the role of examining patients with lupus, and then obviously the medical student answer how you conclude your examination well dip the urine, and I think that's probably the most essential thing, and every patient who you even suspectably person will need a urine dip, because in many cases it's the nephritis that's the early part, and without a urine dip and a prosing creatinine ratio that will go missed. So those are the kind of things that I'm often looking for with an examination. Great, thank you. I wondered if we could talk a little bit about antibodies, so you have mentioned them a little bit. How useful are these? Do you think in sort of clinical practice? Fine, so this is a double ed sword, and I'm probably whichever way answer this will say something controversial, so I'll follow it for that and then go back. Go for it. Anti-clear antibody positivity is an entry criteria for the URACR criteria for a diagnosis of lupus. So ANA positivity is really, really important. There is arguments, and I'm not going to go into those today about ANA negative lupus, but if we're looking at the criteria to get into a study, which I admit is different to clinical practice, a positive ANA is needed. We also know that the cutoff for the ANA for the URACR criteria is 1 in 80, which is actually a pretty low-tighter, and I think that as rheumatologist we're very used to getting referral, saying, "I've checked this patient's blood and they have a positive antinucleurontic and it's 1 in 80, what do I do?" And we often say, "Well, you know, there is a proportion, you know, probably about 5 percent, if the healthy population has a positive ANA." So you're stuck in a position where you have an antibody that can affect about 1 in 20 people incidentally, but also as the crux for a diagnosis of lupus. And so that paradigm makes things very, very difficult. So when I have a patient referred with a positive ANA, I go looking for the immunological abnormalities, and that's where things like the ENA come in, in particular, Smith being an antibody that's strongly associated with lupus, but also just wouldn't fit any other abnormality. So the R&P, ROW, or LAR to suggest that there is another antibody with that ANA, it gives that just an extra weight. And then obviously looking at the markers for disease activity, which would be a DNA binding, and you see 3 and C4. And if you start to pick up a number of those abnormalities in a patient who is very well, I would start being suspicious that that person may have a risk of developing into lupus. But I think this comes back to the matter of ANA testing, which is always a challenge. And I think on one hand, I said earlier, that the time to diagnose this in the UK from the symptom of lupus to diagnosis is about seven years. So I don't think we can say to people, "Don't check ANAs if we want to get that time shorter." Similarly, we need a mechanism for what to do when patients do have positive antibodies, that may not have a disease or any symptoms whatsoever. And this is one of my other piece of clinical work that's involved, is that I, sorry, from my lupus clinic, I have a clinic for patients who are auto-antibody positive, who have that risk of developing lupus, but also may just have a positive antibody that's not causing the many trouble, that may never cause the many trouble. And I think that a better understanding of those antibodies and what they mean on an individual basis is really, really important. But thinking about lupus, among my patients, typically is, go, "ANA, ENA, DNA, C3, C4," and then not forgetting things like phospholipid antibodies, which are really important if you make a diagnosis, but also form some of the classification criteria as well. That's really helpful, thanks to you. And I think it is a tricky one, isn't it? But I always, when it's patient and front of me, always come back to the clinical context, and is there anything to back up what these antibodies are suggesting might be happening, because they're never really going to give you a diagnosis, or they might sort of hint you in the direction of one. Absolutely. And I've had patients who have all of the antibodies associated with lupus, who certainly do not have lupus, but on the basis, was still full for the classification criteria, only on the basis of antibodies alone, that clearly don't have lupus. There are a handful of those patients, but again, it's absolutely correct. It's what the patient is telling you in front of you that I think is the really important thing, and the antibody is there to perhaps confirm what you may or may not be Seven cnt son i chips is. At Valgau vet earlup bien un pro AMG o omd Cuolen sa obyn da i meneillig meneillighawn mu o11 tại a oorsodirio los DIEws wna da ddwe已 cist Cross AMG en wondering AMG a oorodd i ddwe已 cist a oorodd i ddwe已 cist a oorodd i ddwe已 cist a oorodd i ddwe已 cist aorodd i ddwe已 cist aorodd i ddwe已 cist aorodd i ddwe已 cist aorodd i ddwe已 cist I want to ask you about what is the issue of choosing between easy find and prune and mic ifn like because I think we do get to that juncture don't we do you? Is there any evidence or any experience that you have to guide us or do you just sort of want for one? The tends to be asithyparin has been around longer so there is a little bit more data for asithyparin in certain situations. Obviously if I am concerned about pregnancy or whether that is intentional or the risk of unintentional pregnancy then I think asithyparin is likely to drug to go for. I tend to lean slightly more towards micrphenolate and this is my own personal feeling because of the good evidence for renal disease in particular. Also because it is a lot easier to measure drug levels and I think when it comes to framing discussions about adherence, checking drug levels can be useful in those discussions. Clearly you don't want it to be kind of a gocture moment where you say well your levels are zero and I have found the hype. But it can sometimes help us just understand where there has been a slight flip in disease activity and perhaps a bit of loss of adherence. And I used in the right way I think that can help shape some of the discussions. So I knew that micrphenolate levels are a lot easier to do than asithyparin so I tend to move more towards micrphenolate. If there is any question about pregnancy then asithyparin is where I be going and particularly trying to get it in and tolerated and that the right dose before someone tries to conceive I think would be particularly important. That is really helpful. And then wanted to just chat about plasma exchange which is something that I think some people is a little bit mysterious. Could you just tell us a little bit about the sort of types of situations where you think that might be something that people should be considering? Yeah, so I've not really plasma exchange many patients with leopards and that might be because we're starting to get some better treatments. Now I say plasma exchange probably would come towards the end of the spectrum. I you've got someone who's very very sick. I wouldn't be looking at patients and be relating in clinic and saying well we'll bring them in for some plasma exchange but I think many of us are used to the critical care setting where someone is very very sick. I think that the plasma exchange is often kind of it may be seen and I think not exclusive to leopards but maybe seen as kind of a safer halfway house than the setting of infection. I think in a setting of catastrophic antifossil, a bit syndrome which we see occasionally in leopards then the evidence is throw everything that you can at that patient. But Plex isn't something that I've used all that frequently but I think that might be because we have good access to things like cyclophosphamide, redoxamab and bilimumab instead. And there's probably a bit more evidence space for those drugs. And finally on the treatment side I think I just wanted to ask about the rule of caratysale therapy and also just to give a plug for another podcast that we've recorded on that. I think this is a really exciting area isn't it and something that will be new to lots of people. Yeah exactly so further details check out the other podcast that we recently recorded. Yes caratysale therapy is the very very exciting thing at the moment. I've not been in remsodgie for decades but certainly is kind of one of the most exciting things that the I've heard discussed not just as a clinician interested in leopards, but in terms of sparking interest across the field. So, Cardi's health therapy is again another example of us borrowing the ideas that hematologist used to target B cells, but doing it in a much, much more effective way. I think it's important to know that the data that's out there that's published is open label. It's small numbers. It's race select groups. It's not in late phase studies. It's not placebo controlled, but it's hugely, hugely promising. And I think that the thing that's particularly exciting about this and the way I describe it, particularly colleagues in hematology when we discuss this is if you had said, let's design a trial of severe leopus and the outcome is going to be at three months. Many people would say, I don't think that's a good idea because I don't think you can get someone better with severe leopus in three months. If you were to then say, I'm going to make sure that this patient has no clinical activity of leopus, I think they would probably raise their eyebrows and say, well, I really don't think you're going to do that. And then if you went for the hat trick and said, I'm going to bring them off all of their conventional therapy and they're not going to need it, you would probably be laughed out at the room. But this is what the open label data is showing. And I think that it's exciting for a number of reasons. We're still three years out. So we don't know whether this is a long deep remission or something longer than that. I'm not going to use the word that that might potentially be because it's still very early days. It's also a case of patients who come off treatment. And I think that's huge. And speaking to patients, that's one thing that is seen as perhaps the biggest takeaway from this is if you don't have to take a load of these nasty medicines in the long term, you can kind of get on with your life. And I think that's where a lot of interest is from patients. But as clinicians, we know that we don't want patients to get infections from their immunosuppression. We don't want them to get a vasculine of crisis from their steroids. We don't want diabetes from steroids being compounded. And so I think that's where this is really very revolutionary. But we will know more. And I think the things that we'll tell us more in the next few years, this number one is the duration of this response. I.e. Is it one and done? You have this treatment and that's it. Never anything else. Or is it you need recurring cycles? Or is it the disease comes back at certain points? And number two is safety. And we know that and this was mentioned quite extensively in the podcast on Carti Self- Therapy that safety is an important thing for the hematologist using this in the setting of hematological malignancies. We're seeing limited but slightly more promising results in autoimmune conditions. But I think safety is going to be one of the main things that drives this into being used further in the future. So safety and duration will be the things we're looking at in the coming years. But very, very exciting. Thank you. And you did mention a little bit about the disease activity sort of scoring in loopers. Is that something that I realize you do a lot of clinical research as well? But in your sort of routine clinical practice, would you tend to do a disease activity score in patients? Yeah. So obviously I'm a number of by lags. So I would say by lag is a very, very good physical score. So I always do a by lag in clinic and I encourage all of our resident doctors to do the same. We have an electronic record system where we capture all of this. But the ULAR guidelines do say you should measure some form of disease activity at every clinical visit. I would say do a by lag, but I also do a sleigh die. And I also look at other more treat target type endpoints such as loopers, lazy days, activity, state, Doris remission. Now there's another slightly more high level things and I do have a note above my desk to help me remember these things when I look back to do my admin. But I think looking at disease activity is incredibly helpful, whichever measure you decide to use because we need to see where the treatment is being effective. And I think if you see some of these activities score going down, that's good. If it's going up, you're going to keep an eye out. But the one thing I try to impress on anyone that sees patients with me is that the disease activity score does not really give you an idea of how the patient's doing. And we know things like fatigue and other symptoms can remain terrible, terrible, debilitating symptoms. Even if we see a sleigh die score go 10, 6, 4, 0, the fatigue score may say the same. So it's not a case that you fix that person as an individual. You may have made their disease better, but it's always important to think about the other symptoms rather than just kind of pack yourself on the back and say what this person is now considered better because I can see that their disease activity score has normalised. So I would emphasize doing it whenever anyone sees a patient with leopards, a sleigh die is a super easy one to do. If you want to do something more comprehensive, then the buying eye is a good one to do. But then you need to see that activity score is good. But don't forget there are a whole host of symptoms that are not captured in that. They're also a significant role on impacting quality of life for that individual patient in clinic. I think personally I find that doing it just reminds me to ask everything because it's quite a long list isn't it actually. You will sometimes sort of miss something inadvertently, I think, if you don't do that. I also find it helpful when thinking about treatment escalation because there are certain thresholds out there and you kind of see, you know if you cross one, then that's kind of an option in terms of accessing sort of more advanced therapies isn't it, which is really helpful. Yeah, absolutely. And we get a lot of referrals in locally here from other centres that perhaps can't give those more advanced therapies. And it's always nice if they say what they think the therapy the patient might need is and what those these activity scores are because even if you're not delivering that treatment to the patient yourself at your site, it's good to know what those thresholds are because you can tell the patient what's likely to be offered to them when they come to a tertiary centre. And so I always find this hugely helpful and frame a lot of the discussions with the patient. You know many patients will come across and say, I've been told that you might give me a preliminary nap because my Slydidoscore is above 10. Great. Okay, there's been some discussion there. All intensively, you can say it's up to you to choose what treatment is there, but I think getting an idea of disease activity score is often a good way of kind of speaking the language to say where you worries our about a patient and also what type of therapy you may be suggesting that they need. Thank you. And do you sort of, who's in your black book of other specialties to contact and or do you have any sort of MDT's with colleagues, which specialties do you think we need to be really careful to work with to help manage our lupus patients? Yeah, yeah, so first up, this is a double-edged sword again because I used to like getting everyone's telephone numbers to us to help when I had trouble, but people will call you back about it. So which I think is really helpful because you have the face things that we've diagnosed with lupus that have come through from another specialty calling us saying, you should see this patient with lupus is really helpful. In terms of the way that we do it, we meet up with nephrology once a month, sorry, once a week after our weekly lupus clinic. So we have a weekly discussion with nephrology and sometimes I'll go and join them in their clinic as well if one of our patients is going over there to save a second visit. So close working with nephrology goes without saying it's really important. They not only are the experts at the organ and the embryopsies, but they often think about the things that we forget such as ACE inhibition and other types of treatment that go for managing more chronic kidney disease than we know. So we know the definitely really important. Dermatology, as I mentioned, is hugely valuable, members of the team given how much disease is in the skin. And again, biopsy, so you can see it's a procedure type thing that can be helped with, but also the topical treatment of cutaneous lupus is really very complex and having a good dermatologist isn't incredibly helpful. From my perspective, we also have a Neurocyciatric MDT that we do once a month and that's because when we identify these worrying symptoms and patients, it's a good form to discuss there. But also I know that I can contact the members of that team at any time if there's any, if there's any worries about symptoms and have a response there. Hematology, obviously I can't say that hematology having just done our podcast with a hematologist because of Carti cell therapy, but also because we know the flambatius clinic need to be involved. And we're considered about antifusural lipids syndrome or whether we found positive antibodies that need some assistance. Respiratory, so in social lung disease, we have combined ILD clinics running about once every one or two weeks as well. Cardiology, major risk of a atherosclerosis, but also for the macadulant paracyserial involvement, so we have a monthly paracadial MDT here as well. I'm sure I'm missing out on lots of brilliant colleagues, especially immunology with one of my very good friends being a consultant immunologist here at Kings. So essentially anyone, and I think my approach has always been that every specialty looks after lipists to some shape or form, but I think that particularly with nephrology and dermatology, those are where the overlap is perhaps most well established. Great. And what do you think is the most challenging aspect to this condition? So I think that there are a number of challenges. I think that my research was in fatigue, my first ever lipid research was in fatigue, and that was a huge amount of meat, and I think is a real devastating consequence for patients, but also is a major place which clinicians can trip up. And I think being a junior doctor, you can often see patients with active lipists that you then treat and get better. So for example, their creatinine improves, their protein urinvers, and you pat yourself on the back and you go, "I've done a good job of making that person better." And then the person leaves the client when going, "But I still feel really tired and awful." And that's really difficult because you sit there and think, "Well, I thought I made that person better, but clearly they have all of these symptoms that are ongoing." And the way to respond to that is either to, number one, ignore it, and I think as clinicians I ego often sometimes get the better of us. We like to treat things we can treat and make things better that we can make better, but things that are more difficult we may not want to hear about. Or you can embrace it, and I actually think that speaking to patients about fatigue is really important. I often have to say, "Listen, I don't have an easy fix for the symptom for you. I can screen for metabolic causes, and a little bit of exercise can be helpful appreciating that there's a large amount of fatigue that may impair that. But I acknowledge your symptom, and I can see the disruption in schools in your life, and I can see how this makes you suffer. is actually very. a long time to work that height. If you acknowledge the symptom even if there is not much, you can give it a leviate it, which will be welcomed. Those conversations can go very bad, but if you try to acknowledge the symptoms that perhaps are more difficult to see, or more diffuse? I was going to ask you, if there is anything important that we have not discussed, but I realise myself that we have not spoken about steroids, so I just wonder whether I could perhaps ask you to tell me a little bit about the rule of steroids first. And then if there is anything else that you would like to add as a final bit of advice for our listeners, that would be great. So steroids are really good. They are very, very good drugs, they are reliable, they work quickly, they can get you out of a radical situation, when patients are incredibly sick, with actively person of writers or myocarditis or anything that makes you worry that major involvement, if left untreated, will result in significant consequences. We all know that we can rely on steroids. I think it is rheumatologist, we all know that, and we feel reassured about that. But in the long term, there is a big risk with these drugs, and you consider that these patients can be very, very young, and the current guidelines that we have been replacing, you like guidelines, were 5 milligrams a day or less, I deviate from the guidelines and I try to get to zero anywhere that is possible. I think in the past, when we had limited treatment options, there was a vague for long term low-dose steroids. But if you look at rheumatoid arthritis, I don't think you would find any rheumatoid arthritis leaving patients on low-dose steroids, because there are so many more options now. And I hope that as we get more options for leopards, that long-term low-dose steroids will diminish and will no longer become as standard of practice. But yes, very, very important, but with significant limitations in the long term. In terms of other advice, I think it is always important to think about leopards. I think it is always important to test for leopards. And my approach is always, any patient I see wherever they may be, I think could it be leopards, and do I need to test for leopards, because it can take so long to get that diagnosis. And I think, importantly, when you do get that diagnosis, we can sometimes think that we've done a very good job in making what is quite a rare diagnosis for the patient. But often those patients will go through several nest diagnosis before they get to you. And they may not entirely believe that you've got it right this time, because many people may have told them that things are wrong previously. And this is an important relationship between us and our patients. We need to get that right. We need to make sure that we understand the symptoms that are causing the most trouble. We need to have open and honest discussions and patients need to feel that we will look after them when they need help. So I always encourage our patients to let us know if there is any trouble. Between appointments, we will see them, we will get them better, because the problem is, if that relationship breaks down and we don't see patients as frequently as we should, particularly when it's trouble, that when damage happens, sadly, that's irreversible. And I think having a really good relationship with patients is really, really important. I don't think any of us have got it perfect or got it right. And so it's always important to speak to patients to work out from their opinion, from their side, what we need to be doing to give them the best level of care that we can possibly offer them. That's fabulous. Thank you so much for your time. Chris, it's been really, really interesting talking to you. I've learned lots of myself. I know I hadn't realised at all that it was taking so long to get this diagnosis. And I think that has really interesting implications both for us and our patients. And I think my take homes really are to consider very carefully the scope of loopers. Consider that to all of our consultations, particularly thinking about the neuropsychiatric ailments, perhaps. And just to make sure that we are really patient-centered, that we think about what's important to them and we try and deliver to the best of our abilities, patient-centered care. And so thanks again very much for your time today. It's been a real pleasure. Thanks very much. It's always a pleasure to discuss these things with you. And thanks very much for your invitation. And just for our listeners, please do check out our other talking room, etology pods, including the one on CAR T cell therapy, which is very exciting in loopers. And if you'd like to expand your knowledge of this challenging condition, please also check out our digital learning spotlights on BSR digital learning.