March 15, 2026
Updates in Asthma (16 Mar 2026)
In this episode Professor Tom Fardon returns to Clinical Conversations to discuss updates in asthma diagnosis and management from the joint BTS/SIGN/NICE guideline on Asthma.
In this episode Professor Tom Fardon returns to Clinical Conversations to discuss updates in asthma diagnosis and management from the joint BTS/SIGN/NICE guideline on Asthma. Prof Fardon and Dr Ben Warner discuss the changes to practice since the guidelines were released and the evolving role of biologics in asthma treatment.
Professor Fardon is a Consultant Respiratory Physician at NHS Tayside and Honorary Professor at the University of Dundee. They are also the chair of the Scottish Severe Asthma Group within the Centre for Sustainable Delivery.
Dr Ben Warner is a Respiratory Medicine Specialty Registrar with clinical and academic experience of global public health. He is currently undertaking a PhD in multimorbidity in Malawi as part of the Wellcome-funded Multimorbidity PhD Programme for Health Professionals with the University of Glasgow.
Recording Date: 9 December 2025
Useful Links
BTS/SIGN/NICE guideline on Asthma
Algorithm A: Objective tests for diagnosing asthma in adults and young people (aged over 16 years)
Algorithm C: Pharmacological management of asthma in people aged 12 years and over
Optimising inhaled therapy for patients with asthma
Asthma+Lung UK website Inhalers resource
Greener Practice asthma care toolkit (free registration required)
'Greener Practice' Device Choice video
Asthma Guidelines (Plain Language Version)
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This podcast is from the Trainees & Members' Committee (T&MC) of the Royal College of Physicians of Edinburgh (RCPE).
This transcript has not been edited for accuracy.
Transcripts are available on popular podcast platforms.
Dr Ben Warner (00:01)
Hello and welcome to the Royal College of Physicians of Edinburgh Clinical Conversations podcast. My name is Ben Warner and I am a respiratory medicine specialty registrar in the east of Scotland currently undertaking a PhD in multimorbidity. Today, I am delighted to be joined again by Professor Tom Farden, a consultant in respiratory and general internal medicine at NHS Tayside and honorary professor at the University of Dundee, as well as the chair of the Scottish Severe Asthma Group within the Centre for Sustainable Delivery.
We previously heard from Tom on this very podcast in July last year, when we were discussing the management of acute severe asthma, who might be at risk, high risk of deterioration, ongoing inpatient management and discharge planning, and a little about the long-term management of asthma, including the concept of treatable traits. However, as we teased last time, the asthma field is constantly pushing forward.
And in the UK last year saw the publication of for the first time, a joint guideline from the British Thoracic Society, the Scottish Intercollegiate Guidelines Network or SINE and the National Institute for Health and Care Excellence, NICE on asthma, diagnosis, monitoring and chronic management. So one year on from the publication of these guidelines, it seemed only appropriate to invite Tom back on the podcast to bring us up to speed on today's asthma landscape. So we'll go further adi.
Dr Tom Fardon (01:33)
Thanks very much, Ben. Nice to be back.
Dr Ben Warner (01:33)
Tom Fardon welcome.
It's lovely to have you back and thanks very much for joining us. So Tom, last time we spoke on this podcast, I think I asked you for a sneak peek of the guidelines, but as it was still out for a consultation at the time, it was still very much up in the air. Now the guidelines have been published and out in the wild for a year. They've had time to percolate into practice and hopefully they're leading to improved outcomes for patients.
I wondered if we could start with you telling us a bit about what is new in these guidelines, what has changed in asthma diagnosis and care and why.
Dr Tom Fardon (02:10)
Yeah, it seems remarkable that it's been a year since the guidelines came out, but time does seem to move quickly, the older I get. And it's been a good year for asthma because the guidelines released at the British Thoracic Society winter meeting just over a year ago really highlighted the importance of asthma, ignited enthusiasm around asthma because it gave us a lot to do. I don't think I'm understating it. think it's the biggest change in management of asthma, certainly.
since the invention of the inhaler. But I think within respiratory medicine, it's been a big change. I can't think of any other subspecialty area where there's been such a dramatic change for such a large population of people. We have to remember that asthma is by far the commonest respiratory illness. Up to 30 % in some studies in Scotland at least have been diagnosed with a wheezing illness or asthma or have been given an inhaler at some point in their adult life. And it's higher in children. So asthma is a big deal. There's no one who doesn't know somebody who's got asthma.
I think it's part of the landscape. Everybody knows that if someone's got asthma, they've got a preventer inhaler and they've got a reliever inhaler. And that might be even use a brown inhaler, blue inhaler to go back really as far as the eighties and nineties, know, when there wasn't a lot of choice. So that's not just medics and healthcare professionals as general. The public knows brown inhaler, blue inhaler. you taken your preventer? Have you taken your reliever? So to move to something where there is no longer a preventer and a reliever, but there is just one single inhaler that does everything.
is a massive shift and we have to think about not just introducing the changes to patients because that's a big shift, but also to anyone who cares for or comes into contact with anyone with asthma. that's teachers at schools, first aid people, first responders, GPs, primary care, out of hours, nurses, secondary care, urgent care at A &E, emergency departments.
respiratory physicians, but anyone who comes into contact and then some other things like prisons, for example, where there are lots of people with asthma and we need to educate people who are in prisons or people on planes, people on boats. There's a huge amount of impact, which is such a far reaching disease. But what is the change? I'm talking a lot about the impact without talking about what it actually is. So the big change is to move away from the preventer and reliever inhaler to using a single inhaler for all of treatment of asthma.
And why has it come about? We've known since the 1980s with some very compelling data that increased use of short-acting butyragonists or the reliever inhaler leads to an increased risk of death. I mean, the data is well understood. There's data from New Zealand, from Australia, from America, from Europe, showing a clear pattern that the more canisters of salbutamol or albuterol, whichever short-acting butyragonists you use, you get through it a year, the more likely you are to die.
And the converse is true with the inhaled corticosteroids. The more corticosteroid you get through any year as prescribed, the better you'll do. But we all know that human nature is such that we don't remember to take our preventer inhaler, but we will take the reliever when we need it because it helps for symptomatic relief. So we had built for decades guidelines that say you really ought to take your preventer inhaler, but here's your reliever inhaler and when things get worse, take more of it.
And exacerbation management was take more of your reliever inhaler, keep taking that reliever inhaler, keep going, keep going. But the more you take, the worse you do. Another powerful bit of research was the NRAD report in 2013, 2014. So that's the National Report on Asthma Deaths, commissioned by Royal College of Physicians in London. And this looked at all asthma deaths across the whole of the UK and showed very clearly.
that the people who did unfortunately die from asthma in that period were people who had an over-reliance on their short-acting beta agonist. They underused their preventer inhaler as inhaler corticosteroid. They were undertreated in general. 50 % of people didn't seek medical attention during their fatal exacerbation and around 50 % of people, their treatment did not follow guidelines. So all in all, we were
not treating our patients well. were exposing them to have large doses of short-acting beta-agonists, which we know was related to death. We've known that for 40 years. And the NRAD report shows that we hadn't learned from those lessons. So something had to change and it's taken another 10 years to make that change, but that change has now happened. So there are two acronyms which we now need to get into the zeitgeist and those are AER and MART.
AIR stands for anti-inflammatory reliever. And the anti-inflammatory bit is this inhaled corticosteroid and the reliever is that there is a long acting beta-aranginist in the form of formoterole. You have to use formoterole as a reliever because it's the only long acting beta-aranginist that's very short acting, so a quick timeout of action. So the aim for AIR is that you get one inhaler. Your patient gets a single inhaler, a steroid plus formoterole, and there are choices of those and we'll perhaps talk about those choices in a little while.
And that inhaler is the only inhaler the patient gets. And the instructions are very simple. Take this inhaler when you feel you have symptoms and you don't need to take it regularly. You don't need to remember to take it when you brush your teeth in the morning, you brush your teeth at night. You just carry the inhaler around and when you feel symptoms, you take it. And when you have more symptoms, you take more inhaler and that means you get more steroid and that means you do better. And this seems like such a simple idea. We wonder why we've not tried it before, but actually
The rest of world have been doing this for quite some time and the GINA guidelines, the global initiative for asthma, have advocated this approach for many years. But we've not been able to do it in the UK, mainly because we haven't had a drug that's been licensed to do it. So we've been a bit behind, but also I think treatment inertia, sluggish in being willing to accept change and move on. And that often takes a guideline and that's what's happened. So for the majority of people who have mild to moderate asthma,
The decision becomes very simple. You take a single inhaler as your reliever inhaler. And when your symptoms get worse, you take more of it. And when your symptoms are fine or you free up symptoms completely, you don't take anything.
Dr Ben Warner (08:35)
hand.
Dr Tom Fardon (08:38)
Yeah, absolutely. And MARD has been around for some time and if anyone within respiratory medicine who's listening to this podcast will have heard of it at least and asthma specialist are very well averse with it is maintenance and reliever therapy is MARD. And there are a number of inhalers that are licensed to do this, but they all again contain formotrol because the maintenance part is easy enough, but the reliever you have to have formotrol. So this is air, which is the as and when bit, but also with maintenance on top of it. So
It's an easy change from air to Mart because for air you say just take this inhaler whenever you feel you need it. But Mart we say take the inhaler twice a day as well. So you've got some background treatment and then when you need to take more you add on top of it. So as air just fluctuates up and down from a baseline of zero, Mart fluctuates up and down from a baseline of some. And I think Mart has been around for, must be 10 years, maybe 15 years. Certainly for a long time and
For some people, it's been very successful and it's been used, but I think there's been some reticence to move to it because of concerns about overuse of steroid or overuse and long-speed trangness. But the data doesn't support that. And the data that accumulated that led to the ERS consensus statement from a few years ago, the G-net guidelines and now the NICE-SIGN-BTS guideline is that people who'd got mild temodotasma could go take air will on average use
inhalers a year, which is not much at all. Whereas if we had them on maintenance treatment plus salbutamol, then they would get through 12 preventers plus five relievers. So you reduce the inhaler burden quite significantly. And on Mart, so long as people take it as prescribed and suggested, then they can control their asthma much quicker. They exacerbate less frequently. You avoid oral steroids and all those complications and you don't have massive amounts of inhaler use. So you could see that if you're on air,
the asthma progresses and becomes less controlled. You can move on to MART with the same inhaler without any change to the prescription. And then once you're on MART and you're doing well, you may be able to step back down to air again, again with the same inhaler, same prescription. And therefore you only need to do inhaler technique education once. You reiterate it to annual reviews, of course, but it's reinforcement of the same technique, not changing techniques. Same inhaler. I say to people, you know, this is my inhaler. There are many like it, but this one is mine.
And this is the one that I will use. This is all I need to learn, my one inhaler. And my personal view on this is I think it's a really good step forward. It really simplifies how asthma is treated. And most importantly, it aims to get us to a Saber free future. That's a nice tagline of what we're aiming for is to no longer use Sabers, short-acting beta agonists. Because we know they're linked with increased mortality, they can be dangerous. Any asthma death is one death too many.
and we should be aiming to treat an inflammatory disease with an anti-inflammatory treatment, which is what this is trying to do.
Dr Ben Warner (11:35)
Brilliant. Thanks. That's a really nice, clear overview and shows the scale of work that there is to do. But also, as you said, it's almost a simplification or rationalization of what we're doing, actually using the most appropriate drugs for the disease, the pathology underlying it. I guess it's maybe worth just touching on because you've mentioned this association between ovies as sabers, B-dragonists and mortality. And then some of the reticence about for mutarole being used.
long-acting B-trigon is being used repeatedly in Mark or Air. Presumably the actual association is more driven by a reflection of poor asthma control rather than the drug itself. I appreciate there are side effects. Maybe we can touch on those from the sabbers, but someone who's using a lot of sabbers is an indicator that their asthma is poorly controlled. It's not the sabber themselves killing the patients.
Dr Tom Fardon (12:26)
You bring up a really important point because it's hard to tease those things apart, but I think it's a combination of things. For sure, people who have moderately severe asthma, who don't take an anti-inflammatory treatment and rely just on a sabba, are at incredibly high risk. And as you say, the sabba use is a reflection of their underuse of other appropriate treatments. There are reasons for that. Steroids don't necessarily make you feel better, not straight away, whereas a sabba you get some benefit from.
And there's still some worry in some quarters from some patients about, don't want to take a steroid because steroids are bad for me. Which is frustrating for us all of course, because we know that a small dose of inhaled steroid is hugely beneficial and saves lives. What we're trying to avoid is people getting onto oral steroids and that's why biologics is such a win. But there are some social size to this or socioeconomic angles to this that if you're in a country where people have to pay for their prescriptions.
then if you have a preventer and a reliever, that's two prescription charges every two months. And then some people in a position where they can't afford to pay for both of those things, or they make a decision to only cash in the script for one or the other because of financial constraints. So if you have the choice of paying for your brown inhaler or blue inhaler, then often people choose the blue inhaler. And that game, as you say, reflects poor overall understanding of asthma control. There was a study done many years ago.
in America called the SMART study, which looked at long active beta agonist use because there was concern over long active beta agonist use. And there are differences depending on your socio-psychotic background, but also on race. And it was shown very clearly that black women, particularly, did far worse when they were given a long active beta agonist alone without steroid. I think this was maybe in the late noughties. And this is one of the studies which triggered trying to think, how can we
combat the overuse of beta agonists generally and overreliance on beta agonists. And if we look back at the noughties, the landmark studies that showed that long acting beta agonists are very effective. like the Optima study, for example, way, way back in 2000, the outcome measures in those studies that showed that they were effective was FV1 long function. And of course a long acting brocadilator improves your lung function.
But if you look at that data again, and the facet study is the other landmark study, if you reanalyze the data and look at exacerbations, then patients who got more steroid had fewer exacerbations. People who got long-acting beta-agonist had fewer symptoms, got better FV1. And back in the bronchodilator era, we were very keen on FV1, but now we're in the inflammatory era, we're more keen on exacerbations or at least have reduction of exacerbations. So we were driven for a long time pushing long-acting beta-agonists.
Dr Ben Warner (15:03)
we
Dr Tom Fardon (15:16)
pushing for FV1 with less concern about exacerbation. As now we're into the era where we want to reduce exacerbations. It's not that we don't care about FV1. Of course we do. care about lung function, but we have an understanding that the reduction in lung function is generally driven by exacerbations as inflammation, not by smooth muscle by itself. So I think that increased use of short-english vaginus is, as you say, is a signal.
It's a signal that asper control is not good, that their exacerbation frequency is high because people use their short act to be dragunist during exacerbations and that a different approach is needed when patients are rattling through huge numbers of short act to be a dragunist. Again, I think that's what's driven us towards this approach of this is one inhaler, make it simple, make sure we're treating an inflammatory process with an anti-inflammatory drug whilst also giving symptomatic relief on top of it.
Dr Ben Warner (16:08)
That's such a salient point, not just for asthma or even respiratory medicine, but more broadly. It's so interesting that the choice of outcome in a given trial can really change the landscape. And if you're aiming for lung function in a short-term trial, you may see improvement with bronchodilators. But if you're aiming for reducing mortality and exacerbations, as you say, you get a different result with a different drug.
Dr Tom Fardon (16:32)
That's a lesson that's taken us too long to learn. Long function was the primary outcome in so many studies for so long. And if we sidestep into the other main airways disease of COPD, the thing we were trying to alter, the thing we were trying to change, and I always turn to the Eclipse study because it looked very closely at what does FV1 predict. And the only thing FV1 predicted in that study was what the FV1 will be the next time you measure it.
And I think that again changed our view of what is it we're trying to do? What's the most important impactful outcome to measure? And in asthma, it's exacerbations. Because exacerbations ultimately lead to mortality. They drive lung function decline. They drive quality of life. But critically, exacerbations are managed with oral corticosteroids and oral corticosteroid burden is strongly associated with poor outcomes long-term and cost.
So whatever we can do to reduce exacerbation frequency is going to reduce steroid burden and therefore we're going to have better outcomes as we go on. It's not that I don't care about FV1 and I certainly care about lung function. It's not my primary concern now when I'm seeing people with asthma.
Dr Ben Warner (17:46)
Perfect. So let's go in a really nice context to the guidelines and motivation for them and a bit of history. We've touched upon the treatment and I want to come back to that, but just before we do, the structure of the guidelines that begins with talking bit about the diagnosis of asthma, there's an order of tests that they now recommend. Would you be able to explain what that is? Has there been a change to that? Maybe some of the rationale behind it.
Dr Tom Fardon (18:15)
Asthma has always been difficult to diagnose and that maybe sounds a little ridiculous for something which is so common. And I've said earlier on, know, 30 % of people have diagnosed with some sort of wheezing illness, but there is no gold standard test for asthma. There are various different phenotypes of asthma. It presents at different ages in different ways and trying to make a single straightforward test for asthma is impossible. The previous guidelines comprehensively gave a list of
signs, symptoms, patterns that favor a diagnosis of asthma and those which would push you away from a diagnosis of asthma gave you a high probability, a low probability, an intermediate probability and suggested some tests, which I think was a good approach, but was complicated and required a lot of subjectivity. The new guidelines try to make this more straightforward and try to tilt us a bit more towards doing tests of inflammation earlier.
So once you have a clinical history which suggests asthma and that is wheeze, intermittent breathlessness, nocturnal symptoms, worsening symptoms with viral infections, et cetera, A to P allergy, the usual things that we associate with asthma. Then the suggestion is to do some tests of inflammation. So in adults, it's check eosinophils, do of exhaled nitric oxide, of phenol as the first line tests. My view is that this is a good thing to do.
The earlier we can do tests of what we call TH2 inflammation, the TH2 T-Helper cell type 2, the earlier we can do that, the better it is for me as a severe asthma doctor because the sooner we will recognize people who have TH2 inflammation driving their asthma and the sooner we can see people to offer them biologic therapy. And the most powerful measurement of that by some margin is eosinophils. Eosinophils are linked to
exacerbation frequency, they're linked to decline lung function, they're linked to symptom control, they're also strongly linked to responsiveness to treatment, which is helpful. But the eosinophil really does drive asthma in this cohort of patients. So if you've got TH2 driven asthma, the eosinophil count is really, really important. And we've been measuring eosinophils for free, effectively for decades, because it's part of your full blood count. It's one of those tests that is underneath white cells and neutrophils that perhaps no one really looks at.
But I try to drill into people. It's really important to look at sinophils and to look back historically at ear sinophils. You'll know that when people come in with an asthma exacerbation, they've often been given steroids by ambulance service out of our GP, ED, et cetera. We then measure their full blood count. Their ear sinophils are zero. So looking historically to say, well, what was the ear sinophil count when they were sick is incredibly helpful. And we will see often that ear sinophils have been very high.
periods in the past than they're low when they're measured in hospital when they've had some steroids. So the ESNFL cap at diagnosis is really helpful. They're not had treatment, they're not had any steroids. And what is it right now when they're feeling rubbish because they've come to see the GP? Opheno is valuable. It's easy, it's relatively cheap and it's quick. There are machines that you can have on your desk. The test takes a
about all told probably a minute. It's 10 seconds of breathing out and 45 seconds of booting up and giving you a result. And these machines are getting cheaper and it comes out to probably about between five and 10 pounds a test. So that price will come down, but in terms of cost benefit analysis, if you can prove that a pheno is very high at presentation, it's very strongly suggest that someone has worse asthma and then you can titrate treatment to reduce exacerbations, et cetera. So
An ear sinophil is a simple blood test. A pheno is a test, which I think we need to get into primary care everywhere so that there's access to it. And if those tests are positive, then you've nailed your diagnosis of asthma. And also, you know what kind of asthma it is. And as soon as people exacerbate twice, then the Scottish severe asthma pathway is that there are two exacerbations. Then you should consider referral onto a severe asthma center for consideration biologics. And if you know from the beginning, then you can get early referral onto definitive treatment.
The old school tests of doing a peak flow chart and doing FFV1 and reversibility and ultimately a bronchial challenge test, bronchopropatication, so a mannitol, methicolin or histamine charge, they're still in there, but they're later on in the algorithm. And I think that reflects that, well, for peak flow charts, a positive peak flow chart, if it's done properly and the patient hasn't cheated and filled it in in the waiting room beforehand, then is a very powerful thing. it's, you you feel...
confident the patient's done the peak flow chart well and it shows variability, diagnosis is nailed down. But a normal test, its negative predictive value is very, very poor. So always be cautious with that. I quite like peak flow charts for the right patients, but only when it's positive. Reversibility is great again if it's positive, but if you have a hundred percent FV1 before pre bronchodilator, then it's not going anywhere. You need to see people when they're their worst, not at their best. And a bronchial challenge is hard to do.
Not every center has it. Certainly no one in primary care is doing them. And even in big centers in secondary care, they're time consuming. You have to get your patients off treatment if they're already on it. So there are challenges with that. So you have at one end, simple tests, which are very powerful. And then in the middle, some tests, which are powerful if they're positive and at the far end, things which are difficult to do. So we're not there. We don't have a gold standard test of what is asthma or what isn't, but we've certainly got tests which now help us.
place people into a phenotypic bucket so we can say, you have TH2 high asthma? This is the likely time course and this is the journey you're likely to have. But also we've got some tests in our back pocket that say, well, if it's tricky, we can always send you for a bronchial challenge test.
Dr Ben Warner (24:01)
Brilliant. That's a great overview and absolutely nice description of how you can try and get people off the diagnostic pathway early on, or rather, you know, onto a diagnostic label as early as possible to get them on the right treatment as early as possible. I suppose on the point of the peak play variability, you mentioned about the right patients for it. I imagine, my experience, occupational asthma is quite a nice setting for that. If you want to see the context where things are worse.
Dr Tom Fardon (24:28)
So in occupational asthma, really the only meaningful way you can make that diagnosis is with a peak flow chart, but it has to be detailed. And that's difficult for most people to do. We need six weeks of data with time at work, time off work, ideally with a period of vacation or fourth time away from work of at least a week. And we say to do a peak flow six, eight, 10 times a day.
Every time the patient has symptoms or takes a reliever inhaler or takes their air or mart, every time they take an inhaler, take their peak flow beforehand. And most people simply just can't do that because of their workplace that they're in or just because it's very, very arduous to do. So again, if you get a good peak flow chart, which you can put into the Oasis machine and get the data out, that's powerful diagnostic tool, but it can be so difficult when the data is sparse. And beyond that doing
Challenge tests in an occupational asthma pathway is very difficult and requires super specialist centers.
Dr Ben Warner (25:30)
Okay. Sticking with peep throat, among other things, I suppose, having talked about diagnosis, perhaps it might be worth thinking about what we review when a patient with asthma then comes back to clinic or to their GP or, you know, opportunistically, if they present with an asthma exacerbation. So I wondered if we could talk a bit about the kind of things that you would want to review with a patient in terms of...
How well controlled their asthma is, their understanding of their condition and of their treatment. What sort of questions you ask at review, what you want to cover.
Dr Tom Fardon (26:08)
So I mentioned earlier, thing that I'm most interested in is exacerbations. So my first concern is how many exacerbations have you had? So we define exacerbations by have you had some steroids? So that can be straightforward. can look up on the prescribing system, how many steroids have you had? People have at home steroids, they get steroids through ED and through pharmacies and out of hours. So all is important to delve into that to find out how many steroids people have had.
And if people have had over two courses of steroids, then that pushes you towards referral onto severe asthma centers to try to think about biology. If they're not exacerbating frequently and are not at that sort of threshold point, then symptom scores. So your ACT, Asthma Control Test is straightforward, simple thing to measure. We use ACQ and the Severe Asthma Service. It's five or six questions, depending on whether you need ACQ-5 or ACQ-6, that look at symptoms in the previous week.
And we know that a score of 0.75 or less is very well controlled, but 1.5 is poor and something in the middle is kind of okay. And it takes about five minutes to go through the questions, but it's really valuable because you can track how patients are going. So although because the questions are quite subjective, between patients is not very good. You can't compare me and you, for example, because we might have a different perception of breathlessness or a different perception of what's limiting us. But within a person,
It's very valuable because your perception remains the same always. So I can track how you're doing. getting those scores done and tracking them through time is valuable because if you've been trucking along at 0.6 for years and then suddenly it's 1.5, something has changed and that's very valuable. And then always check inhaler technique. That's really important. Check inhaler technique at every opportunity you have to see people because people do slip and people do the strangest things. People blow into inhalers. People do sort of
double sooks or they don't hold their breath or they do. So it's always worth checking. And then we want to know how is it limiting your life? How is it impacting on what you can and can't do? Have you got any other new diagnoses of things? And if people are having exacerbations, oftentimes when people get referred on to me, the referrer will say that they're exacerbating frequently and getting chest infections.
Dr Ben Warner (28:18)
or
Dr Tom Fardon (28:29)
one or the other or both. And the patient will come to me and I say, can I help? What's the problem? And they'll say, I'm getting lots of chest infections. So what is an exacerbation? What is a chest infection? How people refer to what's going on. think is actually really important because what we don't do very well at exacerbation times. And you mentioned, you know, if you see people at ad hoc, as with opportunistic times to see people, sometimes that's in hospital.
We don't do very well as phenotype exacerbations. We don't say what is actually going on right now. We often see someone who's got an asthma diagnosis. They come in, they're not as good. They get antibiotic steroids and it's called something. The patient thinks they've got a quote chest infection. They may have been told by someone it's a chest infection, but there's no clear evidence that they have actually gotten infection and what it is. Is it bacterial? Is it viral? Is it none of those things? Is it actually an inflammatory episode?
versus an infective episode. So what is an exacerbation? think is one of my personal sort of hobby horses and things that I really want to try to get people to dig down to is what is phenotyping those exacerbations. So when I see people for review, I say, have you been in the last six months or the year? I've had three chest infections. And okay, what do you mean by a chest infection? What happened? Did we get an eosinophil count? Did we get a neutrophil count? CRP? Was a chest x-ray done? Did you have cough and spit, yellow sputum, fevers and RIGORs?
Or actually were you much more wheezy? You woke up in the night, you were really tight in the chest, you were really wheezy, you just bought a new cat. We did your eosinophilic amputic with 1.2, your neutrophils were normal, your CRP was normal. Which is a very different story, and it's a very different pathology and a very different treatment. So I think you've got at one end the people who are on air, they're doing very well, you review them, they've not exacerbated no steroids, you can do an ACQ and ACT, their scores are stable, their inhaler technique is great, you reinforce that they should keep taking it.
And that's great. You've got the people then in the middle, they're not exacerbating, but their ACT is a bit high. They're not so well controlled. You might consider going on to Mart and then the people who are exacerbating and you think, well, this is not so great. Can we phenotype those exacerbations? Can we look at whether it's infections or inflammation and then early referral onto a severe asthma center. You can follow the Scottish Severe Asthma Pathway in England and Wales. There's the accelerating access pathway to look at instead.
Dr Ben Warner (30:50)
Brilliant. And I think the guidelines now talk about actually not using peak flow so much for monitoring, but like you're saying, trying to phenotype what's going on, would you use pheno? You mentioned, obviously we often take bloods and end up by happy coincidence, having a full blood count and therefore in a full count when someone's unwell. But would you be using pheno, exhalometric oxide routinely in the monitoring, the review of patients?
Dr Tom Fardon (31:16)
So I do, I think it's really valuable, it's because it's so simple to do, it takes, can you breathe out for 10 seconds at a constant rate, as long as you can do that, then you can get a phenol and you get an immediate result, it's a bedside or deskside test. Whereas one of the challenges that's pushed back to me by primary care often is that if they're seeing a patient for seven minutes in their clinic room on a Tuesday morning and I'm saying to them, we'll get an eosinophil count, it's more like that will require booking in to see the phlebotomy service at some point.
getting the result back 24 hours later from that, by which time three days has gone by in the what you do. And I completely accept that. But a phenol you could do right there and then and gives you a hard number, which, and if you've done it before at diagnosis, you know what the baseline is. So I increasingly do that. I think it can be very helpful. We see patients where the diagnosis is challenging. So people who have been treated for asthma for some time or they have very bad symptoms, episodic symptoms and asthma is high up the list of possible diagnoses.
But all the tests are negative and continue to be negative. And if we can see them during exacerbation and then we do their eosinophils and their pheno, we wait for their eosinophils, we get their pheno immediately and it's 200. That's incredibly helpful. It's also very helpful to me to see people who I think they have a diagnosis of asthma, but their symptoms are something else. That they're not exacerbations of asthma. They have a well-controlled asthma, but it's something else as well. A normal pheno at that time helps.
build the body of evidence that there is something else going on. And we talk quite a lot in severe asthma clinic about asthma plus syndrome. So asthma plus something else, just cause you're a labor with asthma, then it can be easy to attribute everything to asthma. But if your aspect is well controlled, you're starting symptoms, your feeder remains normal, your ethanophils remain normal. What else is it that's driving things that first of all helps make us look harder. So rather is this asthma again, have some steroids. It makes us look harder for the extra thing.
but it also helps the patient to understand that there is something else driving the symptom. So the archetype of this is ILO. So if you've got intermittent laryngeal obstruction, which we used to call varicocortis function, the symptoms can mimic asthma very closely. And by perverse fate, ILO is more common in people with asthma than it is people who don't. And when someone who has both diagnoses presents to us with breathlessness, tight chest, feeling in their throat, cough, whatever,
If you can get the pheno done and it's zero or negative, then that helps build the evidence that this is an ILO episode. The patient comes in with the same symptoms, their pheno is 150. Well, this may well be asthma and then say to the patient afterwards, well, did you notice anything different? This was an asthma attack. The previous one was ILO. What?
you feel that helps you differentiate between the two and help build that dialogue and so we can help in the future. So I think pheno is a great tool. think you need to be cautious because there are false negatives, false positives, but as part of the package of trying to personalize treatment for patients by phenotyping each exacerbation, I think it's really valuable. I'd love that to be more phenomachines. I think it would be great if we could get them into EDs and into our acute services and crucially into GDP practices.
Dr Ben Warner (34:23)
Brilliant. On that, trying to personalize the treatment, think that leads quite nicely onto our treatment algorithm that forms the next part of the guidelines. You've you've mentioned about AIR and MARQ. Briefly, could you talk us through the first steps? And I think an important point to think about here, you mentioned it's such a step change, these guidelines from what we had before. This, and the reason I mentioned about the reviews is that
Dr Tom Fardon (34:32)
touched on this
Dr Ben Warner (34:50)
This is both for people that are newly diagnosed and we're thinking what do we start with? Where do we start in this algorithm? But also when you're reviewing an existing patient with asthma, I guess it's a chance to see how do we get them into this new paradigm of treatment and where should they fit in that?
Dr Tom Fardon (35:08)
For the new patient, new fresh diagnosis of asthma, the guidelines are very straightforward because you make an assessment of the severity of asthma. Is it mild or is it moderate? And how do you make that assessment? Well, I think you think about how did they present? Was it an insidious, mild thing and they've presented early. They're generally very well, but have a worsening of symptoms with a certain pollen or in certain weather conditions. And generally they're okay. You'd say that's mild asthma. If they presented to you with what in retrospect is an exacerbation and you're thinking about, well.
they would have had oral steroids for this or maybe they will get oral steroids and they have a significant deterioration in their baseline, then you might think that that's moderate disease. So for mild disease, then air anti-inflammatory reliever, spend some time with the patient explaining what you're doing. This is my inhaler. There are many like it, but this one is mine. This is all I need to take. I just take this one, I'm unwell. It's very simple to understand. That's me. If you think they have moderate asthma and you think that they will need more than just an anti-inflammatory, that's strata mart. That's a bit
more of a conversation, but it's still the same thing. This is my inhaler. There are many like it. This one is mine and I will take it twice a day and then I will take it whenever I need it. That's fine as well. And then I think you then safety net with the, you exacerbate, as in you go to see somebody somewhere in the land and you are given steroids and you get to two of those in a year, then you must come back and see me because of those things we can then do. We'll do some more tests and you may be referred onto a specialist. And that's important to do at the start because I don't think we do that very well.
And people linger out in the wild frequently exacerbating without being referred. So I think for the new starts, that's relatively straightforward. But the person who's had asthma for some time, it's more difficult because we have a parallel system that's running, which is the old system of reliever and preventer. And running two systems at the same time is difficult. The analogy I always think of is when Sweden in 1967 changed which side of the road they drive on.
So they used to drive on the left as we do in the UK and they made a decision to move to driving on the right, presumably so that when they drove into Norway or Finland they didn't crash their cars. But they did it overnight, just one day in September in 1967 and for one day the traffic lights were all switched round and the road signs were all switched round and people crashed into each other for a day because they didn't know what to do. But very quickly after that they quickly moved to driving on the right.
We've not done that. What we've effectively said is if you've started to learn to drive, drive on one side of the road, but if you've been driving for some time, it's all right. You can be on the other side, but you can swap over if you like. The natural thing here is that it's going to be complicated and that people will be confused. But we're a year into the guidelines now. And actually I worry about people being confused. We're bit overly worried about it. But what we have seen is that people are reluctant to make the switch. So we've always said is if you were driving on one side of the road, just stick to it. It'll be okay.
What the guy then actually says is that at review, if the patient is stable, then you can leave them alone and that's fine. But you should consider in all people whether it's appropriate to move across to the new treatment of air or MART. So for example, if you review someone and it's evident from their dispensing, prescribing data, or you just ask them, they're not taking their preventer, they're just taking their reliever. Absolutely those are the people that you should move on to air.
because we know that those are high-risk people, they're not taking their steroid, they're overusing their sabber, sabber reliance, so get them switched over. So that's one group where you can really make a difference. Group two are those people who are underusing their ICS, so it's those people who are only prescribed a sabber, and we should absolutely not do that. The people who are overusing their sabber, and we should switch those. Then there's the people who are poorly controlled, so they're taking in their inhaled steroid, they're using a lot of sabber, they're exacerbating...
It's an opportunity to say, we could switch you to a different process here because if we can move you onto Mart, that may be all you need to change to get you better control. If that change to Mart doesn't work, then we'll do some phenotyping and we'll maybe refer you onto a biologic. And it's the start of a conversation. And then it review that are people who are exacerbating very frequently despite best efforts and then they should be referred. So I think in my head, we have these groups of people who are prescribed a sabbat only. They should definitely be changed.
The people who are either only taking their sabba or they're overly reliant on it, they should definitely be changed. The people who are under using their inhaled steroid certainly strongly consider changing. And those people who are already effectively doing PRN treatment. So they take their inhaled steroid when they feel worse and they stop taking it when they feel better, which is the human nature of just taking things when you feel bad. They would be much better off moving formally onto the air and mouth rather than just sort of doing it by the back door.
So certainly opportunity to make those changes and don't be afraid to do it. People said to me, well, they're fine. They're fine on there twice a day, bit of preventer and then some reliever. Well, they are fine, but they might be better if you put them on to modern treatments. So I think don't be afraid to make those changes, but be prepared to have the conversation.
Dr Ben Warner (40:12)
There's a BMJ article last year optimizing it, health therapy for patients with asthma. actually one of the things it suggests that we do is raise expectations of asthma control. And I think, you said, if somebody is stable on treatment, then we might leave them alone. But actually what is stable, a patient may have lived with their condition in a fairly poor state of control for many years and they expect that's as good as they are going to achieve. And actually what we should be aiming for, well, perhaps you could share with us, what would you...
see as being stable? What is control of asthma? What should we be aiming for?
Dr Tom Fardon (40:47)
You bring up a really interesting but difficult topic of remission. What is remission in asthma? It's talked about much more in the severe asthma sphere and talk about biologics because we want to think if we've given biologic treatment, have we achieved remission? And the severe asthma community across the UK and worldwide is slowly coming together to what does remission mean?
Remission is most commonly used, I think, in oncological circles. So in cancer, if you are in remission, your cancer has gone away and you're no longer at risk. You you're quote cured. We can't cure asthma. We can control it very well, but we can't cure it. can't take away the disease. So what does going into remission mean? So you could argue that it's not having any symptoms, having a normal peak flow every one being on no treatment or minimal treatment. Then you could add in.
Your inflammatory markers, are they low? Is your phenol low? Is your ESNF low? Is your ACQ less than 0.75? So that's at one end. But then is that unreachable in some of our patients? Because some of those tests, ACQ particularly, is so subjective, you may never reach that. So we've spoken about total control in the goal study back in 2004, I think around there, talked about achieving total control of asthma. And that was a high bar.
The high bar being no symptoms, no sabber use, no nocturnal awakening and certainly no exacerbations. And at the time we would still, well, that's too high a bar. We can't reach that in our pages. They're always going to have something. But actually most people can get to at least very mere total control. If you take four out of the five criteria, most people can get there. And I think we have normalized steroids use in severe asthma. We've normalized symptoms in asthma, even just in popular culture.
Often there's references to, this kid couldn't do sport, I'll pee at school because they had asthma. Often there's sort of the wheezy kid that's a bit sickly and can't do things. And anxious people in TVs and movies puffing on inhalers. We've kind of normalized that, yeah, if you've got asthma, you're going to be sickly and wheezy and your goal is going to have symptoms. So I think you're right. We need to push harder to say that if you are, as you said, stable, but that stability means three courses of steroids every year.
That's not good enough and those people should be referred to as vrasma center. bit stable, but I don't do any sport because it makes me wheezy is not enough. And we should be saying, well, why can't you do that? What's the trigger for that? What can we do to help you have a healthy lifestyle? You can go for the run that you want to do or play badminton with your kids, whatever it may be. And I think that we have more options now. We have options because we have different inhaler devices, different routes of inhalers.
We can try to make it so that it's not a crime, sin to have asthma and that because you have asthma suddenly you can't do a whole load of different things. You should still be able to live an active life and still have a good quality of life. If you've got asthma, it gives us lots of options.
Dr Ben Warner (43:52)
options, I appreciate we not got limitless time, but it would be great to hear a bit more about these options of inhalers. So obviously we've talked about the sort of high level theory of air and marts and lab ICS. Could you give us a very brief overview of what inhalers there actually are, what the choices are and how you decide which inhaler to give to which patient?
Dr Tom Fardon (44:15)
In general, sort of globally, the best inhaler for the patient is the one that they can take. Whether you're talking about control of asthma, about cost, about carbon footprint and impact on the environment. The worst thing for patients is to have an exacerbation. And if they've got exacerbations lead to increased morbidity and ultimately mortality and worse quality of life. They're expensive to go to hospital, use out of hours, it's expensive to get steroids. So reducing exacerbations is really important.
And if you don't take your inhaler, you increase your risk of exacerbation. So time spent at the beginning of the journey, exploring inhaler technique so that we can get that nailed down early is the best thing for the patient. Now, having said that, if we assume that most inhalers these days are easy to use, straightforward, they all require very little in the way of inspiratory flow and the patient is able to follow instructions, then you're left with
what inhalers actually can be used for this. So we're limited a little bit by licensing and the licensing in the UK at the moment for air are three inhalers and they're all formotrol containing inhalers because they have to have formotrol in them. And they are Cymbicort, which is Bidesonide plus formotrol in its turbohaler form, which will be familiar to most people who listening to this podcast, I'm sure, been around since the early nineties. There's an inhaler called Wokair, which is probably not
well known to people, but it's the same contents as Simbicort, but in a different inhaler device. And then the SpiroMax DuoResp, which is an inhaler, which looks like an MDI, but it's actually a DPI. So all three of these inhalers are dry powder inhalers. There isn't a metered dose inhaler, old school as it were, poosh and squish sort of inhaler. They're all dry powder inhalers. So they all require a more forceful inhalation rather than a slow and steady inhalation because there's no propellant. You need to drive the inhalation with your own inspiratory flow and then a deep
breath hold at the end of it. Each individual health board or down south the trusts will make their own formative decisions about which of these inhalers to use. But the choice is familiarity with the inhaler, cost of it obviously important and evidence base, most of which the research was done with Simbicort in the build up to the licensing and the change of guidelines and Simbicort is very familiar to people. You need to spend some time explaining what the inhaler is, how it works, what you do with it.
And of course, if the patient is unable to use a dry powder inhaler for whatever reason, then you have to move to other inhalers with other propellants, an MDI and a spacer, which then at the moment there's no license indication for those. I was at the British Thoracic Society meeting last month. I chaired a session on inhalers and there were a number of studies that were presented using the air process with other inhalers. So with Beclamethasone and Fomotrol, for example. So the treatments like foster or Lufobec.
So rather than Bidestinide, it's Beclomethazone. And of course the evidence was these treatments worked very well. There was non-inferiority to Bidestinide and the same sorts of results. So it's my suspicion that the licenses will extend and that we'll have a lot more choice. There's no rationale why you wouldn't work with Beclomethazone rather than Bidestinide. I don't think anyone would argue that Bidestinide has anything special in it that's any different from Beclomethazone in this context. And the BTS Sign Nice guideline does say
use the licensed drugs, but you may wish to consider other drugs that contain formoterol. So I think it's up to local health boards, local formularies, Trust Damn South to have these discussions and to make sensible, realistic medicine type decisions about what inhalers you can use. But at the moment, the license indication is limited to those three choices. My experience has been that the vast majority of people are absolutely fine with a dry powder inhaler and that we've had
very very few people who we've had to move back to an MDI with a propellant because the DPI's are so straightforward to use.
Dr Ben Warner (48:16)
That's really helpful just to remind us that the inhalers are both a device and the combination of drugs within it. So as you said, the dry powder inhalers and the pressure metered dose inhalers driven by a propellant. You mentioned the dry powder inhalers, you need to take a sharp breath in. So obviously somebody needs to have the capability to do that. But conversely, I guess the metered dose inhalers, they may be historically what people picture when they think of asthma, as you said, someone puffing away on it, but actually it's not.
All that simple is it. mean, you need some coordination to get that down into your lungs and not just hit the back of your throat.
Dr Tom Fardon (48:49)
Yeah, and this is what the irony of things is that we've been using MDIs for a long time and it is in the public eye of, you know, what is the pooch and squish type of inhaler, the pressurized metadose inhaler, but it does require quite a lot of coordination of initiating the breath, the inhalation, pressing at the right time, continuing in a slower, steadier inhalation. And if you use a spacer, then that is made a lot easier, but then you need to carry a spacer around as an extra bit of kit, which a lot of people don't like carrying around with them.
And we know that the evidence is that the older you get or the less likely you are to be able to use an MDI inhaler properly. Yeah. In the UK, we're really married to MDI use. And I'm sure that many who are listening will be well aware of the comparison to the Nordic countries where well over 80 % of inhaler use is DPI, less than 20 % is MDI. And we're the other way around that in the UK, over 80 % is MDI. Yet they have no worse outcomes than we do. In some regards, they have better outcomes than we do.
And there's a very clear carbon footprint benefit to using DPI's than there is MDI's. And in the ASPA community and the CPD community, we've been, think for years now trying, albeit slowly, but we have been trying to push towards using DPI's rather than MDI's and also to push the manufacturers MDI's to make them easier to use better propellants, lower carbon footprint, really push that along. And that has started to happen.
but you can be more confident if you pick a DPI as your first line inhaler, that it's going to be easy to use. It's going to be good for carbon footprint or better than other inhalers and it's going to be reliable and most people will be able to use it with good outcomes.
Dr Ben Warner (50:27)
think that it's so important that people do understand the benefits and the rationale for those different devices. Because as you say, I think it is increasingly entering the consciousness of clinicians that there is a carbon footprint to what they're doing. you know, 13 % of the NHS's carbon footprint related to delivery of care is from inhalers. And that is massively driven by these MDIs. But that's not the only reason, or in fact, it's not the most important reason for the decision.
around what you give a patient. There are all these other benefits to DPI's in certain contexts. And as you say, even not all MDI's are created equally. There are some that have much worse greenhouse gases within them than others. And ultimately, absolutely an inhaler that gets used within a couple of weeks and then needs another prescription is much worse than two inhalers in a year that are used well, whatever the inhaler is.
There is a really nice website, GreenupFactus, which I'll put a link in the description about the carbon footprint of inhalers and how we can improve our prescribing. But a lot of it is around actually having a discussion with patients about how to best control their asthma.
Dr Tom Fardon (51:39)
Yeah, absolutely.
Dr Ben Warner (51:41)
So you've given a really clear overview of a lot of the inhalers that we might use. think just very briefly, I lamas and leukotriene receptor agonists, they're still in the guidelines, as a sort of give it a try and importantly, if it's not making a difference, stop it. But you said again and again, if somebody is needing repeated steroids, we should be referring to specialists for specialist interventions. And predominantly nowadays that means biologics. So it's a massive topic. It's a huge field.
We've got maybe two or three minutes. Perhaps you could just give us a very brief overview of what biologics are, which ones there are, broadly what they're targeting on Higuis and Fo.
Dr Tom Fardon (52:23)
Yeah, so obviously biologics are my favorite topic and we could spend another hour, but I'll try and be brief. First thing, just importantly, you mentioned about lamas and leukotriene, septuene, antagonists and all those other things. They are still in the guideline, but they're in a box below the point of referral onto biologics. And if at the point in the guideline where people have exacerbated more than twice, fully controlled asthma,
Measure TH2 markers, so an incident-filled count of phenol, and if they're high, then straight to a severe asthma center for biologics. If they're low, so we think it's not TH2 asthma, there's no TH2 signal, then go on to give Lammers and to give lymphocytogenesis to antagonists, et cetera, et cetera, as you've described. Trial, stop if it don't work, and then consider referral. So the point is that if there's a TH2 signal, then the evidence is very strong to use biologics rather than playing around with other things.
So that's an important message. So what happens when you get referred on a severe asthma center? What we're looking for is trying to find patients who've got a strong TH2 signal. And therefore we know that eosinophil driven inflammation is what's causing their exacerbations. And those are the people we want to find out about early because we know early intervention improves outcome dramatically. The license indication for biologic is for people who've had three or four exacerbations in the previous 12 months, depends on which biologic.
In Scotland, when we looked at this in 2024, the mean number of steric courses in the year prior to initiating biologic was seven. So people were waiting a long time before we think about referring for biologics. So we can refer much earlier and we can treat much earlier. The biologics are all centered around TX to inflammation. The aim is to reduce eosinophil proliferation, maturation, and migration into the lung tissue.
because eosinophils are increasingly convinced they're not just a marker, they're not just like pheno, a marker of their big inflammation. They are the effector cell that is causing the damage. They degranulate and produce lots of toxic materials which cause damage. They make extracellular traps, which are DNA rich secretions, which we knew came from neutrophils, but we now know come from eosinophils as well. They increase mucus production, they lead to Charcolydon crystals and mucus plugging.
We think that they are really important cell in the middle of asthma. The biologic treatments are targeted at IL-5, which is a very potent driver of es-nfil activity. IL-13 and IL-4, which as well as driving es-nfil activity are involved in IgE production and class switching of IgG to IgE. And the most modern of the biologists is anti-TSLP. TSLP is an alarming. So alarmins are...
the IL-33, IL-25 and TSLP, they are the signals that are triggered by the epithelium. And we think it doesn't really matter what the trigger of the epithelium is. The alarm ends are released in response to epithelial trauma. They then start the cascade, which then leads to increase ultimately IL-5 production and IL-13, IL-4, and then the es-NFL activation, mast cells, IgE, et cetera. So we can act to suppress the es-NFL function.
and activation by giving biologics early. The choice of what we give depends on a number of things and there's a little black box of what happens in severe asthma MDT. But ultimately we need to see the patients early who have a TH2 signal so that we can then put them through the process of evaluation phenotyping and come up with the best biologic for them as early as possible. And they work. They really work. It's one of the most rewarding things about doing severe asthma clinic is that
Patients come in for assessment and they're miserable. They're getting up to on average seven courses of steroids in a year. Their quality of life is terrible. Their side effects from the steroids are high and they've spent years like this, years and years and years. We put them through the process. They get a biologic. They come back three or four months after initiation and they are delighted. I I couldn't believe that this is what everyone else feels like. I've not had any steroids. I've not touched my blue inhaler. They often say.
And they're asking, can I reduce the treatment? This is amazing. So for the right patient who has eosinophil driven disease, and we can measure that for the right patient, can literally transform lives. It doesn't work for everyone. And sometimes it's second line, third line treatment. But as we've been doing this for the last five or six years, I think we increasingly have the confidence that we can pick the patients who are going to benefit. And they really do benefit.
It's phenomenal how the improvements in quality of life we see with some people.
Dr Ben Warner (57:07)
And these are monoclonal antibodies, they're targeting part of your immune system. But I know we think of other drugs in the same sort of category as being quite, you you treat them tentatively, cautiously, but eosinophils, evolutionarily they're your response to helminths and parasites, which happily we have less exposure to, at least in the UK now. Are there concerns about patients' exposure to infection or can we just say the side effects are pretty minimal from these really?
Dr Tom Fardon (57:36)
I like you was taught that eosinophils were evolutionary. They dare to treat helminthic infections and to stop us getting worms. So when the IL-5 monoclonal antibodies, particularly Benrylizumab, which is very, very potent at suppressing eosinophils, it could almost go as far as say eradicate eosinophils. That though people will be at high risk of those infections, but that signal just simply isn't there. that
Trials have been carried out in South America and in Africa where there is a much higher incidence of helminthic infections and there is no signal for those infections. If you look in the BNF, it will say that these drugs have a side effect of increased infections, but that doesn't bear out in clinical trials and in the severe asthma community, it's not something we worry about at all. The side effects of the drugs are generally mild, they're generally short-lived, injection site irritation.
headache, can sometimes last a few hours after the injection. Sometimes abdominal pain again, which is short-lived. is an unusual incidence in some people of hair loss, but you can generally detect that quite early and switch to a different biologic. Dupillomab has been associated with some eye complications. Again, this is usually in people who already have eye issues and we have alternatives and tesapillomab, which is the anti-TSLP biologic has around a perhaps 10 % incidence of arthralgia. So apart from that,
And we consent all our patients to understand these risks. The risk benefit ratio is very strongly in favor of these drugs. Other biologics, other monoclonal antibodies that are immune suppressants. We mustn't conflate the asthma drugs with those drugs. So TNF alpha blockers, adalimumab, Tannaceps, infliximab, Anikira, IL-1 suppression. They are different ball game.
and they're hugely immunosuppressive and the hugely increased risk of developing bacterial infections. These are not they. So I get asked frequently by concerned anesthetists, preoperatively or surgeons or dentists as they're about to some teeth out. When should we stop the biologic? How long will we stop it before an operation? This patient has got an infection of the something. How do we reverse the biologic? And that's not the case for these. And I think it's important to get that message out. Locally we've done that.
is that the astrobiologists should continue regardless they don't suppress anything apart from TH2 inflammation. ESNFL suppression does not lead to an increase risk of bacterial infection, viral fungal, helminthic worms, anything. And that it's important to continue these drugs pretty operatively because the last thing the anesthetist wants is loss of asthma control whilst doing an anesthetic. So we tell the patients this, we give them information leaflets to say, if you have an operation you should carry on.
If they need to just ask the question, tell them to phone me and we can have a conversation. You cannot say any drug is a hundred percent safe. Of course you can't, but I think that there are minimal side effects. And in the seven years of clinical practice with monoclonal antibodies across the world, no serious side effects signal or adverse event signal has been identified as yet. And in that regard, I'm very reassured that they are a safe approach to asthma treatment. And what I can say fairly definitively.
is that they are much safer than repeated courses of oral steroids.
Dr Ben Warner (1:00:55)
I guess you mentioned about perioperative cancer and I suppose the other big situation people worry about is in pregnancy. But again, as you said, oral steroids and asthma exacerbations, these things are very well known risks.
Dr Tom Fardon (1:01:07)
And the BTS sign guidelines from 2024 did not broach this. And the sign guideline from 2019 has a section on pregnancy. But because the evidence base is so sparse, because there are no studies done in people who are pregnant, the advice, the mantra, I suppose, is that the best thing you can do for both the mother and the baby is to keep the mother as well as possible. And that for us has been patients who are stable on a biologic or in remission, you might even say on a biologic.
should remain on biologic. There have been some cases of people stopping their biologic in pregnancy and then exacerbating and end up in ICU whilst pregnant. And this obviously an incredibly high risk situation. are worldwide, many, many people have gone through pregnancy on biologics and there is no signal. We haven't had any reports of adverse outcomes in pregnancy. So in the same way that we continue all treatments that are keeping the patient stable during pregnancy, that includes biologics as well. This obviously needs to be discussed on it.
case by case basis with each patient to the clinician. Certainly my experience has been to continue biologics through pregnancy.
Dr Ben Warner (1:02:15)
I think there's such a great example of really targeted precision medicine and personalized medicine. And he said, although there is a sort of black box of the asthma MDT, a lot of it is about getting the right medication for the right patient. And that's not something you can really put in a phlejart or an algorithm. need to consider them holistically.
Dr Tom Fardon (1:02:33)
Yes. And if you do look at the Scottish severe asthma pathway, much of it is flow charted, but the bit when you get to asthma MDT, we just simply can't flow chart that. There are considerations and those considerations at the top of the list is patient centeredness and realistic medicine. they are dose frequency. Can people take it every two weeks, every four weeks or every eight? So there's some degree of patient preference in that phenotyping, genotyping.
There's a lot of things to think about and trying to personalise those things to each individual. It's not just a first line, second line, third line. If only it were as easy as that. It takes time to consider each individual patient, but it's very rewarding because as I say, people come back to clinic in tears, happy tears about how much it's changed their life.
Dr Ben Warner (1:03:20)
That's wonderful. One very last question because it's a real bugbear of mine. You've mentioned Cezerpillumab, Dupillumab, Benrelizumab. These are impossible names to say. Why are they all called that? There is a rationale, isn't there?
Dr Tom Fardon (1:03:32)
Yeah, there's a naming convention for all monoclonal antibodies. I sometimes think I should look this up and work out what's going on. All of the monoclonal antibodies have a naming convention that's based on what they're targeting. So I'm afraid we're kind of stuck with benvolizumab, methylizumab, dupilumab and tesipilumab for now. And in the next year or so, we've got another one. It's called depakimumab. So it's something to add to the tongue twisters of astrobiologics, I'm afraid. We are stuck with it.
Dr Ben Warner (1:04:01)
Wonderful. Well, we've got to end our kiks somehow, at least by learning the language. Tom, thank you so much. That was another tour de force of asthma from point of diagnosis through to specialist care. I really appreciate your time and picking apart those new guidelines, which I really hope we will see the benefits of an outcome patient and population level in the years to come. Any final thoughts, any last pearls of wisdom you wish to share before we wrap up?
Dr Tom Fardon (1:04:27)
Thanks for inviting me back. it's also a pleasure to chat about asthma. I just encourage people to have a look at the guidelines. It's a lengthy document, but the flow charts are really helpful. There are some summaries you can read the headlines. And when you see someone with asthma, whether it's because they're presenting fresh brand new, whether they're presenting just of exacerbating our problem, or you're just seeing them coincidentally have some thought about those guidelines and what's the best for the patient. It's not what we learned at medical school.
or nursing school or pharmacy school. It's not what we learnt. It's changed. It's changed a lot. Changed for the better. And I think a bit of time spent with the patient explaining why we've changed, why it will benefit them in the long run. think is time well spent. It is also helpful, I think, to signpost people to the plain language version of the guidelines, which is now available on the sign website. So if you just search for sign.
plain language asthma guideline, or I'll perhaps send you the link Ben, so you can put it into the description of this podcast. Then there is what it says on the 10, a plain language version of the guideline to explain to patients in simple terms what that guideline is and how we treat asthma these days. It's not yet on the right decision service, but it will be. So I would encourage people to have a look at that. And if you think your patient has severe asthma, they probably do. And think about referring onto a severe asthma center. We're really keen to see these patients.
Dr Ben Warner (1:05:51)
Fantastic. Thank you so much. will put that link in the description along with the guidelines and all the other topics we've covered. So that just remains for me to say thank you once again. Really appreciated your time and your insights, Tom, and I hope we can get you back on the podcast at some point in the future.
Dr Tom Fardon (1:06:09)
Thanks very much.
Dr Ben Warner (1:06:10)
you
