Aspirin-Exacerbated Respiratory Disease (AERD) and the Role of Type 2 inflammation (Recording)
Published: August 28, 2023 Revised: October 21st, 2024
This webinar was recorded on September 26, 2023
AERD, also known as Samter’s Triad, is a condition that impacts more than 1 million people in the US. People with AERD live with asthma, sinus disease and recurrent nasal polyps, and are sensitive to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDS). Many are undiagnosed. In this webinar, Dr. Rajan Merchant will review the symptoms, causes, diagnosis, management and treatment options for those living with this challenging condition.
Speaker:
Rajan Merchant, MD, FACAAI
Woodland Clinic Medical Group, Woodland, CA
Dignity Health Medical Foundation
Common Spirit Heath Research Institute
Common Spirit Health
CNE for nurses, and CRCE’s for Respiratory Therapists is available through Allergy & Asthma Network’s Online Learning HQ
CME is available through ACAAI for this webinar.
Sponsored by the American College of Allergy, Asthma and Immunology
Transcript: While this transcript is believed to be accurate, errors sometimes occur. It remains your responsibility to evaluate the accuracy and completeness of the information in this transcript. This transcript is not intended to substitute for professional medical advice.
Lynda Mitchell: Welcome Everyone. We’re going to wait a minute to let some people enter the Zoom webinar room, and then we’ll get started. Okay, I’ll wait one more minute and then we’ll get started. Welcome, everyone. All right, well, why don’t we get started? Hello, everyone. Thank you for joining us here today. I’m Linda Mitchell, CEO for Allergy and Asthma Network. Welcome to this afternoon’s webinar. I’m looking forward to hearing Dr. Merchant talk about Aspirin Exacerbated Respiratory Disease. We have a few housekeeping items before we start today’s program. First, all participants will be on mute for this webinar. We will be recording today’s webinar and will post it on our website within a few days. You can find all of our recorded webinars on our website at allergyasthmanetwork. Org. All you have to do is scroll to the bottom of the page to find the webinars, and then you can find the recordings there if you just click on the Look at Older Webinars link. This webinar will be one hour in length, and that includes time for questions. We will take those questions at the end of the webinar, but you can put your questions in the Q&A box at any time.
The Q&A box is at the bottom of your screen. We have some monitoring the chat if you have any questions you put in there or if you need any other help. We will get to as many questions as we can before we conclude today’s webinar. We offered this webinar in partnership with the American College of Allergy, Asthma, and Immunology. Members of the college are eligible to receive CME for this webinar through the college member website. For everyone else, we’ll be offering a certificate of attendance if you need it for your records. A few days after the webinar, you will receive an email with supplemental information about the webinar topic and a link to the recording, as well as a link to download a copy of the certificate of attendance. We will also try to add the link to the certificate in the chat, but sometimes that works and sometimes it doesn’t. Let’s get started. Today’s topic is aspirin exacerbated respiratory disease and the role of type 2 inflammation. Aerd is a condition that impacts more than 1 million people in the US. People with AERD live with asthma, sinus disease, and recurrent nasal polyps and are sensitive to aspirin and other nonsteroidal, anti-inflammatory drugs.
Today, Dr. Merchant will review the symptoms, causes, diagnosis, management, and treatment options for those living with this challenging condition. It is my pleasure to introduce our speaker, Dr. Rajan Merchant. Dr. Merchant is an allergy, asthma, and clinical immunology specialist at the Woodland Clinic Medical Group, which is part of Common Spirit Health and Dignity Health Medical Foundation in Woodland, California. Dr. Merchant focuses on adult and pediatric, seasonal and perennial allergic rhinitis, asthma diagnosis and management, food allergy, drug allergy, and immunodeficiency disorders. He is a fellow of the American College of Allergy Asthma and Immunology and won the Sacramento Magazine Top Doc Award from 2016 to 2022. Thank you for being here today, Dr. Merchant. I’ll turn it over to you now.
Dr. Rajan Merchant: Thank you, Linda. Good afternoon, and thank you for that introduction and for everybody joining this webinar. Again, hosted by the Allergy and Asthma Network and sponsored by the ACAI. Today is September 26th and is actually Aspirin Exacerbated Respiratory Disease Day. I’m excited to again share some history and updates about this unique condition. Here are my disclosures, I don’t have any specific conflicts that are associated with this presentation as it relates to my disclosures. And so we have three learning objectives today that we’ll try to focus on, basically to identify the clinical features associated with AERD, describe some of the components of type two inflammation, and go over some of the basic treatment options and recommendations for management associated with this disease. Let’s see. So before we get started on actually talking about AERD, I wanted to provide some historical context. Willow trees, as pictured here, have been long known for medicinal purposes and was known to have properties to reduce fever and pain. This was actually first described almost 1500 years ago by Padonius dyschoridus, a Greek physician, pharmacologist, and botanist who wrote about the properties associated with salicylic acid. It was actually first purified by a German scientist in 1820 and and then synthesized in 1859.
And then 1897 is when Felix Hoffman, a scientist who was working for Bayer, Bayer actually produced acetylsalicylic acid to reduce the bitterness that was associated with the original form. And in 1899, that’s when Bayer patented the drug and called it aspirin. Behr aspirin is still widely recognized as the wonder drug and is the standard to which all other nonsteroidal anti-inflammatory drugs or NSAIDs are compared to. And so 1922 is when the first reported case of aspirin exacerbated respiratory disease was described by Wydahl et al. At that point, it was just focused on asthma being worsened by aspirin. And in 1968 is when Samter and Beers published The Intolerance of Aspirin, where they described the classical triad as we now know it to be where we had nasal polyps, bronchial asthma, and aspirin hypersensitivity. Back then, it was again described as an acquired disease that develops usually in middle age and predominantly in non-on atopic individuals. And so as Linda mentioned, AERD affects approximately 1.5 million people in the US, approximately, again, seven % of adults who have asthma have AERD and among patients with severe asthma, the prevalence is almost twice as high. About the same number of individuals with chronic rhinosinusitis and nasal polyps also have AERD, estimated to be about 15 %.
However, there is a little bit of discrepancy as many patients again may not be aware of their sensitivity to NSAIDs and in one study, almost 50 % patients that were diagnosed with chronic rhinosinusitis with nasal polyps challenged with aspirin had features of AERD. Some risk factors that are associated with the disease. Typically, again, this is thought to be a non-atopic condition. And so we see that the majority of individuals or triggers or risk factors are associated with respiratory tract infections. Allergen exposure again seems to be less prevalent as a whole. And again, surprisingly, aspirin or NSAID use is not a specific risk factor, but does obviously play a key role in the pathogenesis. And in a good number or almost 30 %, again, we don’t really have a clear understanding of what triggers or what leads to the disease itself. So clinical features associated with the disease, a fully developed ARD, usually again diagnosed in adults. We see progression of the disease over several years and sometimes decades and that recognition of aspirin or NSAID sensitivity will also be dependent on the overall frequency and use in this age group. So typical symptoms start with rhinitis, move on to again, sinusitis and nasal polyp development, asthma a couple of years later, and then the NSAID tolerance again anywhere between four years to up to a decade after the onset of symptoms.
Some key clinical features. Obviously, we see respiratory features are again the primary components of AERD as based on the name, but there are a number of non-respiratory symptoms that have also been associated in this demographic or patient group. We know aspirin or NSAIDs can trigger urticaria and angiodema and that is also seen in patients with AERD as well as some of the classical GI symptoms that we see with use of NSAIDs and aspirin and some unusual symptoms that may again sometimes be attributed to other diseases, specifically hypotension, a loss of consciousness may be considered an anaphylactic reaction to NSAIDs or aspirin, but also again highly likely to be a part of the disease process associated with AERD. So generally again, most patients that have AERD, we see that 60 % of patients… Oops, go back a slide. Yeah, have again, a more severe course of symptoms, generally more refractory disease compared to individuals who don’t have AERD. Typically, patients require greater levels of medications and treatments that seem to be a little bit more resistant. We see that patients with asthma, 60 % are considered to be severe asthma, 25 to 50 % of these patients are considered to be uncontrolled and almost about a quarter of patients that have required mechanical ventilation for asthma were sensitive to aspirin.
Over time, we do see that the disease does lead to some fibrosis and airway remodeling. Additional complications associated with nasal polyps, again let me go back one slide, involve again recurring sinus infections, facial deformations and tympanic membrane perforation as well as again, invasion into the brain with nasal polyps because of how aggressive they can be in terms of their development. So typically again, we’ve talked about again the features, the definition again is a combination of these three components of having asthma, chronic rhinosinusitis and nasal polyps with the key element that again inhibition of COX-1 by aspirin or NSAIDs within 20 minutes to up to three hours leads to a worsening of symptoms with congestion or bronchoconstriction. Reactions to NSAIDs or patients with AERD are considered to be pseudo allergic. Again, most of the time we think of allergy being a type one or IgE-mediated reaction in the circumstance for AERD, these are pseudo allergic. It’s an abnormal pharmacological manifestation of what’s going on within the physiology. And this was actually described again by Samter back in 1968 when he had seen structurally different molecules that were causing similar reactions in terms of AERD manifestation. So here we see that a variety of NSAIDs that can inhibit both COX-1 and COX-2, NSAIDs or a strong COX-1 inhibition can induce AERD or NERD, which is again nonsteroidal exacerbation of respiratory disease, which is again commonly used in Europe versus the AERD which is used here in the US.
And specific NSAIDs such as naloxicam that are more selective COX-2 inhibitors do not seem to induce the symptoms associated. So it is really that COX-1 inhibition that seems to be the driver of the diagnosis and the pathogenesis. So before we go into again, the type two inflammation that’s associated with the disease, a little bit of, again, the physiology. So aspirin or NSAIDs are again one component of this diagnosis. But the overall physiology again is a complex dysregulation where we have an increase of glucotriin C4 and prostaglandin where we have a dysregulation of the anti-inflammatory and inflammatory mediators. So again, a little bit of that described here, an increase specifically of LTC4, a decrease in PGE2 as it relates to COX2 or sorry, COX1 inhibition, which then leads to, again, an activation of mast cells. And this is a little bit of a better visualization of that. We can see that specific markers of LTC4 or system nihalucotrienes that again activate or induce specific cytokines that relate to mast cell activation and the mast cell activation then drives the inflammatory components leading to basophils, T-cells and eosinophils being increased production. So specific to type two inflammation, we see that the particular interleukins that drive type two inflammation are associated with all three of the major phenotypes.
So IL-4, IL-5, and IL-13 are again inflammatory signals that cause cell trafficking to the specific tissues. We can see increases in IgE production as well as again barrier dysfunction, tissue remodeling, smooth muscle proliferation and contractility, specifically when it talks to asthma, some microbiome alterations associated with chronic sinusitis and hyperplasia and goblet cell production leading to increased mucus production. This again nicely gives us a very good visual of all of the mechanisms that are going on with regards to both the inflammatory pieces and the anti-inflammatory component where PGE2 is being inhibited by aspirin. And again, this pathway is a little bit different than what we see with the atopic pathway where the ILC2 cell, which again drives the type two inflammation and leads to IgE production. Here we see that the dysregulation of the system, neolucotriens and the increase in the Prostaglandins, these pro-inflammatory mediators really are the mechanisms which activate the mast cells and then those pieces lead to the increase in the type two mediators associated with the inflammation. And so we go back to this triad of what’s going on. So the aspirin or NSAID hypersensitivity again inhibits or decreases PGE2, which again is the stabilizer for mast cells, mast cell activation because of this dysregulation of glandins and glucotriene leads to an increase pro-inflammatory condition, which then allows the mast cells to drive the type two inflammation, leading to the mechanisms of asthma and worsening of the nasal polyps and sinus disease that we see in terms of the severity.
So the overall next step is going over the different recommendations and treatments associated with the management of AERD. The basic goals of treatment are not that dissimilar to treating asthma or nasal polyps, basically control asthma symptoms, try to manage the underlying inflammatory pieces associated with chronic rhinosinusitis, prevent again nasal polyp regrowth. And for most individuals, again, understanding that this is a lifelong process of an underlying disease and that will take some time to get the treatments to be optimal and that there can be setbacks based on, again, various triggers that may come into play. So for most individuals, specifically for asthma, a trial of a glucotryin-modifying agents again will probably be beneficial to help decrease or inhibit the effects of the increased glucotryin productions, whether this is with Montelukas specifically or with Xyluten, which affects the five-lipoxygenase pathway. Both can be used to modify the activity or severity associated with AERD. Specifically, avoidance of obviously COX1 NSAIDs, a key player of treatment. And then we’ll go over a little bit about the biologics associated with type two inflammation. So counseling and avoidance of patients of identifying all of the different mechanisms of COX1 inhibitors, including Tylenol, which can be at a high dose a week COX-1 inhibitor.
So trying to identify medications that patients can well tolerate when they do need it for specific indications. Foods also play a key role again. We know that salicylic acid was derived from again, natural substances are found and again most medicinal products are found from food or plant derivatives. And so understanding where these foods contain high levels of salicylic acid would be again a key role. And also knowing that most individuals, even with careful avoidance, likely will continue to have disease progression even with avoidance as again, the underlying mechanism is again a dysregulation of the inflammatory and anti-inflammatory mediators and that inhibition of COX-1 with NSAIDs or aspirin just exacerbates the entire physiology. So this table again gives us a nice overview of all of the different treatment options associated. Again, most of these treatments are very similar to treatments that we currently use for underlying allergic rhinitis, sinusitis, nasal polyp disease and/or asthma. We usually will always start with topical steroids as a way to control disease and inflammation. Lucotrine modifying drugs, as stated, to block the lucotriene effects. Oral steroids when severity seems to be particularly problematic or or affecting again, multi-organs. Inhaled steroids, again, similar for asthma management.
And then again, a key component of treatment, aspirin desensitization to actually improve or reduce the symptom severity associated with AERD. This was actually first described, aspirin desensitization in 1922, when Wadau actually diagnosed the aspirin-associated respiratory disease. He actually did a desensitization during that time and was able to show that individuals who were desensitized were able to have less severe or less frequent exacerbations. Subsequently, again, described in 1970 and then most recently when it became more widely used, when Dr. Stevenson, in 1980, documented the sustained benefit after desensitizing patients and where the Scripps protocol for aspirin desensitization became standard of care. Typically, all patients who have aspirin exacerbated respiratory disease can be desensitized to aspirin. Patients who can take daily aspirin without adverse side effects once they have been desensitized and desensitization can be generally maintained indefinitely as long as the patients again take aspirin regularly. Typically, if they stop treatment for a couple of days, again, they lose that protective component and will likely react to aspirin or NSAIDs within a few days of stopping daily treatment as the desensitization wears off. Surgical management again is a key component. Nasal polyps again play a significant role and cause a significant role in quality of life.
And so generally when medications are not allowed to reduce symptoms or impairing a quality of life, surgical management had been again a key player to try to reduce symptoms, usually with a polypectomy or endoscopic sinus surgery. There were the initial recommendations. The biggest challenge with surgeries was that treatment usually led to recurrence of nasal polyps, usually at a much again faster rate than individuals who did not have AERD. And then specifically now talking about again, the monoclonal antibodies associated with treatment for type two inflammation. We have a couple of different targets that have been looked at for AERD or with AERD. Anti-ige treatment with omalizumab, anti-IL-5 treatment with mepolizumab, benralizumab or reslizumab, and then anti-IL-4, anti-IL-13 with dupilamab. And so here again, we try to illustrate how these specific monoclonal antibodies can affect the inflammatory pathways. And we can see that the different targets for these inflammatory mediators, these interleukins that cause or drive the inflammation can be blocked and where we can then have an improvement in disease severity, disease modification and disease elements where other treatments may have not worked, particularly when we talk about topical or inhaled steroids or nasal steroids for disease management.
So with regards to IgE or anti-IgE therapy, again, there was a study published again back in 2019 looking at the effects of omalizumab in patients with AERD. They saw that there was again a significant reduction in the total number of steroid courses and total use of Saba while patients were on omalizumab during their first year. Concordantly, again, the treatment was only beneficial if again, IgE or atopy was noted. Patients who did not have a significant factor for atopy or allergy did not seem to have the same level of benefit with omalizumab. There was again, another component of looking at omalizumab where there was a decrease in urinary LTE4 and a reduction in overall cystoneal glucotriene production and led to NSAID tolerance on patients who were on omalizumab. And this was again published back in 2020. When it goes to specific treatment regarding anti-IL-5, mepolizumab has been studied and was shown to improve both upper airway symptoms, including anosmia, congestion, and asthma control in patients. Again, this was a retrospective look at patients that were on mepolizumab and are known to have AERD. I did not specifically see any clear clinical trials looking at benralizumab or eraselizumab with AERD, although these again would work similarly with IL-5 inhibition.
And then finally, the dual therapy targeting trial for alpha receptor with dupilumab again highly effective as add on therapy for patients with nasal polyps and AERD. Again, reported outcomes to decrease sinus inflammation, sinus imaging and the markers associated with T2 inflammation. And here we have again, a nice outline that looks at all of the different monoclonal antibodies as well as aspirin treatment with desensitization across a variety of clinical components with regards to symptoms as well as adverse events. And the top line again, specific to dupilumab showed the greatest benefit with the least among side effect profile with regards to patients who have chronic sinusitis with nasal polyps. The one key piece of this table that I think is fascinating is that again, initially, prior to monoclonals being available, aspirin desensitization was again, the mainstay of treatment for most of these patients on top of again the topical steroids. And we see a clear benefit from aspirin desensitization, but there is a greater side effect profile that was again less appreciated at the time. And then when we look at again a greater view, we see that aspirin desensitization does have again, a greater side effect and is considered to be more harmful than beneficial with management.
And so there has been a little bit of a shift of maybe not using aspirin desensitization as much, given that we have some other treatment options where the overall risk benefit profile may favor or may not be treating the risk of transfusion. This is the study that we’re trying to show you. We’re not using aspirin desensitization anymore. So in summary, basically AERD or NERD again is defined as asthma with chronic rhinosinusitis, nasal polyps with symptoms associated with aspirin or NSAID use that specifically inhibits COX1 inhibition. Again, this is a complex dysregulation of pro-inflammatory and anti-inflammatory mediators that lead to an increase in LTC4 and a decrease in PGE2 production which affects mast cells. This dysregulation as a whole leads to an increase in type 2 inflammation with increases in again IL-4 or IL-5 and IL-13. Treatment again basically has evolved around treating the underlying conditions of pharmacological options to treat asthma and nasal polyps and sinusitis with topical steroids, a surgical management for the individuals who have significant sinus disease to open up the nasal and/or endoscopic sinus passages. Aspirin desensitization again was a hallmark of treatment and maybe again considered to be maybe a little bit less of a consideration.
Now that we have some specific treatments targeting type two inflammation where the risk benefit profile seems to favor use of biologics over aspirin desensitization but still again an option for treatment that may be discussed with patients as you go through the different options and where they may respond. And that comes to the end of the presentation and we will be ready to take it up for questions.
Mitchell: Thank you, Dr. Merchant. Really informative. It’s a very complex topic. Really, you’ve deciphered that very well, and I appreciate you going through it in a very clear manner. We’ll go ahead and we’ll take some questions and answers. I didn’t get a whole lot of questions, but I do have some for you, so let me go ahead and ask them. So is there any contraindication to aspirin desensitization in these patients?
Merchant: Yeah, there’s not a clear contraindication of aspirin desensitization. It still works extremely well to reduce symptoms and to reduce the inflammatory conditions that are associated with it. I think the biggest challenge associated with aspirin desensitization is again, the potential for needing high doses of treatment over a sustained period of time. And that the biggest negative outside of some of the harms that may be associated are that if you stop treatment or forget to take treatment over a couple of days, you lose that productive benefit and have to go through that desensitization process again to be able to go back to tolerating aspirin. The main benefit I think that aspirin desensitization provides where monoclonals may not be necessarily known yet, again, we see a little bit with omalizumab showing a benefit where other NSAIDs are tolerated, is that you can use COX-1 inhibitors with aspirin desensitization to be able to use those other medications. Whereas again, they may not still be available for use with a monoclonal antibody because you would still likely potentially exacerbate symptoms with use.
Mitchell: Okay, thank you for that. So for my information, I don’t know if anybody else is wondering. So if you do aspirin desensitization, does that also desensitize to NSAIDs?
Merchant: Yeah, typically you can better tolerate all NSAIDs under aspirin desensitization. So whether that’s Ibupofen or any of the other COX1 inhibitors, they are all better tolerated or are not likely to cause an exacerbation of the underlying physiology when you are on aspirin desensitization.
Mitchell: Okay, very interesting. You might have said this and I missed it, but do all patients that have AERD also have type 2 inflammation or just a subset of the patients with AERD?
Merchant: Yeah, so all patients do seem to manifest this type 2 inflammation associated with AERD. There is a little bit of, again, a driving factor which comes first? Is it the dysregulation that starts to develop that then leads to some of the inflammatory conditions? Or are there other mechanisms that are leading to the inflammation? And again, I think the clear difference is in atopy, we see the mechanisms driving the inflammation earlier in life and where we get a higher level of IgE production versus again, an AERD that seems to be a lesser component of the path of physiology. And again, being mediated by those respiratory infections or triggers seem to be a driving factor leading to that inflammatory state.
Mitchell: Got it. One of the questions from the audience, what pain relievers do you recommend if there is no aspirin desensitization done?
Merchant: Yeah, so typically I would say, naloxicam, which is again a selective COX2 or a cellaroxib, a cellabrex, which is a COX2 as well, are probably pretty well tolerated medications that don’t seem to cause any specific issues associated with AERD.
Mitchell: Okay. Has any of the recent COVID research shown any new clues regarding AERD and the loss of smell?
Merchant: That’s a good question. I’m not directly aware of any specific studies looking at COVID and asthma and if that has any clear components where it drives the inflammatory conditions. That’s not to say that there isn’t any, I’m just not aware of them.
Mitchell: Okay. Do any foods exacerbate or cause additional inflammation for patients with AERD?
Merchant: Yeah. So there is an entire list of foods and probably a topic of itself where you can talk about all of the different ways that aspirin or salicylic acid is found in both natural substances as well as again in other forms. There are again foods that have high levels of salicylic acid, which would then drive some of the inflammatory components associated with AERD. I didn’t go through a list of those, but those are commonly available and again can be something that can be looked up to say here are foods that contain salicylic acid or high levels of salicylic acid, which would then be things that you would want to try to avoid.
Mitchell: So that’s a low salicylate diet.
Merchant: Correct.
Mitchell: Yes. Okay, very interesting. Okay, let me see. I noticed through this presentation you were using CRSWNP. That’s a piece of this whole constellation of problems that are all part of AERD. Is that correct?
Merchant: Yeah. Depending on, again, the definition and how different ways of the physiology, some describe having chronic rhinosinusitis with nasal polyps as one component. Others describe both of those as independent factors, but fall in actually not as a triad, but as a tetrology of having asthma, chronic sinusitis, nasal polyps and aspirin sensitivity or NSAID sensitivity. But that is a key element that you have to have nasal polyps and sinusitis based on imaging or underlying visualization of both to be able to really characterize this as AERD.
Mitchell: Thank you. Is. There any effects on the liver on aspirin desensitization and daily aspirin therapy that has to be conducted after desensitization?
Merchant: I don’t think there are specific effects on the liver that require liver monitoring on aspirin therapy. Most of the symptoms associated, again, are going to be GI related. Again, a little bit of a higher risk for bleeding disorders associated. Those are the things that we typically worry about. But you don’t have to specifically monitor liver function or kidney function on aspirin desensitization.
Mitchell: Okay. And is there a standard dose of aspirin that’s taken like a baby aspirin or some other dose or does it vary?
Merchant: Yeah, sorry. And I didn’t go into the details of the dosing, but typically it is a high dose of aspirin. So anywhere from 650 milligrams once a day to twice a day. So some of the literature has a high dose of 650 twice a day. And others say after a period of time, 650 milligrams once a day can be used. But it is a high dose of aspirin on a daily regimen that is recommended for ongoing treatment.
Mitchell: Okay. What are the goals of AERD therapy from a 30,000 foot perspective?
Merchant: Yeah. So the goals of therapy ultimately again are primarily to try to keep patients as symptomatic and/or free of symptoms as possible, just like for all of the underlying conditions. Try to control their asthma, understand what’s going to drive their asthma in terms of symptoms or triggers. Similarly, for the chronic sinusitis components or nasal polyps, obviously try to minimize nasal polyp growth, try to minimize the recurrence of active infections or inflammation underlying in terms of the sinusitis. And ultimately, again, trying to maintain high quality of life in terms of treatments that are potentially lifelong in terms of the burden of disease. So if you’re having to take treatments with nasal steroids, inhaled steroids, oral tablets to try to control it, that also adds a pretty significant stressor in terms of daily management outside of just the disease itself. And so sometimes simplifying these regimens or options with the newer type 2 mediators for the biologics may actually reduce the burden of disease and the impact, as well as improve overall control and inflammation.
Mitchell: Okay. Is there a preferred surgical method if someone chooses surgery?Merchant: I’m not the surgeon, so I couldn’t tell you if there’s a preferred surgical method. I think it depends on how extensive the nasal polyps are and how extensive the underlying sinus inflammation is. Again, if typical treatments haven’t been working or disease has progressed, the surgeons will obviously go through a variety of options. Generally speaking, again, if they’ve already had one surgery done with polypectomy and ethmoidectomy, typically there’s not more to do in the sinuses and they’ll just continue to try to cut out the nasal polyps on reoccurring surgeries.
Mitchell: Okay. And let’s see, is there any other questions from the audience? I’ll ask another question is with the advent of the new drug treatment options with biologics and with the availability of aspirin desensitization, would you say that if someone does have a diagnosis of AERD that they do have some hope for an effective treatment option among what’s available now?
Merchant: Yeah, certainly I think there are again a number of treatment options that are very effective, including aspirin desensitization as well as the monoclonal antibodies targeting the type two inflammation. Both of them lead to, again, a general improvement in symptoms, a reduction in severity and again prevent or decrease progression of disease and the need for recurring surgeries, particularly for nasal polyps and sinus issues. All of the treatments have been very effective and a number of studies have now looked at where again treatment early may even lead to a decreased need for surgical intervention for chronic sinusitis and nasal polyps. I think there are lots of options. I think the biggest challenge is again understanding that this progression can happen over four or five or more years before it gets recognized. They may have already had a sinus surgery because it presented with sinus symptoms before the other components were presented. And so I think that’s one of those elements is that we know this is a progressive disease and that initial symptoms may warrant a treatment that start out with one option. But as the disease progresses, it becomes easier to recognize or determine that this is again actually AERD and not just sinusitis or something else and that then we can target these other treatments.
Merchant: And there’s also again some data that may come out that suggests that early treatment with monoclonals because again, monoclonals are now specifically approved for nasal polyps and sinusitis. And so maybe treatment may prevent progression of disease and that may be yet to be determined. But again, I think there’s some interesting literature looking at those elements as well.
Mitchell: Well, thank you. I just want to tell the audience, if you need resources, educational resources for patients and caregivers regarding AERD, we do have a number of them on our website, and you’ll get information about those in the follow-up email that happens after this webinar. In a day or two, you’ll see that, along with a link to the recording. So, Dr. Merchant, that’s about the last of the questions that we have for you. Very interesting. I learned a lot. I really appreciate your time today, and thank you for joining us. I’ll just go ahead and move on to announcing the next webinar, which will be on October fifth. It’s Real-world tobacco cessation strategies in under-resourced community. It’s with Dr. Jessica Feno, who has a program like this that she leads in her community. You’ll learn more about that. Thank you again, Dr. Merchant, for joining us. Really do appreciate it. Our next advances webinar is going to be on October 19th, where we’ll welcome Dr. Clint Dunn to discuss atopic dermatitis, JAK inhibitors, and beyond. Like I said, you’ll receive an email from Zoom in a few days with a link to the recording, link to those AERD resources that I referenced, and other information that will assist you with the diagnosis of AERD patient education. Thank you again for all of us at Allergy and Asthma Network. Join us as we work every day for everyone to breathe better together. Bye, everyone. Thank you, Dr. Merchant.
Merchant: Thank you.
