Are there similar clinical manifestations in both asthma and autoimmune disease?
Dr Pavord: Asthma is a very heterogeneous disease and you can certainly see aspects of asthma in people with autoimmune disease. In rheumatoid arthritis, for instance, it’s not uncommon to see patients with airflow obstruction, which is one feature of asthma —but the mechanism of that obstruction is very different from the mechanisms we typically see in asthma, for example, type 2 airway inflammation.6 I would see them as very different, very separate conditions.
How are some of the new biologic treatments able to mitigate clinical worsening in asthma and comorbid autoimmune disease?
Dr Pavord: The biologics have had a massive impact on asthma and chronic rhinosinusitis, particularly for those patients living with more severe airways disease. Not only do biologics have good clinical traction — particularly on the risk of having an asthma attack, which is significantly reduced on biologics — but also improvement in symptoms, lung function, and quality of life.4
One feature of biologics is that their clinical effects are predictable. There are simple biomarkers that you can measure in the clinic, such as blood eosinophil count and exhaled nitric oxide, which are very predictive of response to treatment.
We also have low failure rates with biologics in clinical practice because we’re able to target them very effectively. That has been one of the important features of biologics in asthma.
How can specialists collaborate to better manage and treat asthma/allergies and potential comorbid autoimmune disorders?
Dr Pavord: One issue is that a lot of people with asthma and chronic rhinosinusitis are looked after in nonspecialist care.
I’ve seen a revolution in airways disease over the last 10 years. We recognize that measuring biomarkers of type 2 airway inflammation is a very important part of assessment in patients with asthma, but this thinking hasn’t really permeated down into nonspecialist primary care. We really need to start getting these tests done in general practice, because it’s clear that they’re very predictive of the likelihood of an asthma attack.
All other things being equal, if you have asthma and high blood eosinophils and FeNO, you’re at between a 3 and 5 times increased risk of having an asthma attack, compared with someone who has low blood eosinophils and FeNO with the same severity of asthma.4,7
It is possible for patients to go to their general practitioner to have their asthma assessed, but they may not have either of these measurements taken and we need to change that. Why wouldn’t a patient want to know that they’re at an increased risk of having an asthma attack? And, if they did have that information, would it help them make a better decision about treatment?
In specialist care, we’re getting interesting, new insights into asthma from these biomarkers and identifying a process that we can treat really well, but these measurements need to be taken in more patients with asthma in primary care.
Is there anything else you would like to add?
Dr Pavord: Before we had these biologics, a patient living with severe asthma had a pretty miserable time — experiencing symptoms, recurrent asthma attacks, and frequent courses of steroids for their asthma. Biologics have transformed the outcome.
Running a severe asthma clinic is a real pleasure now because we have good options for patients for the first time in 20 years. We’re seeing results that we wouldn’t have dreamed of seeing 10 years ago, so it’s been an exciting time to be in this field.
Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.
1. Mukherjee M, Nair P. Autoimmune responses in severe asthma. Allergy Asthma Immunol Res. 2018;10(5):428-447. doi:10.4168/aair.2018.10.5.428
2. Wenzel SE, Vitari CA, Shende M, Strollo DC, Larkin A, Yousem SA. Asthmatic granulomatosis: a novel disease with asthma and granulomatous features. Am J Respir Crit Care Med. 2012;186(6):501-507. doi:10.1164/rccm.201203-0476OC
3. Mukherjee M, Bulir DC, Radford K, et al. Sputum autoantibodies in patients with severe eosinophilic asthma. J Allergy Clin Immunol. 2018;141(4):1269-1279. doi:10.1016/j.jaci.2017.06.033
4. Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention, 2020. Updated December 20, 2020. Accessed March 24, 2021. https://ginasthma.org/gina-reports/
5. Dixon AE, Kaminsky DA, Holbrook JT, Wise RA, Shade DM, Irvin CG. Allergic rhinitis and sinusitis in asthma: differential effects on symptoms and pulmonary function. CHEST. 2006;130(2):429-435. doi:10.1378/chest.130.2.429
6. Mori S, Koga Y, Sugimoto M. Small airway obstruction in patients with rheumatoid arthritis. Mod Rheumatol. 2011;21(2):164-173. doi:10.3109/s10165-010-0376-5
7. Price DB, Bosnic-Anticevich S, Pavord ID, et al. Association of elevated fractional exhaled nitric oxide concentration and blood eosinophil count with severe asthma exacerbations. Clin Transl Allergy. 2019;9:41. doi:10.1186/s13601-019-0282-7
This article originally appeared on Pulmonology Advisor