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Characteristics of T2-low asthma revealed with Finnish real-world data

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Characteristics of T2-low asthma revealed with Finnish real-world data

AstraZeneca Finland, Medaffcon and Turku University Hospital (TYKS) have carried out one of the first real-world studies into the prevalence and stability of the type 2 low-inflammation endotype of asthma among patients with severe uncontrolled asthma (1).

Understanding the endotype better is a prerequisite for optimising treatment for patients afflicted with what can be a debilitating condition, states Dr. Klaus Tamminen, head of medical affairs at AstraZeneca Finland.

“Severe asthma exacerbates regularly, causing for example absences from work and a burden on health care resources and society more broadly,” he reminds. “Type 2 low-inflammation hasn’t been studied as extensively as its high-inflammation counterpart (2). There were a lot of pertinent questions to answer: How common it is, how frequently does it exacerbate and how do the basic metrics used to monitor it behave over time?”

The endotype is an interesting research topic also because it has a weaker response to corticosteroids and because the first biological medications have proven effective against eosinophilic asthma, (2) adds Dr. Arja Viinanen, a specialist of pulmonary diseases at TYKS.

“We basically wanted to define the disease burden for non-eosinophilic asthma and approximate the size of the patient group who need new treatment options,” she tells. “We also didn’t know the extent of change from one endotype to the other and whether severe T2-high and T2-low asthmas differ from each other in terms of severity and exacerbations.”

The first step, however, was establishing a definition of type 2 low-inflammation asthma with metrics that are available not only in research but also in everyday clinical settings (1).

The research team set two biomarker-based cut-offs to define the endotype: a fractional exhaled nitric oxide (FeNO) concentration of less than 25 parts per billion and an eosinophil count of less than 150 cells or 300 cells per microlitre (1). The two eosinophil cut-offs were selected because both have been utilised as markers of eosinophilic disease in previous research, explains Dr. Viinanen.

Rare data

The approach dictated the source of the research data.

Auria, the data lake at TYKS, was essentially the only source that offered structured data on not only spirometry tests but also the results of eosinophil and FeNO measurements, according to Dr. Mariann Lassenius, real-world evidence lead at Medaffcon.

“These are data that can’t be found easily elsewhere without extensive manual data mining,” she comments. “The FeNO counts especially were something we had to look into to determine whether they were available in the first place. We found that they’re available in a structured, easily usable form – basically in a table – and started the study.”

“Structured data are enormously helpful especially when you want to monitor an occurrence over time and compare one year to another,” tells Dr. Tamminen. “The Finnish real world data landscape is great because clinical data is so readily available.”

Another unique feature of the country is the existence of legislation governing – in practice, facilitating – the secondary use of healthcare register data (3).

Biomarker levels remained low in up to 72% of patients

The data enabled the team to identify all of the over 9,600 asthma patients who had contact with the pulmonary diseases ward at TYKS. The cohort was reduced to 637 by excluding patients whose disease was under control and then to 169 by excluding patients whose biomarker counts had not been monitored sufficiently frequently (1).

Thirty-one of the patients fell below the lower eosinophil cut-off and 66 the higher cut-off for type 2 low-inflammation asthma. The biomarker profile was stable in 55 per cent of patients in the former and 72 per cent of patients in the latter group with follow-up measures (1).

“Of course it would’ve been nice to have a larger patient cohort and more statistical power,” admits Dr. Lassenius. “Still there aren’t too many places in the world where studies with this kind of a follow-up period have been conducted. We were able to monitor these patients and disease events for four years.”

First step on road from control to cure

Dr. Tamminen states that the study fundamentally improves understanding of type 2 low-inflammation asthma and its implications for patients, thereby paving the way for a shift from controlling symptoms to inducing remission and, ultimately, curing the condition for patients who get no relief from existing medications.

“Perhaps one of the more paramount takeaways for clinicians is that even though the disease is defined through a low eosinophil count and the count remains fairly stable in most patients, the count can spike during exacerbations, for example,” he analyses.

“In general,” he adds, “real-world studies that improve understanding of disease endotypes and burden are also an important guide for research and development work at AstraZeneca.”

Of note is also that type 2 low-inflammation asthma manifests relatively uniformly regardless of the cut-off for eosinophil count, adds Dr. Viinanen.

“For instance, if you think about other morbidites linked to eosinophilic asthma, such as nasal polyps, neither of these groups presented these kind of clinical characteristics,” she elaborates. “Another key finding was that these two endotypes of severe asthma are, broadly speaking, similar in terms of severity: there wasn’t a dramatic difference in exacerbations.”

AstraZeneca, Medaffcon and the scientific committee formed for the study also intend to conduct follow-up studies with the data.


  1. Viinanen A, Aakko J, Lassenius MI, Telg G, Nieminen K, Kaijala S, Lehtimäki L, Kankaanranta H. Type 2 Low Biomarker Stability and Exacerbations in Severe Uncontrolled Asthma. Biomolecules. 2023 Jul 13;13(7):1118. doi: 10.3390/biom13071118.
  2. Kuruvilla ME, Lee FE, Lee GB. Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease. Clin Rev Allergy Immunol. 2019 Apr;56(2):219-233. doi: 10.1007/s12016-018-8712-1.
  3. Secondary use of health and social data. Ministry of Social Affairs and Health, Finland. (accessed 31.10.2023)
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