T2-high asthma was associated with increased rates of emergency department visits, hospitalizations, and all-cause mortality (HR 1.45; 95% CI 1.05-1.99; p=0.023) compared to T2-low asthma.
Cohort (n=2,803)
No
Is Type 2 inflammation associated with higher BMI and worse clinical outcomes in adults with asthma?
In adults with asthma, Type 2 inflammation is associated with higher BMI, worse spirometric parameters, and increased rates of hospitalizations and mortality.
Effect estimate: HR 1.45 (95% CI 1.05-1.99)
p-value: p=0.023
Abstract Rationale Type 2 (T2) inflammation drives eosinophilic airway inflammation in asthma and is associated with more severe disease and worse outcomes. Obesity commonly complicates asthma and is associated with worse asthma control, but prior studies on obesity’s effects on T2 inflammation in asthma have been limited and conflicting. To address this knowledge gap, we investigated the association between T2 inflammation and obesity in asthma using an institutional electronic health record (EHR) biobank. Methods We performed a retrospective observational cohort study of adults with asthma in BioVU, Vanderbilt’s de-identified longitudinal EHR biobank. Asthma was identified using a previously validated EHR algorithm (PMCID: PMC6203662). Demographics, BMI, clinical labs (blood eosinophils, serum IgE), spirometric parameters (FEV1 and FVC), visits, and mortality data were extracted from the EHR. T2-high asthma was defined as a highest lifetime measured eosinophils ≥300 cells/uL or IgE ≥100 IU/L. We used linear mixed effects regression to test the association between T2 inflammatory lab values with BMI and spirometric parameters matched within ±30 days. We assessed difference in clinical outcomes based on T2-status using negative binomial regression to estimate incident rate ratios (IRR) for emergency department visits or inpatient admissions, and Cox proportional hazards regression to estimate hazard ratios (HR) for mortality. All analyses were adjusted for age, sex, recorded race/ethnicity, smoking status, and BMI. Results We identified 2803 BioVU participants meeting the EHR asthma phenotype. EHR length between first and last visits was 17.4 11.6-21.4 years (median, IQR), and 1,226 (43.7%) were T2-High. Lifetime median BMIs of T2-high and T2-low asthma were 31.2 26.2-37.2 and 30.6 25.6-36.7. In linear mixed effects regression, each 1-unit change in BMI was associated with a 1.7% increase in eosinophil levels (95%CI: 1.4%-2.1%, p 0.001), and higher eosinophil levels were associated with worse FVC and FEV1/FVC ratios (Figure 1A). No significant association were seen for IgE levels due to lower numbers. T2-high asthma had increased rates of emergency department visits (IRR: 1.39, 95%CI: 1.24-1.56, p 0.001), inpatient hospitalizations (IRR: 1.53, 95%CI: 1.35-1.72, p 0.001), and increased all-cause mortality (HR = 1.45, 95% CI: 1.05-1.99, p = 0.023) (Figure 1B). Conclusions Contrary to prior studies reporting lower T2 inflammatory markers in obese asthma patients, in our asthma cohort T2 inflammation was associated with higher BMIs, worse spirometric parameters, and worse clinical outcomes. Elucidating the biological interplay between obesity and T2 inflammation in asthma may reveal new treatment opportunities for this common and debilitating airway disorder. This abstract is funded by: K01 HL157755; UL1 TR002243; F99 HG013870; F99HG013879
Haimerl et al. (Fri,) conducted a cohort in Asthma (n=2,803). T2-high asthma vs. T2-low asthma was evaluated on All-cause mortality (HR 1.45, 95% CI 1.05-1.99, p=0.023). T2-high asthma was associated with increased rates of emergency department visits, hospitalizations, and all-cause mortality (HR 1.45; 95% CI 1.05-1.99; p=0.023) compared to T2-low asthma.
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