Abstract Rationale Large population-based studies have shown that asthmatics of female sex have poorer disease control and greater healthcare utilization compared to asthmatics of male sex. When comparing serum biomarkers, female sex is associated with lower type 2 (T2) inflammatory biomarkers, which in turn have less therapeutic options. As phenotyping becomes standard in asthma management, biological sex may influence treatment. The aim of this study is to evaluate the association between select biomarkers and sex in a cohort of veteran asthmatics. Methods This study consists of a single-center cohort of adult veterans with asthma. Patients were excluded if currently smoking, vaping, on systemic steroids, or on immunosuppressive medications. Females were excluded if pregnant, lactating, post-menopausal, or with ovariectomy. Those who met inclusion criteria completed a REDCap (Research Electronic Data Capture) questionnaire for demographics followed by biospecimen collection. Descriptive analysis was performed on demographics. Biomarkers were analyzed with standard linear regression or rank-based regression. Results In descriptive analysis, there was no significant difference between male and female sex in age, race, level of education, deployments, exacerbations, GINA step therapy, comorbid sleep-disordered breathing, gastroesophageal disease, or body mass index (BMI). Male sex had higher incidence of depression and anxiety than females (81% vs 27%, p-value 0.002). Female sex had higher incidence of allergic rhinitis (88% vs 53%, p-value 0.038). Evaluating the association between biomarkers and sex, IL-18 was significantly lower in female sex compared to male (estimated coefficient -6.09, p-value 0.036). Females had higher neutrophil percent (estimate coefficient 10, p-value 0.034). Notably there was no difference in eosinophil, IgE, TSLP, or IL-5 when comparing male and females asthmatics. Conclusions Although population-based studies have linked female sex to poorer asthma control, this was not reflected in this cohort. T2 biomarkers were also not different between the groups. Interestingly, the higher neutrophil percent in the female group can be supportive of neutrophilic (non-T2) asthma which would be consistent with literature. The significant difference in IL-18 may have future implications given its role in T2 and non-T2 inflammation and its contribution to chronic airway inflammation and hyperresponsiveness. Blocking IL-18 and associated pathways may play improve asthma management, particularly, in severe cases as an additional option for treatment. Limitations of this study include small sample size. This cohort had minimal exacerbation history and generally well-controlled asthma. Future directions would be to specifically evaluate the subgroup of severe asthma for biomarker differences. This abstract is funded by: U.S. Department of Veteran Affairs grant IK2 BX4004219 (K.J.W.)
Bowles et al. (Fri,) studied this question.