Anti-IL-5/5Ra biologics improve work productivity and activity in severe asthma: a RAPSODI registry-based cohort study.

INTRODUCTION: Severe asthma is associated with a serious disease burden, partially caused by limitations in activity and work impairment. AIMS AND OBJECTIVES: This study aims to relate treatment with biologics targeting IL-5/5Ra to work productivity and activity in the long term in a real-world context. MATERIAL AND METHODS: This is a registry-based multi-center cohort study evaluating data from adults with severe eosinophilic asthma included in the Dutch Register of Adult Patients with Severe Asthma for Optimal DIsease management (RAPSODI). Patients that started with anti-IL-5/5Ra biologics and completed the work productivity and activity improvement questionnaire, were included. Study and patient characteristics were compared between the employed and unemployed patients. Work productivity and activity impairment are related to accompanying improvements in clinical outcomes. RESULTS: At baseline, 91 of 137 patients (66%) were employed which remained stable throughout the follow-up period. Patients in the working age category were younger and had significantly better asthma control (p = 0.02). Mean overall work impairment due to health decreased significantly from 25.5% (SD2.6) to 17.6% (SD 2.8) during 12 months anti-IL-5/5Ra biologics treatment (P = 0.010). There was a significant association between ACQ6 and overall work improvement after targeted therapy (ß = 8.7, CI 2.1-15.4, P = 0.01). The improvement of asthma control of 0.5 points on the asthma Control Questionnaire was associated with an overall work impairment of -9%. CONCLUSIONS: Work productivity and activity in severe eosinophilic asthma improved after starting anti-IL-5/5Ra biologics. Clinically relevant improvement in asthma control was associated with an overall work impairment score of -9% in this study.

Obesity and asthma: co-morbidity or causal relationship?

There is substantial evidence that obesity and asthma are related. "Obese asthma" may be a unique phenotype of asthma, characterized by decreased lung volumes, greater symptoms for a given degree of lung function impairment, destabilization or lack of asthma control, lack of eosinophilic inflammation and a different response to controller medication. Whether this relationship between obesity and asthma is causal or represents co-morbidity due to other factors is unclear. In previous reviews concerning the relationship between obesity and asthma, five hypotheses were put forth. One of these hypotheses is that a low grade systemic inflammation caused by adipokines from the fat tissue causes or enhances bronchial inflammation. In animal models, there is an increasing amount of evidence for the role of adipokines derived from fat tissue in the relationship between obesity and asthma. The data are conflicting in humans. Since obesity is a component of the metabolic syndrome and the metabolic syndrome is also a form of systemic inflammation, it is to be expected that there is a relationship between metabolic syndrome and asthma. The few data that are available show that there is no relationship between metabolic syndrome and asthma, but there is one between the metabolic syndrome and asthma-like symptoms. Further research is needed to confirm the relationship between obesity and asthma in humans, where a rigorous approach in the diagnosis of asthma is essential.