D2.115 - Association of chemokine levels with types of reactions after alcohol consumption in patients with nonsteroidal anti-inflammatory drugs exacerbated respiratory disease (N-ERD)
Background
The airway epithelium is now considered an important component controlling airway inflammation. In response to variuos factors, it actively secretes mediators involved in the initiation of inflammatory reactions, including many chemokines that recruit immune cells to the tissues involved in this process. Nonsteroidal anti-inflammatory drugs exacerbated respiratory disease (N-ERD) is an asthma phenotype whose clinical picture has been widely described, but the pathomechanism is not fully understood. It is believed that alcohol hypersensitivity, manifested mainly by respiratory reactions, is more common in patients with N-ERD than in other groups of asthmatics. The aim of the study was to determine the relationship between the level of chemokines of epithelial origin and the type and severity of reactions to alcohol consumption in patients with N-ERD.
Method
The study involved 72 people (including patients with N-ERD, asthma without hypersensitivity to NSAIDs and healthy volunteers from the control group). Participants underwent a questionnaire and functional tests of the respiratory system (spirometry and FeNO measurement). In the obtained biological material (serum, exhaled air condensate and urine).The level of chemokines (CCL17 / TARC, CCL26 / Eotaxin-3, CCL5 / RANTES, CXCL10 / IP-10, CCL22 / MDC, CCL11 / Eotaxin-1) was determined using the ELISA method.
Results
Symptoms after drinking alcohol occurred in 20 (48%) patients with N-ERD, 7 (35%) patients with NTA (asthma without NSAID hypersensitivity) and 1 (9%) patient from control group. Any nasal or bronchial symptoms were found more frequently in patients with N-ERD as compared to healthy subjects. Dyspnea was more frequent in patients with N-ERD versus those with NTA and to the control group. Analyzing a group of patients with N-ERD, it was shown that patients who experienced alcohol-related nasal blockage had lower levels of CCL17/TARC in exhaled air condensate (EBC) than those without such a reaction. People with alcohol-related dyspnea had lower serum CCL26/eotaxin-3 levels. Patients with lower urinary CCL5/RANTES values were more likely to experience wheezing after drinking alcohol.
Conclusion
In patients with N-ERD, the type and severity of symptoms after drinking alcohol may be related to the existing inflammation of the upper and lower respiratory tract.
