Abstract

Severe asthma is a heterogeneous disease consisting of several endotypes and phenotypes diagnosed due to different biomarkers. Frequency of different endotypes and phenotypes in real clinical practice needs further investigation.The aim of this study was to assess biomarkers of T2-inflammation in patients with severe asthma in a single secondary care center.Methods. We examined 96 adult outpatients (34% male) with severe asthma. Data collected included demographics, smoking history, asthma exacerbations during previous 12 months, medication use, comorbidities. Lung function tests were assessed by using the Spirograph 2120 (Vitalograph, Great Britain). Blood eosinophils (Eos) were measured by automatic haemoanalyser. Atopic status was determined by positive skin prick-test (> 3 mm) and/or serum specific IgE to common inhalant allergens. Serum total IgE levels were assessed by immunofluorescence assay. FeNO was measured by a chemiluminescence analyzer (Model LR4000; Logan Research, Rochester, UK). Presence of allergy, need for regular oral steroid use, blood Eos ≥ 150 cell/μl and FeNO ≥ 20 ppb were considered as markers of T2-driven inflammation. Asthma control and quality of life were assessed by using Russian versions of ACQ-5 and St. George's Respiratory Questionnaire (SGRQ). Statistical analyses were performed with Statistica Ver. 10.0 (StatSoft, Inc., USA).Results. The majority of patients with severe asthma (93%) have at least one or more elevated markers (presence of allergy, need for regular oral steroid use, Eos ≥ 150 cell/μl or FeNO ≥ 20 ppb) of T2-inflammation. Biomarkers levels did not differ in non-steroid-dependent and steroid-dependent patients. The most frequent markers were allergy and blood Eos ≥ 150 cell/μl. Two or more elevated biomarkers were revealed in 72% of patients.Conclusion. The majority of patients with severe asthma in real clinical practice have signs of T2-inflammation. It seems that many severe asthmatics have indications for prescription of biological and can be treated by more than one of monoclonal antibodies against major cytokines of T2-inflammation.

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