Most symptoms of chronic rhinosinusitis manifest in adulthood, in this connection it is not always possible to assume the endotype of the disease by phenotype in a child. An early identification of the disease’s endotype is necessary for optimization of diagnosis and choice of personalized management of children with chronic rhinosinusitis.
OBJECTIVE
To develop an algorithm for diagnosis of endotypes of chronic rhinosinusitis in children.
PATIENTS AND METHODS
The study included 160 children diagnosed with «chronic rhinosinusitis». Inflammatory markers, namely IL-5, IFN-γ, IL-17α, TNF-α, IL-22, IL-6, IL-33, IL-35, ECP, MPO, TGF-β1, total IgE, were determined in the blood serum and nasal secretion by enzyme immunoassay. The endotypes of chronic rhinosinusitis were determined by cluster analysis. The coupling of the endotypes with the phenotypes of the disease was done and markers with high discriminant power for each endotype were identified.
RESULTS
After comparison of the coupling between phenotypes and all endotypes, it has been found that the phenotype of chronic rhinosinusitis with polyps and concurrent diseases (allergic rhinitis and bronchial asthma) has the Th-2 endotype by nasal secretion markers, but 3 different subendotypes by blood serum markers. The phenotype of chronic rhinosinusitis without polyps and concomitant pathology has the same set of markers in nasal secretion and in blood serum — Th-1 endotype. The phenotype of chronic rhinosinusitis associated with hypertrophy of the pharyngeal lymphatic ring has its own endotype with high degree of coupling.
CONCLUSIONS
ECP and IL-33 are nasal secretion markers for the Th-2 endotype, IFN-γ is the Th-1 endotype marker, IL-35, MPO and TGF-β1 are markers for the endotype associated with hypertrophy of the pharyngeal lymphatic ring. The blood serum markers can be used for the identification of subendotypes of the Th-2 endotypes: IL-17 and IL-22 — for the subendotype of chronic rhinosinusitis with polyps, ECP — for the subendotype with allergic rhinitis, a decrease in the IL-35 level — for the subendotype with high risk of bronchial asthma development.
