Abstract

Chronic rhinosinusitis with nasal polyposis (CRS with NP) is a clinical syndrome including several clinical phenotypes and endotypes with differences in pathophysiology and is divided into neutrophilic (non-type 2) and eosinophilic (type 2) according to the dominant endotype, which is the most severe variant associated with therapy resistance and frequent recurrence. Such pheno-endotype requires personalized treatment, and pharmacotherapy based on endotyping is prospective. Aminocapronic acid (ACA) competitively inhibits plasminogen and plasmin formation, inhibits C3a and C5a, which can affect the pathophysiological mechanisms of eosinophilic inflammation and polypous growth, since, in addition to hemostatic properties, it also has desensitizing, anti-enzymatic, and anti-proliferative properties.
 The aim of the research: to evaluate the influence of additional administration of aminocapronic acid on the degree of regression of nasal polyps in comparison with patients receiving standard therapy of Chronic rhinosinusitis with nasal polyposis according to clinical recommendations.
 Material and methods. The study included 120 outpatients, divided into two groups: the main (n - 60) and control (n - 60) ones. The average age of the main group was 45.8 years; the control group was 47.0 years. Patients were prescribed basic treatment (irrigation therapy with saline solutions and mometasone furoate), and in the main group – additionally aminocapronic acid (ACA). The evaluation of treatment effectiveness was based on the analysis of the dynamics of nasal congestion and the regression of nasal polyps at V2 (day 5±1), V3 (day 10±1), V4 (day 20±1) and V5 (day 30±1) compared to V0. Indications for surgical treatment were determined at V3.
 Results. The use of aminocapronic acid in Chronic rhinosinusitis with nasal polyposis contributes to a reliable reduction in the severity of the main clinical symptoms (rhinorrhea, postnasal drip, nasal congestion, reduced sense of smell), nasal congestion starting from V2, regression of polyps – from V3 compared to patients of the control group. This ensured a statistically significant 25% reduction in the number of operated patients: 56.7% in the main group versus 81.7% in the control (p<0.05). Conservative treatment was continued by 43.3% of patients of the main group and by 18.3% of patients of the control group (p<0.05). After the operated patients were removed from the groups, they did not significantly differ in the dynamics of regression of nasal congestion and nasal polyps at V4 and V5 (p>0.05). Differences in the results of treatment are attributed to the clinical effects of Aminocapronic acid (ACA), since the group characteristics of the patients were commensurable.
 Conclusions:
 
 the additional appointment of Aminocapronic acid (ACA) to patients with Chronic rhinosinusitis with nasal polyposis contributes to a faster regression of nasal congestion associated with edematous changes of the mucous membrane of the nasal cavity, compared to the regression of polyps during the fifth day of treatment;
 there is a significant difference in the severity of symptoms in the main group during the 10th day of treatment compared to patients in the control group;
 the reliable positive dynamics of clinical symptoms correlates with a reliable, at 25%, decrease in the number of operative interventions in the main group.

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