Abstract

Viral upper respiratory infection (VURI)-associated acute cough is the most common symptom worldwide among children and adults. It causes serious economic and social problems both for individual patients, patients’ families, and the health care system as a whole. There is still no effective pharmacological agent capable of interfering with all the main pathophysiological mechanisms involved in VURI-associated acute cough. This circumstance partly explains the increased prevalence of the prolonged course of acute respiratory infections, when the cough takes on the features of subacute or post-infectious course. The pathophysiology of this symptom is being actively investigated to optimize the treatment of cough. A viral infection provokes an acute cough induced by various irritative stimuli, the main one being secretions from the respiratory tract, which directly acts on reflexogenic areas of the mucosa. Inflammatory mediators also play an important role, acting on the peripheral sensory terminations of airways. Inflammatory mediators also induce post-infectious bronchial hyperreactivity, which is an important component of the pathogenesis of post-infectious cough. Recently, researchers are becoming increasingly interested in the role of the voluntary or conscious cough component, which is implemented due to the cortical response to afferent information from the receptors of the upper respiratory tract.This hypothesis explains the ineffectiveness of central antitussive agents in patients with viral infection-associated dry cough and expands the possibilities of peripheral antitussive agents represented by levodropropizine. In addition to the action on nerve endings, the agent also affects inflammatory mediators, which enhances its ability to break the “vicious circle” of this symptom, prevents the development of post-infectious cough and promotes rehabilitation of the bronchial tree. The efficacy and safety of levodropropizine has been demonstrated in clinical trials in both children and adults.

Full Text
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