Secondary Symptoms
Mucus Trafficking through the Laryngopharynx IgE-mediated histamine liberation, in conjunction with other inflammatory mediators, precipitates mucosal oedema, augmented mucus secretion, bronchial smooth muscle constriction, and airway architectural alterations in both the nasal and bronchopulmonary regions[34, 37-40]. Enhanced mucus translocation from the bronchi or nasal cavity towards the larynx may instigate epithelial irritation, compromise glottic closure, and provoke airway reflexive responses, culminating in a diverse array of aerodigestive manifestations[25, 41]. Although post-nasal drip (PND) is posited as a pivotal component of the UACS hypothesis, its attribution as the aetiological agent for symptoms such as throat clearing and cough in patients with AR and ARS remains a subject of academic debate, especially when nasoendoscopic observations do not corroborate anomalous secretions[26]. Additionally, the UACS paradigm may be insufficient in addressing the multifaceted symptomatology accompanying or occurring independently of cough in UTCS. Nasal Airflow Obstruction Nasal congestion in AR leads to a compensatory shift towards oral respiration, bypassing the nasal humidification and filtration mechanisms. This change may undermine the laryngopharyngeal epithelial barrier by promoting mucosal desiccation, increasing allergen deposition in the aerodigestive tract, and exacerbating lower airway constriction [28]. Secondary Phonotrauma Phonotrauma, often linked to vocal misuse or overuse[42]., refers to epithelial damage induced by excessive vocal cord vibrations or contact[43] [44]. Chronic airway symptoms such as persistent cough and throat clearing, which necessitate robust laryngeal contraction and elevated glottic pressure, can secondarily induce phonotrauma[44]. This may initiate a self-sustaining feedback loop of irritation and reflexive symptoms over time, as depicted in Figure 2 [45] [46]. United Airway effects A growing corpus of literature advocates for the ”Unified Airway Model,” in which different segments of the respiratory tract are considered as functionally interconnected[40, 47, 48]. Inflammatory mediators, specifically vascular cytokines, circulate locally, enabling inflammation in one segment to influence others. While this concept has been well-studied in the context of lower airway and nasal interactions[29, 39, 48], its implications for the laryngopharynx remain largely unexplored yet offer a plausible mechanism linking nasal and lower airway inflammation with non-specific chronic laryngitis.