Rhinitis goblet cells replace ciliated columnar epithelial cells in the nasal mucous membrane. This results in mucin hypersecretion by goblet cells and decreased mucociliary activity. Nasal secretion are not adequately cleared with clinical manifestation of nasal congestion, sinus pressure, post-nasal dripping, and headache. Over-expression of transient receptor potential (TRP) ion channels, such as TRPA1 and TRPV1, may be involved in the pathogenesis of non-allergic rhinitis. Neurogenic inflammation produced by neuropeptides released from sensory nerve endings to the airways is a proposed common mechanism of association between both allergic and non-allergic rhinitis with asthma. This may explain higher association of rhinitis with
Rhinitis medicamentosa Rhinitis medicamentosa Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose. The characteristic presentation of RM involves nasal congestion without rhinorrhea, postnasal drip, or sneezing following several days of decongestant use. This condition typically occurs after 5–7 days of use of topical decongestants. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening