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Concept
Rhinitis medicamentosa
Summary
Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion suspected to be 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, although evidence has been contradictory.
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 the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in permanent turbinate hypertrophy, which may block nasal breathing until surgically removed.
Common issues that lead to overuse of topical decongestants:
Deviated septum
Upper respiratory tract infection
Vasomotor rhinitis
Cocaine use and other stimulant abuse
Pregnancy (these products are not considered safe for pregnancy)
Chronic rhinosinusitis
Hypertrophy of the inferior turbinates
The pathophysiology of RM is unclear, although several mechanisms involving norepinephrine signaling have been proposed. RM is associated with histological changes that include: an increase in the number of lymphocytes and fibroblasts, epithelial cell denudation, epithelial edema, goblet cell hyperplasia, increased expression of the epidermal growth factor receptor, increased mucus production, nasociliary loss, inflammatory cell infiltration, and squamous cell metaplasia.
Direct acting sympathomimetic amines, such as phenylephrine stimulate alpha adrenergic receptors, while mixed-acting agents, such as pseudoephedrine can stimulate both alpha and beta adrenergic receptors directly and indirectly by releasing norepinephrine from sympathetic nerve terminals.
Official source
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