Allergic Rhinitis

• Seasonal (intermittent) — the classic hay fever, driven by tree, grass and weed pollens and by outdoor mould spores. Predictable timing, which makes pre-emptive treatment possible.
• Perennial (persistent) — year-round, driven by house dust mite, animal dander, cockroach and indoor moulds. Nasal blockage tends to dominate over sneezing.
• Occupational — triggered by a workplace allergen (flour, latex, laboratory animals, wood dust), and improving away from work.
• Local allergic rhinitis — an allergic nasal response with negative skin-prick and blood tests, because the IgE is produced locally in the nasal mucosa. It is often misdiagnosed as non-allergic rhinitis.

Not everything that runs is allergic. Non-allergic (vasomotor) rhinitis, rhinitis medicamentosa from overused decongestant sprays, hormonal rhinitis in pregnancy, and drug-induced rhinitis all mimic it and do not respond to antihistamines.

The mechanism is a two-phase reaction, and knowing which phase a treatment targets explains most of the pharmacology.

Sensitisation comes first: on early exposures the immune system produces allergen-specific IgE, which coats mast cells in the nasal mucosa. Nothing is felt at this stage.

The early phase takes minutes. Re-exposure cross-links IgE on the mast-cell surface, triggering degranulation — the release of preformed histamine, tryptase, prostaglandins and leukotrienes. Histamine acting on H1 receptors produces the immediate sneezing, itch, watery discharge and vasodilation.

The late phase takes 4–12 hours. Eosinophils, basophils and T-cells are recruited into the mucosa, producing the sustained congestion, reduced smell, and the “priming” that makes each subsequent exposure worse through a season. This is why antihistamines help itch and sneezing far more than blockage, and why nasal corticosteroids — which suppress the late phase — outperform them for a truly blocked nose.

Allergic rhinitis and asthma are one airway. Most people with allergic asthma have rhinitis, and untreated rhinitis worsens asthma control. New wheeze, breathlessness or chest tightness deserves assessment rather than more antihistamine.

See a clinician for symptoms only on one side, blood-stained or one-sided discharge, facial pain or complete loss of smell, or for symptoms not responding to standard treatment — these suggest polyps, a structural problem, or something else.

Distinguish from: viral upper respiratory infection (the common cold — shorter, with sore throat and sometimes fever, and coloured discharge), influenza, bacterial sinusitis, non-allergic rhinitis and nasal polyps.

Intranasal corticosteroids are the most effective single treatment for moderate-to-severe allergic rhinitis, better than oral antihistamines for congestion. Second-generation oral antihistamines are effective for sneezing, itch and rhinorrhoea and are non-sedating. Allergen immunotherapy is the only treatment that modifies the underlying disease rather than suppressing symptoms.

Topical decongestant sprays must not be used beyond a few days — rebound congestion (rhinitis medicamentosa) is a common and self-perpetuating trap.

Non-herbal measures carry real weight in allergic rhinitis. Allergen avoidance is effective where it is practical — dust-mite covers, keeping windows shut at peak pollen, showering after being outdoors — and saline nasal irrigation has reasonable evidence for washing allergen and mucus from the nasal cavity, is cheap, and is safe to combine with anything.

Among supplements, quercetin is the most commonly recommended on the basis of mast-cell stabilisation in vitro; human evidence in allergic rhinitis is limited and does not yet support a confident claim. Vitamin D deficiency is associated with more severe allergic disease, though correcting it has not been shown to treat rhinitis.