Allergic rhinitis represents a global health problem. It is an extremely common disease worldwide affecting 10 to 25% of the population (IRMWG 1994) and an increasing prevalence has been recognized in the few last decades (Togias 2000).

Allergic rhinitis is clinically defined as a symptomatic disorder of the nose induced by an IgE‐mediated inflammation following exposure of the membranes lining the nose to allergens such as dust mites, moulds and pollens. Symptoms of rhinitis include rhinorrhoea, nasal congestion, nasal itching and sneezing, which are reversible spontaneously or under treatment.

Allergic rhinitis was previously subdivided, based on time of exposure, into seasonal, perennial or occupational. A new classification has been developed which is based on duration of symptoms and distinguishes allergic rhinitis as "intermittent" or "persistent" (Bousquet 2001). According to this classification, intermittent allergic rhinitis (symptoms for less than four days per week, or for less than four weeks) would correspond most closely with seasonal allergic rhinitis (hay fever). Persistent allergic rhinitis (symptoms for more than four days per week, or for more than four weeks) would correspond most closely with perennial and occupational allergic rhinitis. The validity of the new classification has, however, been recently challenged (Demoly 2003).

A diagnosis of allergic rhinitis is made by:

‐ positive history;
‐ positive skin test for prevalent aeroallergen and/or by allergen specific serum IgE;
‐ demonstration that the symptoms are the results of IgE‐mediated inflammation (Skoner 2001).

Patients with non‐allergic rhinitis with eosinophilia syndrome (NARES), where nasal eosinophilia are present yet skin tests or serum IgE levels reveal no evidence of an allergic cause, will not be considered in this review.

The concept of "minimal persistent inflammation" is a new but important hypothesis that was recently proposed by Ciprandi et al (Ciprandi 1995) and is a feature of perennial and seasonal allergy (Ricca 2000). It is characterized by an inflammation made up of different cells. The symptomatology is currently considered to be caused mainly by the accumulation and activation of infiltrating cells, such as mast cells, basophils and eosinophils, which release mediators and cytokines and result in allergic inflammation.

Non‐specific nasal hyperresponsiveness is also an important feature of allergic and non‐allergic rhinitis. It can be defined as increased nasal responsiveness to a normal stimulus resulting in sneezing, nasal congestion and secretion (Gerth 1999). This phenomenon is believed to result from the effect of allergic inflammation on the sensory nerves that supply the upper airway mucosa. The nerves present in nasal mucosa include cholinergic nerves and nerves of the non‐adrenergic, non‐cholinergic system (NANC). Sensory C fibers contain neuropeptides, such as substance P, neurokinin A and K, and calcitonin gene‐related peptide (Bousquet 2001). Various non‐allergic triggers have been shown to act on the nasal mucosa through sensorineural stimulation. Also in allergic rhinitis stimulation of sensory nerves per se can produce inflammatory changes, a phenomenon known as neurogenic inflammation (Togias 2000).

Management options for allergic rhinitis include allergen avoidance, medication, immunotherapy and education. Medications include oral and topical H1‐antihistamines, decongestants, leukotriene antagonists and chromones, topical glucocorticosteroids and anti‐cholinergics. However, medication has no long‐lasting effect when stopped (Bousquet 2001).

A pharmacologic agent that has proved useful in the investigation of effects of neuronal stimulation is capsaicin (8‐methyl‐n‐vanillyl‐6‐nomamide), the pungent component of hot pepper. Intranasal capsaicin specifically stimulates afferent nerves consisting mostly of unmyelinated C fibers and some myelinated a delta fibers. As a result it can trigger central and axonal reflexes, the latter being putatively mediated by the release of neuropeptides (Sanico 1997). Capsaicin as a blocking agent of neuropeptides, especially substance P, blocks the axon reflex and exerts a curative effect on allergic rhinitis (Zhang 1995). Capsaicin pretreatment of the nasal mucosa may result in a long‐lasting amelioration of symptoms upon allergen challenge in patients with allergic rhinitis (Stjarne 1998) and non‐allergic rhinitis (Lacroix 1991). Neurogenic mechanisms play a role in nasal allergic inflammation and repeated topical capsaicin applications induce desensitization of the human nasal mucosa in vivo, with a reduction in the tissue content of neuropeptides (Lacroix 1991).

We plan to systematically review the safety and effectiveness of capsaicin in the treatment of allergic rhinitis in adults.