It is an immunologic response of nasal mucosa to air-borne allergens and is characterised by watery nasal discharge, nasal obstruction, sneezing and itching in the nose. This may also be associated with symptoms of itching in the eyes, palate and pharynx. Two clinical types have been recognised:
Seasonal : Symptoms appear in or around a particular season when the pollens of particular plant, to which the patient is sensitive, are present in the air.
Perennial: Symptoms are present throughout the year.
AETIOLOGY
Inhalant allergens are often the cause. Pollen from the trees and grasses, mold spores, house dust, debris from insects or house mite are common offenders. Food allergy is rarely an important cause.
Genetic predisposition plays an important part. Chances of children developing allergy are 20% and 47% respectively, if one or both parents suffer from allergic diathesis.
PATHOGENESIS
Inhaled allergens produce specific antibody in the genetically predisposed individuals. This antibody becomes fixed to the blood basophils or tissue mast cells. On subsequent exposure, antigen combines with antibody at its Fab end. This reaction produces degranulation of the mast cells with release of several chemical mediators, some of which already exist in preformed state while others are synthesised afresh. These mediators are responsible for symptomatology of allergic disease.
Depending on the tissues involved, there maybe vasodilation, mucosal oedema, infiltration with eosinophils, excessive secretion from nasal glands or smooth muscle contraction. A ‘priming affect’ has also been described, i.e. mucosa earlier sensitised to an allergen will react to smaller doses of subsequnt specific allergen. It also gets ‘primed’ to other non-specific antigens to which patient was not exposed. Clinically, allergic response occurs in 2 phases:
Acute or early phase : It occurs immediately within 5-30 min. after exposure to the specific allergen and consists of sneezing, rhinorrhoea nasal blockage and/or bronchospasm. It is due to release of vasoactive amines like histamine.
Late or delayed phase : It occurs 2-8 hours after exposure to allergen without additional exposure. It is due to infiltration of inflammatory cellseosinophils, neutrophils, basophil, monocytes at the site of antigen deposition causing swelling, congestion, thick secretion. In the event of repeated or continuous exposure to allergen, acute phase symptomatology overlaps the late phae.
CLINICAL FEATURES
There is no age or sex predilection. It may start in infants as young as 6 months or older people. Usually the onset is at 12-16 years of age.
The cardinal symptoms of seasonal nasal allergy include paroxysmal sneezing, 10-20 sneezes at a time, nasal obstruction, watery nasal discharge and itching in the nose. Itching may also involve eyes, palate or pharynx. The duration and severity of symptoms may vary with the season.
Symptoms of perennial allergy are not so severe as that of the seasonal type. They include frequent colds, persistently stuffy nose, loss of sense of smell due to mucosal oedema, postnasal drip, chronic cough and hearing impairment due to eustachian tube blockage or fluid in the middle ear.
Signs of allergy may be seen in the nose, eyes, ears, pharynx or larynx.
Nasal signs include transverse nasal crease a black line across the middle of dosrum of nose due to constant upward rubbing of nose simulating a salute (allergic salute), pale and oedematous nasal mucosa which may appear bluish. Turbinates are swollen. Thin, watery or mucoid discharge is usually present.
Ocular signs include oedema of lids, congestion and cobblestone appearance of the conjunctiva dark circles under the eyes (allergic shiners).
Otologic signs include retracted tympanic membrane as a result of eustachian tube blockage.
Pharyngeal signs include granular pharyngitis due to hyperplasia of submucosal lymphoid tissue. A child with perennial allergic rhinitis may show all the features of prolonged mouth breathing as seen in adenoid hyperplasia.
Laryngeal signs include hoarseness of voice and oedema of the vocal cords.
DIAGNOSIS
A detailed history and physical examination is helpful, and also gives clues to the possible allergen. Other causes of nasal stuffiness should be excluded.
INVESTIGATIONS
□ Total and differential count. Peripheral eosinophilia may be seen but is an inconsistent finding.
□ Nasal smear shows large number of eosinophils in allergic rhinitis. Nasal smear should be taken at the time of clinically active disease or after nasal challenge test. Nasal eosinophilia is also seen in certain non-allergic rhinitis, e.g. NARES (non-allergic rhinitis with eosinophilia syndrome).
□ Skin tests help to identify specific allergen. They are prick, scratch a intradermal tests.
□ Radioallergosorbent test (RAST) is an invitro test and measures specific antibody concentration in the patient’s serum.
□ Nasal provocation test. A crude method is to challenge the nasal mucosa with a small amount of allergen placed at the end of a toothpick and asking the patient to sniff into each nostril and to observe if allergic symptoms are reproduced. More sophisticated techniques are available now.
COMPLICATIONS
Nasal allergy may cause:
□ Recurrent sinusitis because of obstruction to the sinus ostia.
□ Nasal polypi.
□ Serous otitis media.
□ Orthodontic problems and other illeffects of prolonged mouth breathing especially in children.
□ Bronchial asthma. Patients of nasal allergy have four times more risk of developing bronchial asthma.
TREATMENT
Treatment can be divided into:
□ Avoidance of allergens
□ Treatment with drugs
□ Immunotherapy
Avoidance of allergens : This is most successful if the antigen involved is single. Removal of a pet from the house, encasing the pillow or mattress with plastic sheet, change of place of work or sometimes change of job maybe required. A particular food article to which the patient is found allergic can be eliminated from the diet.
Treatment with drugs:
□ Antihistamines. They control rhinorrhoea, sneezing and pruritis. All antihistamines have the side effect of drowsiness; some more than the other. The dose and type of the antihistamines has to be individualised. If one antihistamine is not effective, another may be tried from a different class.
□ Sympathomimetic drugs (oral or topical). Alpha-adrenergic drugs constrict blood vessels and reduce nasal congestion and oedema. They also cause CNS stimulation and are often given in combination with antihistaminics to counteract drowsiness. Pseudoephedrine and phenyl-propanolamine are often combined with antihistaminics for oral administration.
Topical use of sympathomimetic drugs cause nasal decongestion. Phenylephrine, oxymetazoline and xylometazoline are often used to relieve nasal obstruction, but are notorious to cause severe rebound congestion. Patient resorts to using moreand more of them to relieve nasal obstruction. This vicious cycle leads to rhinitis medicamentosa.
□ Corticosteroids. Oral corticosteroids are very effective in controlling the symptoms of allergic rhinitis but their use should be limited to acute episodes which have not been controlled by other measures. They have several systemic side effects.
Topical steroids such as beclomethasone dipropionate, budesomide, flunisolide acetate fluticasone and mometasone inhibit recruitment of inflammatory cells into the nasal mucosa and suppress late-phase allergic reaction, are used as aerosols and are very effective in the control of symptoms. They have also been used in rhinitis medicamentosa while withdrawing topical use of decongestant nasal drops. Topical steroids have fewer systemic side effects but their continuous use may cause mucosal atrophy and even septal perforation. It is wise to break their use for 1-2 weeks every 2-3 months.They may promote growth of fungus.
□ Sodium chromoglycate. It stabilises the mast cells and prevents them from degranulation despite the formation of 19B-antigen complex. It is used as 2% solution for nasal drops or spray or as an aerosol powder. It is useful both in seasonal and. perennial allergic rhinitis.
Immunotherapy : Immunotherapy or hyposensitisation is used when drug treatment fails to control symptoms or produces intolerable side effects. Allergen is given in gradually increasing doses till the maintenance dose is reached. Immunotherapy suppresses the formation of 19B. It also raises the titre of specific antibody. Immunotherapy has to be given for a year or so before significant improvement of symptoms can be noticed. It is discontinued if uninterrupted treatment for 3 years shows no clinical improvement.