Allergic Rhinitis



It is an IgE-mediated 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:

1. Seasonal. Symptoms appear in or around a particular seasonwhen the pollens of particular plant, to which the patient is sensitive,
Are present in the air.

1. 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 IgE antibody in the genetically predisposed individuals. This antibody becomes fixed to the blood basophils or tissue mast cells by its Fc end. On subsequent exposure, antigen combines with IgE 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 may be 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:


(a) Acute or early phase. It occurs immediately within 5-30minutes, after exposure to the specific allergen and consists ofsneezing, rhinorrhoea nasal blockage and/or bronchospasm. It isdue to release of vasoactive amines like histamine.


(b) Late or delayed phase. It occurs 2-8 hours after exposureto allergen without additional exposure. It is due to infiltration ofinflammatory cellseosinophils, neutrophils, basophil, monocytes andCD4 +T cells at the site of antigen deposition causing swelling,congestion, thick secretion. In the event of repeated or continuousexposure to allergen, acute phase symptomatology overlaps thelate phase.


Clinical Features