ALLERGIC RHINITIS (hay fever, seasonal allergic rhinitis) is the most common form of respi allergy presumed to be mediated

by an immediate (type 1 hypersensitivity) immunologic reaction, and it is among the top 10 reasons for visits to primary care physicians. Symptoms are similar to those of viral rhinitis but are usually more persistent and demonstrate seasonal variation; rhinitis is considered to be the allergic form if the symptoms are caused by allergen specific IgEmediated immunologic response. COMPLICATIONS Allergic asthma Chronic nasal obstruction Chronic otitis media with hearing loss Anosmia (absence of the sense of smell) In children, orofacial dental deformities SEASONAL OCCURRENCE Early spring- tree pollen (oak, elm, poplar) Early summer- rose pollen (rose fever), grass pollen (Timothy, red-top) Early fall- weed pollen (ragweed) PATHOPHYSIOLOGY Sensitization begins by ingestion or inhalation of an antigen nasal mucosa reacts by slowing of ciliary action, edema formation and leukocyte (primarily eosinophil) infiltration trigger release of histamine in the mucosa tissue edema results in vasodilation and increased capillary permeability CLINICAL MANIFESTATION Sneezing and nasal congestion Clear, watery nasal discharge Nasal itching Itching of throat and soft palate is common Headache, pain over the paranasal sinuses, and epistaxis can accompany allergic rhinitis Fatigue Loss of sleep Poor concentration ASSESSMENT AND DIAGNOSTIC FINDINGS Diagnosis is based on history, PE, and diagnostic test result. Nasal smear Peripheral blood counts Total serum IgE Epicutaneous and intradermal testing RAST Food elimination and challenge Nasal provocation Results indicative of allergy as the cause of rhinitis includes increased IgE and eosinophil levels and positive reactions on allergen testing. MEDICAL MANAGEMENT Goal: to provide relief of symptom Avoidance therapy, pharmacotherapy, and immunotherapy. Verbal instructions must be reinforced by written info Avoidance Therapy Every attempt is made to remove the allergens that act as precipitating factor. Examples includes: use of air conditioners, air cleanser, humidifiers, and dehumidifier; removal of dust- catching furnishings, carpets, and window covering; removal of pets from the home or bedroom; use of pillows and mattress covers that are impermeable to dust mites; smoke-free environment. HEPA (high-efficiency particulate air) purifiers and vacuum cleaner filter may also be used

Pharmacotherapy AntiHistamines- Dipenhydrmine (Benadryl), Hydroxyzine (Atarax), Cetirizine (Zyrtec), Loratadine (Alavert, Claritin), Fexofenadine (Allegra) Adrenergic Agents- are vasoconstrictor of mucosal vessel, used topically in addition to oral route.topical route less side effects. However, used in minimal days to prevent rebound congestion. Mast Cell Stabilizers- Intransal cromolyn sodium (NasalCrom) is a spray that acts by stabilizing the mast cell membrane, thus reducing the release of histamine and other mediators of the allergic response. Corticosteroids- intranasal corticosteroids are indicated in more severe cases of allergic rhinitis that cannot be controlled by more conventional meds such as decongestants, antihistamines, and intranasal cromolyn. E.g. Beclomethasone (Beconase, Vancenase), Budesonide (Rhinocort), Dexamethasone (Decadron), Flunisolide (Nasalide), Fluticasone (Cutivate, Flonase) and Traimcinolone (Nasacort) Leukotriene Modifiers- Zileuton (Zyflo), Zafirlukast (Accolate) and Montelukast (Singulair) block the synthesis or action of leukotriene and prevent signs and symptoms associated with asthma Immunotherapy Allergen desensitization Involves the administration of gradually increasing quantities of specific allergens to the patient until dose is reached that is effective in reducing disease severity from natural exposures. GOAL: reducing the level of circulating IgE, increasing the level of blocking antibody IgG, and reducing mediator cell sensitivity.