Divided into seasonal or perennial types.
Seasonal allergic rhinitis triggered by outdoor allergens such as pollens and molds.
Perennial allergic rhinitis induced mainly by indoor allergens such as dust mite, molds and animal dander.
Seasonal and perennial allergic rhinitis can coexist in the same patient.
Characterized by sneezing, rhinorrhea, nasal congestion, itching palate, red, watery and itching eyes which may be seasonal or persistent.
Many patients have mild symptoms which are ignored, while others have more significant symptoms treated with antihistamines or topical corticosteroid sprays.
Mostly associated with clear nasal discharge caused by IgE mediated reactions against inhaled allergens and involves mucosal inflammation driven by type 2 helper T (Th2) cells.
Exposure of individuals to an allergen against which they are sensitized cross-linking by the allergen of IgE bound to mucosal mast cells results in nasal symptoms within minutes.
Nasal symptoms is due to release of neuroactive and vasoactive substances such as histamine, prostaglandin D2, and cysteine like leukotrienes.
Allergens include: seasonal pollens, molds, and perennial indoor allergens such as dust mites, pests, pets, and some molds.
The pattern of allergens depends on geographic location, and degree of urbanization but the overall prevalence of sensitization does not vary across the US.
Sensitization to inhaled allergens beginning next during the first year of life.
Sensitization to indoor allergens precede sensitization to pollens.
Frequency of sensitization to inhalant allergies is increasing.
Sensitization to inherent inhaling allergens occurs in more than 40% of the population in the US.
Coexisting conditions include: chronic sinusitis, asthma, otitis media, nasal polyps, and upper respiratory infection.
It is difficult to diagnose allergic rhinitis in children in the first 2-3 years of life because of frequent frequent viral infections that occur in young children.
Prevalence peaks in the 2nd to 4th decades of life, then gradually diminish.
Affects about one fourth of adults in developed countries.
Affects 20-40% of US population.
Diagnosis can usually be made on the basis of history and clinical exam.
Edema and venous engorgement of nasal mucosa causes eustachian tube blockage, sinus pressure and cough.
Diagnosis often made on the basis of clinical characteristic symptoms and response to empirical treatment with an antihistamine or nasal glucocorticoid.
Formal diagnosis requires evidence of sensitization measured by allergen specific IgE in the serum or by positive skin tests and history of symptoms that correspond with exposure to the sensitizing allergen.
It is easier to diagnose the process when seasonal symptoms are present or when the patient can clearly identify a single trigger than when symptoms of chronic with the patient has more than one trigger, including allergens and irritants.
Skin testing and testing for allergen specific IgE have similar sensitivity, but they do not identify sensitization in overlapping groups of patients.
Blood testing does not require stoppage of antihistamines whereas skin testing advantage is that it provides immediate results.
19-38% of patients have coexisting asthma.
Differential diagnosis includes forms of rhinitis nonallergic in origin such as vasomotor rhinitis and nonallergic chronic rhinosinusitis.
Having multiple older sibs and growing up on a farm associated with reduced risk of allergic rhinitis.
Children with the allergic rhinitis are more likely than unaffected children to have myringotomy tubes placed and have their tonsils and adenoids removed.
Complications include sinusitis, asthma and nasal polyps.
Severity assessed by assigning numerical values for eye symptoms, nasal itching, sneezing, rhinorrhea, and nasal congestion with 0,1,2 and 3 ratings from no symptoms to severe symptomatology and the interference with sleep, leisure, school or work and the duration of such symptoms from minutes to hours daily.
Symptomatic disorder IgE mediated inflammation after allergen exposure.
Allergic specific IgE antibodies bind to high affinity Fc receptors on mast cell and basophil cell surfaces.
Following reexposure to allergens Fc receptors are crossed link activating mast cells in the nasal mucosa with release of histamine, leukotrienes, cytokines and chemokines.
The chemicals released cause vascular dilation, endothelial leakage of fluid, and irritation of sensory nerves.
As secretions accumulate sneezing and rhinorrhea occur and nasal congestion appears as vascular sinusoids in the nasal mucosa fill with blood.
For a few hours recruitment of inflammatory cells such as neutrophils, eosinophils, and T cells occur prolonging the inflammation and this delayed response is dependent on the initial IgE mediated response, but responds to medications differently than the initial response.
Glucocorticosterids suppress the late phase but does not affect the immediate allergic response.
Inherited predisposition to phenotype type 2 helper T (TH2) cells, atopic individuals exhibit exaggerated responses to normal substances.
The type 2 helper T cells initiate type 1 hypersensitivity reactions seen in allergic rhinitis and seen in pollen induced rhinitis.
The immune system identifies an allergen as foreign and forms specific IgE antibodies in response.
Allergens originating from animals, insects, plants and fungi are airborne antigens that react with specific IgE antibodies.
When sensitizing allergens are reexposed specific IgE antibodies bound to mast cells are cross linked with resulting mast cell degranulation and release of histamine and other chemical mediators initiating the early phase response of the allergic reaction.
Following above an interaction of mast cells, epithelial cells, cells, T cells, innate lymphoid cells, eosinophils, basophils, Th2 inflammation develops in the nasal mucosal with the participation of chemokines and cytokines produced by the cells.
Mucosal inflammation leads to nasal symptoms that can persist for hours after allergen exposure and the mucosa can become more reactive to the precipitating allergen as well as the other allergens and non-allergenic stimuli such as odors and other irritants.
Affects 10-40% of the worldwide population.
One of the top 10 reasons for patient visits to a primary care physician.
Affects approximately 16% of the U.S. population.
Most patients with asthma have rhinitis.
The presence of allergic rhinitis significantly increases the probability of asthma of to 40%.
Atopic eczema frequently precedes allergic rhinitis.
Patients with allergic rhinitis usually have allergic conjunctivitis is well.
Symptoms relieved by H1 antihistamine-diphenhydramine or chlorpheniramine and second generation H1 antihistamines loratidine, desloratidine, fexofenadine and cetirizine.
Topical intranasal corticosteroids are the most effective agents for the prevention and symptomatic care.
Topical intranasal corticosteroids takes at least one week to be maximally effective relieving sneezing, nasal congestion, discharge and itching.
Intranasal steroids are the most effective pharmacotherapy for seasonal allergic rhinitis, but overall efficacy remains moderate.
The clinical effect with intranasal steroids appears within a day, but its peak effect is not reached for several weeks.
The superiority of intranasal steroids over at the histamines in the treatment of perennial allergic rhinitis remains uncertain.
There is insufficient data to determine effectiveness differences among various intranasal glucocorticoids.
Oral histamines and intranasal corticosteroids are recommended as first line therapy.
Cysteinyl leukotrienes are released in the nasal mucosa during allergic inflammation.
Oral leukotriene receptor antagonist montelukast has modest benefits in allergic rhinitis.
The effect of leukotriene-receptor antagonists on the symptoms of allergic rhinitis is similar to or slightly less that of oral antihistamines.
Some studies have shown a benefit of adding Leukotrienes-receptor antagonist monteleukast to an antihistamine.
Initial pharmacologic treatment of seasonal allergic rhinitis in patients aged ?12 years include:
routinely prescribe monotherapy with an intranasal corticosteroid rather than an intranasal corticosteroid in combination with an oral antihistamine.
The initial treatment of seasonal allergic rhinitis in persons aged ?15 years, recommend an intranasal corticosteroid over a leukotriene receptor antagonist.
For treatment of moderate to severe seasonal allergic rhinitis in persons aged ?12 years, it is recommend that the combination of an intranasal corticosteroid and an intranasal antihistamine be the initial treatment.
Allergic rhinitis affects about 1 in 6 people in the US.
Often, antihistamines are the first line of treatment but intranasal corticosteroids should be the first line of approach.
Can be associated with decreased quality of life, sleep deprivation, and impaired school and work performance.
Head to head trials of nonsedating antihistamines have not shown superiority of any specific agent over another.
H1 antihistamines are also available as nasal sprays and appear similar to oral preparations in efficacy but may be less acceptable due to a bitter taste.
As the effect on antihistamines and symptoms, especially nasal congestion, is modest, they can be combined with oral decongestants.
Topical nasal decongestants are more affective than oral lesions, but rebound congestion or reduced effectiveness can become a significant problem, and short term use is recommended.
Two forms of specific immunotherapy utilized for management: sublingual and subcutaneous.
1/3 of children and almost 2/3 of adults report partial a poor relief for pharmacotherapy for allergic rhinitis.
Sublingual immunotherapy involves placing the allergen under the tongue for local absorption to desensitize the patient over an extended treatment time to diminish allergic symptoms.
Moderate evidence on systematic review that sublingual immunotherapy reduces rhinitis and rhinoconjunctivitis by more than 40% in 9 of 36 studies vs a comparator (Lin SY et al).