Allergic Rhinitis


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Maria Patricia S. Abes, MD; Maria Remedios D. Ignacio, MD; Nanneth T. Tiu, MD – a group of expert Filipino ALLERGISTS bond together as the H & L Allergy Team, whose aim is to give advice, to help readers understand and find relief in dealing with common allergic disorders.

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Allergic Rhinitis (AR) is an inflammation of the nose that affects approximately 25 percent of adults and more than 40 percent of children.1 Although, It is not life threatening, it should not be sneezed at! A significant health burden like impairment in physical and social functioning, daytime sleepiness and fatigue, irritability, depression and attention deficit, learning and memory deficits, loss of productivity at work, sexual dysfunction, and sleep disordered breathing may occur. Epidemiological surveys also have shown that 38 percent of patients with AR have asthma and about 78 percent of asthma patients have AR.2 Therefore, it is important that AR patients should have an accurate diagnosis and adequate treatment.

Signs and symptoms

Allergic rhinitis is caused by inhalation of allergens such as pollen, dust, or animal dander that trigger an abnormal reaction in the nose of susceptible people, especially those with asthma or a family history of atopy. It can also be triggered by irritants such as wearing perfumes, using scented soaps, etc. Within minutes of contact with an allergen, IgE-sensitized mast cells degranulate and release mediators that lead to the symptoms of:

• nasal congestion
• rhinorrhea
• sneezing
• itching

Allergic Rhinitis may be classified as:

1. Temporal pattern and context of exposure to a triggering allergen
a. seasonal (eg, pollens)
b. perennial (year-round exposures, eg, house dust mites)
2. Frequency and duration of symptom
a. intermittent (<4 days per week or <4 weeks per year)
b. persistent (>4 days per week and >4 weeks per year)
3. Severity
a. mild (when symptoms are present but are not interfering with quality of life)
b. severe (when symptoms are bad enough to interfere with quality of life).

Factors that may lead to a more severe classification include sleep disturbance; impairment of daily, sport, or leisure activities.

Diagnosis: history, PE, tests

Allergic Rhinitis is mainly diagnosed based on clinical history, supported by nasal examination, and the the presence of allergic shiner, allergic salute, nasal crease, mouth breathing and Dennie–Morgan fold. Allergy testing may be done and is indicated for patients with severe, persistent AR who do not respond to regular treatment, or when a specific causative allergen must be identified to target therapy. This is performed by putting a drop of a suspected allergen and is pricked on the surface of the skin. If the patient is allergic to the substance, a redness or swelling can be observed within 20 minutes.

Treatment

• Environmental control – eg. removal of stuffed toys,cleaning of aircon filter
• Pharmacologic therapy – antihistamines (oral, intranasal), intranasal corticosteroids, Leukotriene Receptor Antagonists (LTRAs )
• Allergen immunotherapy – involves giving gradually increasing doses of the substance, or allergen, to which the person is allergic and is indicated for severe, persistent AR.
• Education – allergy is not curable but it is preventable and proper management is a must!

Pharmacologic Therapy

1. Oral antihistamines target the histamine1 (H1) receptor and relieve the itching, sneezing, and rhinorrhea of AR. Antihistamines are available as oral (first- and secondgeneration) and intranasal preparations.

First-generation antihistamines (eg. diphenhydramine, chlorpheniramine, and hydroxyzine) cross the blood-brain barrier easily and bind central H1-receptors abundantly, which can cause sedation. They can also cause dry mouth, dry eyes, urinary retention, constipation, and tachycardia. Cumulative use of first-generation antihistamines has been associated with higher risk of dementia.

Second- generation antihistamines (eg. fexofenadine, cetirizine, levocetirizine, loratadine, desloratadine, ebastine, epinastine, and bilastine) have limited penetration of the blood-brain barrier, thus reducing sedation.

2. Intranasal antihistamines – Intranasal preparations of azelastine and olopatadine have a rapid onset of action and may aid in reducing nasal congestion. Sedation and bitter taste have been reported with both preparations.

3. Intranasal corticosteroids – Intranasal corticosteroids (INCS) have potent anti-inflammatory properties that reduce symptoms of sneezing, itching, rhinorrhea, and congestion. Intranasal, oral, and injectable corticosteroids are available, but oral and injectable preparations are generally not recommended for AR because of the adverse effects of systematically administered corticosteroids.

Common adverse effects of INCS include: nasal dryness, burning, stinging, blood tinged secretions, and epistaxis. The package inserts for all INCSs recommend monitoring for intraocular pressure, glaucoma, and cataracts; monitoring for growth is also recommended in the pediatric population.

4. Leukotriene receptor antagonists (LTRAs ) inhibit leukotrienes and inflammatory mediators which contribute to the symptoms of AR. Montelukast is the only LTRA approved by the FDA for the treatment of Seasonal AR.

Montelukast has a good safety profile and has been approved for patients 6 months or older. Potential adverse effects include: upper respiratory tract infection and headache. There are post-marketing reports of rare drug-induced neuropsychiatric events, including aggression, depression, suicidal thinking, and behavior. As many as 40 percent of patients with AR have coexisting asthma. Because montelukast has been approved for both rhinitis and asthma, it may be considered in such patients.

Treatment guidelines

Many patients with AR are under-recognised and poorly managed so several guidelines have been developed to address this issue and to improve care of patients, reduce cost and variations in care. However, guidelines should not replace individualization of patient care or clinical judgment. It should be used as a starting point for the clinician and patient to determine, through shared decision making, what would constitute the optimal treatment for AR at the current time.

References:
1. Mark S. Dykewicz, MD et al Ann Allergy Asthma Immunology (2017)
2. Erwin W. Gelfand, MD JACI 2004 Inflammatory mediators in allergic rhinitis
3. Allergic Rhinitis & Impact on Asthma Guidelines

July 2018 Health and Lifestyle

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