3. Delayed-Reaction Allergy
Delayed-reaction allergy is caused by activated T cells and not by
antibodies.
In the case of poison ivy, the toxin of poison ivy in itself does not
cause much harm to the tissues. However, on repeated exposure, it
does cause the formation of activated helper and cytotoxic T cells.
Then, after subsequent exposure to the poison ivy toxin, within a day
or so, the activated T cells diffuse from the circulating blood in large
numbers into the skin to respond to the poison ivy toxin.
The damage normally occurs in the tissue area where the instigating
antigen is present, such as in the skin in the case of poison ivy, or in
the lungs to cause lung edema or asthmatic attacks in the case of
some airborne antigens.
4. Allergic PersonThe allergic tendency is genetically passed from parent to child
and is characterized by the presence of large quantities of IgE
antibodies in the blood.
These antibodies are called reagins or sensitizing antibodies to
distinguish them from the more common IgG antibodies.
When an allergen (defined as an antigen that reacts
specifically with a specific type of IgE reagin antibody) enters
the body, an allergen-reagin reaction takes place and a
subsequent allergic reaction occurs.
A special characteristic of the IgE antibodies (the reagins) is a
strong propensity to attach to mast cells and basophils.
5. Allergic PersonAt any rate, many of the mast cells and basophils rupture;
others release special agents immediately or shortly
thereafter, including histamine, protease, slowreacting
substance of anaphylaxis (which is a mixture of toxic
leukotrienes), eosinophil chemotactic substance, neutrophil
chemotactic substance, heparin, and platelet activating
factors.
These substances cause such effects as dilation of the local
blood vessels; attraction of eosinophils and neutrophils to the
reactive site; increased permeability of the capillaries with loss
of fluid into the tissues; and contraction of local smooth
muscle cells.
8. IntroductionRhinitis is broadly defined as inflammation of the nasal
mucosa.
Allergic rhinitis is the most common type of chronic rhinitis,
affecting 10 to 20% of the population, and evidence suggests
that the prevalence of the disorder is increasing.
In the past, allergic rhinitis was considered to be a disorder
localized to the nose and nasal passages, but current evidence
indicates that it may represent a component of systemic
airway disease involving the entire respiratory tract.
Allergic Rhinitis
9. IntroductionEvidence has shown that allergen provocation of the upper
airways not only leads to a local inflammatory response, but
also to inflammatory processes in the lower airways, and this
is supported by the fact that rhinitis and asthma frequently
coexist.
Therefore, allergic rhinitis and asthma appear to represent a
combined airway inflammatory disease, and this needs to be
considered to ensure the optimal assessment and
management of patients with allergic rhinitis.
Allergic Rhinitis
10. PathophysiologyIn allergic rhinitis, numerous inflammatory cells, including
mast cells, CD4-positive T cells, B cells, macrophages, and
eosinophils, infiltrate the nasal lining upon exposure to an
inciting allergen (most commonly airborne dust mite fecal
particles, cockroach residues, animal dander, moulds, and
pollens).
The T cells infiltrating the nasal mucosa are predominantly T
helper (Th) in nature and release cytokines (e.g., interleukin IL-
3, IL-4, IL-5, and IL-13) that promote immunoglobulin E (IgE)
production by plasma cells.
Allergic Rhinitis
11. PathophysiologyIgE production, in turn, triggers the release of mediators, such
as histamine and leukotrienes, that are responsible for
arteriolar dilation, increased vascular permeability, itching,
rhinorrhea (runny nose), mucous secretion, and smooth
muscle contraction.
The mediators and cytokines released during the early phase
of an immune response to an inciting allergen, trigger a
further cellular inflammatory response over the next 4 to 8
hours (late phase inflammatory response) which results in
recurrent symptoms (usually nasal congestion).
Allergic Rhinitis
12. ClassificationRhinitis is classified into one of the following categories
according to etiology:
IgE-mediated (allergic)
Autonomic
Infectious
Idiopathic (unknown)
Traditionally, allergic rhinitis has been categorized as seasonal
(occurs during a specific season) or perennial (occurs
throughout the year).
allergic rhinitis is now classified according to symptom
duration (intermittent or persistent) and severity (mild,
moderate or severe).
Allergic Rhinitis
13. ClassificationRhinitis is considered intermittent when the total duration of
the episode of inflammation is less than 6 weeks, and
persistent when symptoms continue throughout the year.
Symptoms are classified as mild when patients are generally
able to sleep normally and perform normal activities (including
work or school); mild symptoms are usually intermittent.
Symptoms are categorized as moderate/severe if they
significantly affect sleep and activities of daily living and/or if
they are considered bothersome.
Allergic Rhinitis
14. Etiological Classification
Allergic Rhinitis
ETIOLOGICAL CLASSIFICATION OF RHINITIS
Type Description
IgE-mediated (Allergic) IgE-mediated inflammation of the nasal mucosa, resulting in eosinophilic and Th2-
cell infiltration of the nasal lining
Further classified as intermittent or persistent
Autonomic Drug-induced (rhinitis medicamentosa)
Hypothyroidism
Hormonal
Non-allergic rhinitis with eosinophilia syndrome (NARES)
Infectious Precipitated by viral (most common), bacterial, or fungal infection
Idiopathic Etiology cannot be determined
15. Classification (symptoms, duration & severity)
INTERMITTENT:
Symptoms 6 weeks
PERSISTENT:
Symptoms continue throughout the year
MILD:
Normal Sleep
No impairment of daily activities, sport, leisure
Normal work/school
No bothersome symptoms
Allergic Rhinitis
16. Classification (symptoms, duration & severity)
MODERATE-SEVERE
Abnormal Sleep or
Impairment of daily activities, sport, leisure or
Problems at work/school or
Bothersome symptoms
Allergic Rhinitis
17. TreatmentThe treatment goal for allergic rhinitis is relief of symptoms.
Therapeutic options available to achieve this goal include
avoidance measures, oral antihistamines, intranasal
corticosteroids, leukotriene receptor antagonists, and allergen
immunotherapy.
Other therapies that may be useful in select patients include
decongestants and oral corticosteroids.
Allergic rhinitis and asthma appear to represent a combined
airway inflammatory disease and, therefore, treatment of
asthma is also an important consideration in patients with
allergic rhinitis.
Allergic Rhinitis
19. OVERVIEW OF PHARMACOLOGIC TREATMENT OPTIONS FOR ALLERGIC RHINITIS
Therapy Usual Adult Dose Usual Paediatric Dose
Oral Antihistamines (2nd Generation)
Cetirizine (Reactine) 5-10mg OD 5-10 ml (1-2 teaspoons) OD
(children’s formulation)
Desloratadine (Aerius) 5mg OD 2.5-5 ml (0.5-1.0 teaspoon) OD
(children’s formulation)
Fexofenadine (Allegra) 60mg BD or 120mg OD Not currently indicated for children
under 12 years of age
Loratadine (Claritin) 10mg OD 5-10 ml (1-2 teaspoons) OD
(children’s formulation)
Intranasal Corticosteroids
Beclomethasone (Beconase) 1-2 sprays (42 µg/spray) EN, BD 1 spray (42 μg/spray) EN, BD
Budesonide (Rhinocort) 2 sprays (64 µg/spray) EN, OD or 1
spray BD
2 sprays (64 μg/spray) EN, OD or 1
spray EN, BD (do not exceed 256 μg)
Ciclesonide (Omnaris) 2 sprays (50 µg/spray) EN, OD Not indicated for children under 12
years of age
Fluticasone Furoate (Avamys) 2 sprays (27.5 µg/spray) EN, OD 1 spray (27.5 μg/spray) EN, OD
Fluticasone Propionate (Flonase) 2 sprays (50 µg/spray) EN, OD or BD
(for severe rhinitis)
1-2 sprays (50 μg/spray) EN, OD
Mometasone Furoate (Nasonex) 2 sprays (50 µg/spray) EN, OD 1 spray (50 μg/spray) EN, OD
Triamcinolone Acetonide
(Nasacort)
2 sprays (55 µg/spray) EN, OD 1 spray (55 μg/spray) EN, OD
Leukotriene Receptor Antagonists
Montelukast (Singulair) 10mg OD Not currently approved for patients
under 15 years of age
Allergic Rhinitis