Allergic Rhinitis

 DEFINITION
 ARIA Guidelines
 RISK FACTORS
 PATHOPHYSIOLOGY (Sensitization, Early Phase Response, Late Phase Response,
Systemic Activation)
 TYPES (Seasonal And Perinneal)
 CLINICAL PRESENTATION
 COMPLICATIONS
 INVESTIGATIONS (Skin prick test, RAST, lysine aspirin test)
 TREATMENT
 NON ALLERGIC RHINITIS (include NANIPR, NARES, hormonal rhinitis, Non
allergic occupational rhinitis, Drug induced rhinitis)

DEFINITION

 Clinical hypersensitivity of nasal mucosa to foreign substances mediated through IgE antibodies.
 Rhinitis  any 2 of the symptoms of Running nose, Itching, Blockade, Sneezing. (RIBS)

ARIA (Allergic Rhinitis and its Impact on Asthma) GUIDELINES

Based On Duration:

Intermittent symptoms - < 4 days per week, < 4 weeks

Persistent symptoms - > 4 days per week, > 4 weeks

Based on Severity:

Mild – Normal sleep, Normal daily activity, Normal work and school, No troublesome
Symptoms.
Moderate – severe – vice versa

RISK FACTORS

1. Adolescent males
2. IgA deficiency state
3. Family history of allergy (mainly allergic rhinitis). Seasonal allergy indicates risk of Asthma
4. Environmental factors : -
Hygiene hypothesis – lifestyle changes, increased exposure to allergens, pollution, irritants, and
dietary modifications is responsible for decreased TH1 type immune response.
5. Common allergens –
Seasonal Allergens (Seasonal Allergic Rhinitis aka Hay fever) – Tree, Grass or Weed Pollens.
Perennial Allergens – Dust, Dander, Mites
Occupational allergens – Latex, Flour, Washing Powders, Lab Animals
Food And Drug Allergens – peanuts, egg, meat, fish etc

Comorbidities: Asthma, otitis media, sinusitis, LRTI, dental occlusion.

 Smoking increases IgE but DECREASES incidence of Allergic Rhinitis

PATHOPHYSIOLOGY:

4 phases – Sensitization  Early phase reaction  late phase reaction  Systemic Activation

SENSITISATION

Allergin goes to APC of nose (mainly Langerhans cells), these are CD1 + cells containing Birbeck
granules  process antigen and present it to Naïve T cell in Lymph node. In normal cases co
stimulatory signals including TH receptor are not present for all allergens to induce allergic response,
In allergic patients excess of TH2 cells present  TH2 secrete cytokines IL 4, IL 5, IL13 and also
activate B lymphocyte in local tissue (increase IgE production) IgE rapidly taken up by local mast
cells and patient is sensitised. Chr 5q is involved in increased IgE production. (CD14 maps chromosome
5q)

Cross Linking Hypothesis – Antigen molecules cross react with IgE  lead to opening of calcium
channels  Ca Influx  Leads to histamine release.

EARLY PHASE REACTION (< 24hrs)

Increase in Histamine, LT and PG lead to immediate sneezing, rhinorrhoea and itching (RIS) as mast
cells degranulate. Histamine also causes Vasodilatation, plasma exudation and oedema (B). Histamine
also possesses Pro inflammatory and Immunomodulatory properties. PG D2 is 10 times more potent
than histamine and causes nasal obstruction. LT also increase vascular permeability and increase
eosinophil recruitment. LT B4 induces Neutrophil recruitment.

Kinins cause rhinorrhoea, sneezing, obstruction and pain and have been noted in nasal secretions
following allergen challenge

TH2 cytokines are – IL4, IL5, IL13, Pro inflammatory Cytokines are IL6, IL8, IL10 and TNFα

LATE PHASE REACTION

 Inflammatory in nature, Eosinophils, Neutrophils, Basophils, Mast Cells, T Lymphocytes,

Macrophages etc. are recruited
 GMCSF (Granulocyte macrophage CSF) & IL5 and chemokines like RANTES and eotaxin recruit
eosinophils
 Eosinophils are capable of produces cytokines like IL3, IL5, GMCSF and also PGE1, TX B2, TGF
beta, HISTAMINASE
 Eosinophils cause increased vascular permeability and mucous secretion
 Macrophages are not eliminated by local steroids unlike Langhan Cells which are completely
eliminated from mucosa after 2 week therapy.

SYSTEMIC ACTIVATION

There is evidence of increase in Eosinophil and basophilic precursors being released by bone marrow
in response to allergic contact in nose and lungs.

 NON IgE mediated Mast cell degranulation  MAC (Morphine, Aspirin & Codeine) can lead to
degranulation of mast cells directly