1. Allergic rhinitis
Definition :Rhinitis is defined by a combination of two or more nasal symptoms:
running,blocking,itching&sneezing. Allergic rhinitis occurs when these symptoms are the result of
IgE-mediated inflammation following exposure to allergen.
Prevalence :
Allergic rhinitis is a global health problem &increasing in prevalence. Evidence of allergic rhinitis is
14%.The prevalence of positive Phadiatop & skin prick tests (SPTs)decrease significantly with age
with odds of 23, 21.1 &21 % respectively with every ten year increase in age.
Key notes: Quoted prevalence figures for allergic rhinitis vary widely from .8 to 39.7% with UK having
a high prevalence >20%.
Risk factors
Genetic & family history: genes involved in atopy include loci 5q, 11q &12q. Gene exist for
interleukin IL-4 & IL-13, with marker associated with the presence of a high level of serum IgE.
Environment : many possible factors have been suggested such as lifestyle change,increased
exposure of antigen, pollution & irritants, dietary modification, decrease in infections, leading to a
reduction in Th1-type immune response(hygiene hypothesis) & stress.
Co-morbidities
Others condition associated with allergic rhinitis are asthma, sinusitis, otitis media,sleep disorders,
lower respiratory tract infection& dental occlusion.
Aetiology : pathophysiology
This is complex, involving cells, mediators,cytokine, chemokines neuropeptides & adhesion
molecules which cooperate in a complex network to produce the specific symptoms of allergic
rhinitis. The reaction can be considered in four phases.
1)sensitization ;
2) subsequent reaction to allergen –early phase;
3) late phase reaction;
4) systemic activation.
Sensitization
First exposure allergen (grass pollen, house dust mite, cat danders) enters through the mucosa , is
processed by APCs(Langerhans cells) & then presented to the B& T cells.
Resulting immune response produces a proliferation of cell populations specific for the antigen &
results in the development of memory cells & plasma cells.

2. IgE specific for the antigen is produced & binds to mast cells throughout the body.
Subsequent reaction to allergen: early phase
Second exposure –allergen again enters through mucosa & then cross –links IgE on mast cells.
Degranultion of mast cell releases mediators such as histamine ,heparin.
Activation of arachidonic acid metabolism produces prostaglandins & leukotrienes,(formally
known as SRS-A.)
Memory cells exposed to the allergen produce more IgE.
Histamine causes rhinorrhoea, sneezing, pruritis & nasal obstruction. However , its effects on nasal
obstruction are not marked & require relatively high concentration. Action on sensory nerves
induces itching & sneezing. Histamine also increases ipsilateral glandular secretion by a direct effect
on mucus cells & vessels. And contralateral secretion through neural reflexes.
Histamine also possesses proinflammattory & immunomodulatory properities.
Upregulation of adhesion molecules on vascular endothelial cells.
Increase production of cytokines IL-6& IL-8 by endothelial cells.
Activation of epithelial cells with consequent ICAM 1 expression & cytokine production.
Prostaglandin D2 , it induces a sustained nasal obstruction & ten times more potent than histamine.
Leukotrienes produced by the lipoxygenase pathways. They induce vascular permeability & oedema
in the nose & also involved in eosinophil recruitment.
Kinin also produced by via action of kininogen. Kinin cause rhinorrhoea ,sneezing obstruction & pain.
Late phase response
Occur if high doses of antigen,this is inflammatory in nature & involves the ingress of cells such as
eosinophils, basophils, mast cells , T lymphocyte,neutrophils& macrophases into the local site. The
main symptoms are nasal obstruction & hyperactivity.
Systemic activation:
Although allergic rhinitis appears to be a local phenomena, there is evidence of upregulation of
production & release of eosinophil &basophil precursors from the bone marrow in response to
allergen contact in nose or lung. The resultant circulating precursors are attracted to the reaction
site & to other parts of the respiratory tract by adhesion & selectin molecules &infiltrate the tissue
where they mature. This process is also evident in nasal polyposis & may be responsible for some of
the notable rhinitis /asthma link.
Clinical presentation
Immediate allergic symptoms of sneezing, rhinorrhoea & itching.
Perennial allergic symptoms mainly nasal obstruction, hyperactivity, & often poor sense of smell.

3. The sinus lining is also involved, so that the picture is one of a chronic inflammatory rhinosinusitis.
Perennial allergic rhinitis often present as chronic inflammatory rhinosinusitis without acute allergic
symptoms.
Diagnosis
Most allergic patients can be diagnosed by a combination of history, examination & skin prick
test(SPT) or radioallergoabsorbent tests (RAST) for specific IgE.
Skin prick tests: allergen introduced into the skin causes degranulation of IgE-sensitized mast cells
with mediator release & formation of a wheal & flare.
Skin prick tests should not be performed if the patient is on antihistamine, has severe eczema,has
had previous life-threatening anaphylaxis or has dermagraphism. Oral steroid do not interfere
except at very high dose, dermal corticosteroid may reduce reactivity.
A positive skin prick test is not indicative of clinical allergy unless supported by the relevant history.
Positive skin prick tests occur in 25- 30% of adult, only 10 to 15% develops symptoms.
Blood tests for allergy:
Stabilized allergen is incubated with the patient’s serum, any specific IgE binds to allergen & is
identified by a second incubation with labelled anti-IgE.
Total IgE
Specific IgE by RAST (Radioimmunoabsorbent tests).
Comparision of skin prick test &blood tests in allergy diagnosis.
SPT(skin prick test) RAST(radioimmunoabsorbant test)
Immediate result Days to weeks
Cheap &safe Expensive & safe
sensitive Slight less sensitive
Affected by therapy Not affected by therapy
Training for performance&interpretation Trained operator &interpreters required.
Nasal allergen challenge:
Allergen is introduced into nose & any reaction is measured & compared to placebo. This is the gold
standard of allergy diagnosis but rarely necessary.
It is necessary where a positive history is accompanied by a negative SPT & prior to initiating
immunotherapy.

4. The allergen should be applied in gradually increasing concentrations with careful monitoring of
both upper & lower respiratory symptoms. Both subjective( visual analogue scales ) & objective
(sneeze count, nasal inspiratory peakflow, rhinomanometry, acoustic rhinometry, spirometry or
pulmonary peakflow) need to be employed. It is also possible to collect nasal secretions & measure
mediators, cytokines or cells such as eosinophils.
Lysine aspirin can be used in this test for aspirin sensitivity.
Nasal challenge testing is time-consuming, difficult & requires extensive laboratory facilities.
Most asthmatics have rhinitis; approximately one-third of the rhinitis have asthma.
Treatment of allergic rhinitis:
Management of allergic rhinitis includes allergen avoidance, pharmacotherapy, education & possibly
immunotherapy.
Allergen avoidance
Avoidance strategies can be primary prevention & secondary prevention.
Primary prevention:
Early use of antibiotic with the alteration of gut flora & increased vaccinations in the childhood have
been implicated as possible causal factors in the increasing prevalence of allergic disease.
Similarly ,restriction of allergenic exposure to inhalant allergens &highly allergic foods during early
life have been suggested.
Smoking during pregnancy & early life particularly mother is strongly associated with an increased
prevalence of atopy sensitization, rhinitis, asthma.
Secondary prevention:
Exposure to allergens; Major indoor allergens include house dust mite,domestic pets,cockroach&
moulds.Seasonal rhinitis results from exposure to pollens(tree poolen, grass pollen,weed pollen,)
1)Theoretical approaches to house dust mite avoidance/reduction are summarized below:
Encase mattress & pillow covers or special allergen-proof fabric;
Hot wash bedding(550) & damp wipe mite-proof covers every one to two weeks.
Remove objects that accumulate dust or place in a cabinet.
Store clothing in drawers & remove unused clothing from the bed room.
Remove upholstered furniture & replace with leather ,plastic or vinyl furniture.
Remove carpets, replace with washable rugs, install hardwood floors
Treat carpets with 3% tannic acid, vacuum regularly(ideally not patient)

5. Use washable curtains or venetian blinds, clean every two weeks
Replace or wash air filters on air conditioners every month to remove debris.
2)Patients with allergic rhinitis who are sensitive to cats & dogs should be advised to remove the
animals.
3)Avoidance of pollen is frequently not possible.Recently individual intranasal filters have
demonstrated efficacy .
Pharmacotherapy
1)Antihistamines : These rapidly relieve running ,itching, & sneezing but no effect on blockage
although there are recent exceptions (desloratadine & levocetirizine).
Cetirizine ,fexofenadine& desloratadine do not block the potassium reuptake channels even at
supranormal dose( no arrhythmias)
Antihistamine have some anti-inflammatory effects & may reduce allergic progression in children.
2)Topical glucocorticocoids
These are the most effective treatment for rhinitis especially if started prior to allergen exposure.
Regular treatment is necessary. Side effects are minor & includes epistaxis& nasal irritation in 5-10%
of patients. Their onset of action is slow with some improvement after 6-12hours ,maximum effects
occurring only after several days.
There is no diference in efficacy among the various preparations but bioavailability does differ &
lowest bioavailability is seen with fluticasone& mometasone.
3) Sodium cromoglicate: It is useful for small children less than four years for whom a topical
corticosteroid is not available.
4)Decongestants : These reduce nasal obstruction but increase rhinorrhoea. Regular use more than
a few days can result in rhinitis medicamentosa.
5) Ipratropium bromide: This is atropine like nasal spray is useful against watery rhinorrhoea. Side
effects include glaucoma & prostatism & dry mouth &eyes.
6) Systemic corticosteroid: These can be used to unblock the nose at the start of treatment or very
severe symptoms during the hayfever season.
7) Antileukotrienes : These are effective against congestion & mucous production with efficacy
similar to that of loratadine but less than topical steroid.
Nasal douching
Nasal douching improves quality of life & endoscopic preparations.

6. Immunotherapy
Allergen immunotherapy involves the repeated administration of an allergen extract in order to
induce a state of immunological tolerance. Immunotherapy is more effective in seasonal hayfever &
limited spectrum of allergens.
Special circumstances
Paediatric rhinitis:Diagnosis of paediatric rhinitis in small child who have 6 to 8 colds year .Sodium
cromoglicate, saline drops or spray may also be in children under two years.
Pregnancy : Probably due to high circulating oestrogen levels. These symptoms disappear at
delivery. NO medication is safe in pregnancy. Least absorbed topical nasal corticosteroid would be a
sensible option for existing rhinitis. Nasal decongestant causes foetal abdominal
malformation.Rhinitis in pregnancy is often resistant to treatment.
Asthma : Since most asthmatic have concomitant rhinitis, a treatment which relieves both
conditions simultaneously would be optimal ,since there are problems with concordance with
inhaled & topical nasal steroid.Leucotrienes receptors agonist plus levocetirizine or desloratadine
have some effect on nasal obstruction.

7. Immunotherapy
Allergen immunotherapy involves the repeated administration of an allergen extract in order to
induce a state of immunological tolerance. Immunotherapy is more effective in seasonal hayfever &
limited spectrum of allergens.
Special circumstances
Paediatric rhinitis:Diagnosis of paediatric rhinitis in small child who have 6 to 8 colds year .Sodium
cromoglicate, saline drops or spray may also be in children under two years.
Pregnancy : Probably due to high circulating oestrogen levels. These symptoms disappear at
delivery. NO medication is safe in pregnancy. Least absorbed topical nasal corticosteroid would be a
sensible option for existing rhinitis. Nasal decongestant causes foetal abdominal
malformation.Rhinitis in pregnancy is often resistant to treatment.
Asthma : Since most asthmatic have concomitant rhinitis, a treatment which relieves both
conditions simultaneously would be optimal ,since there are problems with concordance with
inhaled & topical nasal steroid.Leucotrienes receptors agonist plus levocetirizine or desloratadine
have some effect on nasal obstruction.