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ALLERGIC RHINITIS
Dr . Vaishnavi Sreeram
RHINITIS
 Clinical Definition : Having 2 or more symptoms of
Anterior or Posterior Rhinorrhoea, sneezing, nasal
blockage and/or itching of the nose during 2 or
more consecutive days for more than 1 hour on
most days
CLASSIFICATION
 Allergic
 Infectious
 Non-allergic non-infective
ALLERGIC
 Intermittent
 Persistent
INFECTIOUS
 Acute
 Chronic
OTHERS
 Occupational
 NARES
 Hormonal
 Drug induced
 Irritants
 Food
 GERD
 Ideopathic
ALLERGIC RHINITIS
 Rhinorrhoea, blocking, itching & sneezing as a result
of Ig E mediated inflammation following exposure to
an allergen.
 10-25% population
 Male predominance
 Peak age – young adulthood
ALLERGIC RHINITIS
 Characterized by inflammatory changes in the
nasal mucosa caused by exposure to inhaled
allergens
 Diagnosed when the symptoms are caused by
allergen exposure leading to an IgE mediated
reaction
CLASSIFICATION
AETIOLOGY
I. Genetics
• Chromosome 5q- IL-4, IL-13
• Chromosome 11q, 13, 12q
II. Family history
• Allergic Rhinitis
• Asthma
AETIOLOGY contd…
III. Atopy
 Tendency to develop exaggerated IgE antibody
response in response to one or more aero allergens
 Predispose to rhinitis, asthma, eczema
 AD
 Gene on 11q, 13
 Maternal influence
 Allergen exposure to dispose to atopy
AETIOLOGY contd…
IV. Allergens
 Foreign substances which are capable of
provoking an IgE mediated response
 Proteins
 5-20 micron size
 10-40 k dalton molecular weight
Allergens - Intermittent rhinitis
 Symptoms in &around a particular
season when pollen of a particular plant
to which the patient is sensitive is present.
Allergens - Intermittent rhinitis
 Most common grass pollen
 Pollen count >50/m3
develop symptoms
 Pollen count maximum in
evening
& night
 More symptomatic
Intermittent…
 Other allergens
Weeds – Rag weed,Nettle,Dock
Trees-Western red cidar,ash,pine etc.
Fungal spores-
Aspergillus,Alternaria,Basidiospores etc.
Allergen-persistent rhinitis
 Most common cause- House dust mite
 Genus –Dermatophagoides
 Most common type-D.pterosynnus
 Optimal growth at 15-20°C & at a relative humidity of 60 –
70%
 Feed on human skin scales
 Digestive enzymes-cystiene proteases
 eg –Der p1- Excreted through mite faeces –dried up –become air borne
Allergen- persistent…
 Domestic pets-cats, dogs, rabbits..
 Cat allergen Fel d1
 Salivary protein
 Preened on to fur- dried up –air borne
 Remain in air for prolonged period
Allergen- persistent…
 Cockroach –a recently identified allergen
Occupational allergens
 Presence of work related symptoms with
improvement during periods away from work place
s/o
 Flour-bakers,grain workers
 Laboratory animals-guinea pigs,rats , mice-in lab
workers
 Wood dust-saw mill workers
 Biological products enzymes
 Latex –surgeons,nurses etc.
 Chemicals –di iso cyanates ,polyamines
Food Induced rhinitis
 IgE mechanisms
 Sensitivity to food preservatives-
sulphites,benzoates,tartrazine
 More common in children
 Triggers- milk,egg,cheese
 In adults-nuts,fish,shellfish,citrus fruits
 “Pseudo allergy” –histamine containing foods like
cheese,wines,poorly kept fish
 Flushing, headache,rhinitis
Drug induced rhinitis
 Aspirin sensitivity –important cause
 With nasal polyp& Intrinsic asthma
 Other NSAIDS
 Anti hypertensives-propranolol ,other beta
blockers,ACE Inhibitors
Rhinitis medicamentosa
 Rebound hyperemia,nasal congestion& obstruction
with tachyphylaxis occurs following prolonged use
of topical vasoconstrictors
 Not to use topical vasoconstrictors for >2weeks at
a time
Air pollution
 More in developed countries
 Life style changes,dietary modifications, Diesel
exhausts ,tobacco smoke, domestic spray
 Ozone
 Nasal hyper reactivity- sensitivity of nasal
mucosa to non specific allergens
 Seen in ideopathic rhinitis
 Lower level of allergen provokes symptoms
PATHOGENESIS
 IG E
 Heat labile
 Mol. Wt-188000
 2 heavy chains(epsilon)
 2 light chains(kappa or lambda)
 Fc & Fab ends
Pathogenesis contd…
 Sensitisation
Pathogenesis contd…
 Early phase
Pathogenesis contd.. (Early phase)
 Preformed mediators
 Histamine
 Heparin
 Chondroitin SO4
 ECF-A
 NCF-A
 Newly generated
mediators
 PAF
 PGD2
 LT-B4, C4, D4
 TX-A2
 TNF
Pathogenesis contd.. (Early phase)
 Histamine : VD plasma exudation oedema
 Heparin : Enhance phagocytosis
 PGs &LTs : Vasoactive,bronchospastic
 PAF : Plt aggregation, histamine&
serotonin release, chemotaxis of neutrophils &
eosinophils
 TX A2 : Spasmogenic
 TNF : Transmigration of neutrophils,
eosinophils
Late phase
 Starts by 6-12 hrs
 Lasts~24hrs
 Cellular inflammation is characteristic
 Ingress of eosinophils,basophils, mastcells,
neutrophils etc.
 VCAM-1, ICAM-1, E selectin
 Recurrence of sneezing,rhinorrhoea, with congestion
predominating.
Eosinophils
 Synthesis& release of
 Cytokines –IL-3,5
 MIP-1 ,TGF
 PG-E1 ,PAF
 ROIs
 Histaminase
 Cellular permeability & mucous secretion
Endothelial cells
 Release chemotactic factors,adhesion molecules
 Increased expression of adhesion molecules in
allergic rhinitis individuals
Epithelial cells
 Barrier & mucociliary clearance function
 Expression of inflammatory mediators & adhesion
molecules
 More sensitive to air pollutants in allergic rhinitis
Systemic activation
 Upregulation of production & release of
inflammatory cells from bone marrow
 Attracted to reaction site & other parts of
respiratory tract ,produce inflammatory response
Ig E independent response
 By directly inducing cytokines& chemokines
 Eg . House dust mite
 By mast cell degranulation
 Eg morphine,codeine
CLINICAL FEATURES -SYMPTOMS
 Paroxysms of morning sneezing,nasal
blockage,rhinorrhoea,
 Itching eye,palate,pharynx
 Stuffy nose& loss of smell due to mucosal
oedema
 20 symptoms- loss of taste,
sinusitis,ET dysfunction
CLINICAL FEATURES- SIGNS
 Rhinoscopy
 Pale oedematous nasal turbinate with thin clear
secretion
CLINICAL FEATURES -SIGNS
 Dripping nose wiped off by
children with hand
 Thenar eminence rubbed
against tip of nose with rest
of hand stretched out
 “ALLERGIC SALUTE”
CLINICAL FEATURES -SIGNS
 Black line across dorsum of nose due to
constant upward rubbing of nose
 Disappears when tip of nose pulled down
 TRANSVERSE NASAL CREASE
 “DARIERS LINE”
CLINICAL FEATURES -SIGNS
 ‘ALLERGIC SHINERS’
 Dark areas under the eyes
as a result of venous stasis
in the lower orbito
palpebral grooves
CLINICAL FEATURES –SIGNS
 spasm of mullers muscle venous return from skin
& s/c tissue of lower eye lid oedema
 ‘Bags’ under eye
 Tearing, conjunctival injection, periorbital
swelling
CLINICAL FEATURES –SIGNS
 ORAL CAVITY
 Over riding of maxillary incisors
 High arched palate
 Hypertrophied lymph node on posterior pharyngeal
wall- ‘cobble stone’
CLINICAL FEATURES –SIGNS
 LARYNX
 Hoarseness of voice
 Oedema –vocal cord
COMPLICATIONS
 C/C Sinusitis
 Serous otitis media
 Sleep apnoea
 Dental& palatal abnormalities
 Nasal polyp formation
DIAGNOSIS
 History –personal history,family history, occupational&
environmental exposure dietary &drug use
 Physical examination
 Blood-TC&DC eosinophilia
 Nasal smear
 Nasal secreation collected smeared on glass slide
fixed with ethanol May grunwald/ Giemsa stain
eosinophil count
 +ve if >25% cells are eosinophils
DIAGNOSIS- SKIN PRICK TEST
 In vivo test to demonstrate given allergen
 Principle :–Allergen introduced in skin cause
degranulation of mast cell with mediator release
wheal & flare.
 Method:- Drop of allergen extract on volar aspect of
forearm, pricked in to skin
 Positive control-histamine
 Negative control - saline
 Wheal diameter at 15 minutes
 >2mm in below 5 yrs & > 3mm in adults
DIAGNOSIS- SKIN PRICK TEST
 +ve result > 2mm than –ve control
 C/I:-
 On anti histamines
 On high dose steroids
 H/o severe eczema
 H/o anaphylaxis
DIAGNOSIS - Patch test
 To determine delayed type hypersensitivity
 Allergen placed in skin for 48 hrs
 Local reaction
 Used in skin problems & food allergy
RAST
 RADIO ALLERGO SORBENT
TEST
 In vitro test to detect specific
Ig E conc. in patient’s serum
 Method:-
RAST
 Measurement of specific IgE in blood
 Usually reserved for patients who require a diagnosis
but where SPTs are unavailable or inappropriate.
 A blood sample is taken and radio- or enzyme-labelled
anti-IgE is added to the serum.
 A positive result is shown by an IgE level of 0.35 kU/l
or greater.
 As for SPTs, a positive result may not necessarily be
clinically relevant
ADVANTAGES
 Can detect picograms concentration of antibodies
 No risk of allergic reaction
 Results are not affected by antihistamines other drugs
 PLASMA REACTIVE IMMUNO SORBENT TEST(PRIST)
 Total IgE in plasma measured
 FLUORO ALLERGO SORBENT ASSAY(FAST)
 Measures antigen specific antibodies
 MULTIPLE ALLERGEN SIMULTANEOUS
TEST(MAST)
 Test several antigens for specific antibody
simultaneously
 SERIAL ENDPOINT TITRATION (SET)
 Diagnostic test to determine the amount of
sensitivity to each inhalant allergen
 More useful in immunotherapy
DIAGNOSIS - Nasal allergen challenge
 Gold standard of allergy diagnosis
 Used in
Positive history with negative SPT
Prior to initiate immunotherapy if history is doubtful as in
occupational allergy
Nasal allergen challenge
 Method :-
 Relevant allergen obtained without any irritants
 Diluent of allergen used as placebo
 An allergen is applied to the nasal mucosa, or the
patient exposed to an airborne allergen.
 Applied in gradually increasing conc.
 Monitoring of both upper & lower respiratory
symptoms
Nasal allergen challenge
 Reaction is compared with placebo
 Subjective:- Symptom scores, Visual analogue scale
 Objective:- Sneeze count, Nasal inspiratory peak flow,
Rhinomanometry, Spirometry, pulmonary peak flow
 Collect nasal secretions:- Mediators, Cytokines, Cells
Nasal allergen challenge
 Disadvantages
 Time consuming
 Risk of inducing anaphylaxis
 Require extensive laboratory facilities
 Resuscitation equipment & trained staff necessary
Treatment
 Allergen Avoidance& Environmental
control
 Pharmacotherapy
 Immunotherapy
 Surgical treatment
Allregen Avoidance & Environmental control
 PRIMARY PREVENTION
 Avoid smoking during pregnancy
 Promote breast feeding for atleast first 3 months after
birth
 Reducing exposure to house dust mite
SECONDARY PREVENTION
 Avoidance of allergens
House dust mite control measures
 Wash bedding regularly (every 1–2 weeks) at 55–
60°C to kill mites
 Wash pillows and duvets in hot water (55–60°C)
 Encase pillows and mattresses with protective
coverings that have a pore size of 6µm or less
 Sufficient ventilation of dwellings to decrease
humidity
 Use a damp duster when dusting and cleaning surfaces
 Use a good quality vacuum cleaner (if possible, one fitted
with a HEPA filter)
 Remove/reduce curtains and soft furnishings in the
bedroom
 Replace fabric-covered seating with leather or vinyl
 Remove soft toys from the bedroom; wash them at 55–
60°C or freeze them (in a kitchen deep-freezer) to kill
house dust mites
 Exposure of mattresses, rugs and carpets to direct strong
sunlight (for >3 hours) kills mites
Pollen Avoidance measures :
 Keep windows closed at peak pollen times
 Wear glasses or sunglasses to help prevent pollens
entering the eyes
 Consider wearing a mask over nose and mouth to prevent
inhalation of pollens at peak time
 Use air-conditioning where possible
 Install car pollen filters where possible
Pet Allergen avoidance measures :
 If possible, find another home for the pet and do not
introduce new animals into the home.
 If the pet is not removed from the home then:
❍ Exclude pets from bedrooms and if possible keep pets outdoors
❍ Vacuum carpets, mattresses and upholstery regularly
❍ Change clothes before going to school or work if you have had
contact with any animal (e.g. horse/ cat/dog).
Cockroach allergen avoidance:
 Eradicate cockroaches with appropriate insecticidal bait
 Seal cracks in floors and ceilings
 Enclose all food
 Do not store waste in the home
 Scrub floors with water and detergent to remove
allergens.
Mould allergen avoidance:
 Use dehumidifiers in the home if relative humidity is consistently
high (above 50%)
 Ensure heating, ventilation or air-conditioning systems are
properly maintained
 Use 5% ammonia solution to remove mould from bathrooms and
other contaminated surfaces
 Replace carpets with hard flooring and replace wallpaper with
paint
 Repair indoor water damage immediately.
TREATMENT
 The most widely used and effective medications to treat
allergic rhinitis are oral or topical antihistamines and topical
nasal steroids.
 These medications aim to achieve improved symptom control
and are not a cure for allergy.
 Symptom control is better for patients with intermittent
allergic rhinitis if they start treatment prior to exposure to the
allergen to which they are sensitized.
 The basic summary of recommendations for treatment is
according to the ARIA guidelines
Antihistamines
 First-line treatment for symptoms of runny nose,
sneezing and nasal and eye itching
 Little effect on nasal blockage
 Rapid onset of action (usually less than an hour)
 Symptom reduction on a once daily dosing
 Better symptomatic control when used regularly
rather than on an as required basis.
Antihistamines
First generation:-
 Cross BBB & interact with central histamine receptor
 Sedation, psychomotor retardation, learning impairment
 Chlorpheniramine: 4mg tid/qid
 Diphenhydramine:25-50mg tid/qid,
 Hydroxyzine :10-25mg tid/qid
Antihistamines
Second generation:-
 Terfinadine -
 Rapid onset(1-2hrs) & moderate duration(12-24hrs) of
action
 60 mg BD
 S/E - QT Prolongation ECG
 Ventricular arrhythmias in impaired liver function test
& with Ketoconazole, Erythromycin etc.
Antihistamines
Second generation
 Astemizole :-
 Slow onset(2-4hrs) & long duration(2-5days) of action
 Dose 10 mg OD
 D/A –
 Long t1/2 stop ~6 weeks before SPT
 Increased appetite, weight gain
 D/I with Terfinadine- VT
Antihistamines
Second generation
 Loratidine
 Dose 10 mg O D
 Rapid onset of action
 No cardiac S/E
 No interaction with macrolides, antifungals
Antihistamines
Second generation
 Cetrizine
 Dose 10 mg OD/BID
 MOA
Anti histaminic effect
Inhibit release of mediators from platelets
Inhibit eosinophil chemotaxis
 Disadvantage :
Sedation at higher doses
Antihistamines
Second generation
 Azelastine
 Topical – as nasal spray
 Adult dose –2puffs/nostril
 D/A –stinging in nose, altered taste
perception
Antihistamines
Second generation
 Fexofenadine
 Dose - 60mg BD
 Mizolastine
 Clemastine
 Luvistine
Topical Corticosteroids
 Extremely effective in controlling nasal symptoms, eye
symptoms, reduce inflammation& hyper reactivity, improve
sense of smell
 Intra-nasal application allows a high concentration of the
active drug to be delivered to the nasal mucosa with
minimal systemic absorption.
 Onset of action is slow - some improvement after 6~12hrs.
 Can take 2 weeks for full benefit to be noticed
 Dexamethasone(.01%), Budesonide(100mcg/dose)
fluticasone(.05%), Triamcinalone(.1%), Mometasone(.1%)
 Lowest bioavailability with fluticasone & mometasone
Topical corticosteroids
 SideEffects :
 Nasal irritation
 Slight bleeding
 Candida super infection
 Septal perforation
Oral steroids
 Short courses are effective for
 Severe peak pollen seasonal symptoms
 When complete nasal blockage prevent penetration of
steroid nasal spray
Eg: Prednesolone 20-40 mg/day
Decongestants
Oral
 Pseudoephedrine ,Phenylpropanolamine
 MOA- Vasoconstriction, Reduced nasal congestion &
oedema
 CNS stimulation –counteract drowsiness of anti
histamines
Decongestants
Topical
 Phenylephrine, Xylometazoline (0.1%), Oxymetazoline
(0.05%)
 Dose : 2-3 drops in each nostril 8-12 hrly
 D/A
 Continued use cause rebound congestion
Topical anticholinergics
 Ipratropium bromide (0.03%)
 Dose : 2 puffs/nostril BD or TID
 Indication : Excessive watery rhinorrhoea
 S/E : Excess use cause nasal drying and crusting
Mast cell stabilisers
 Sodium chromoglycate
 Effective for prophylaxis of allergic rhinitis
 Dose : 2% solution, one spray into each nostril 4-6
times a day before the onset of symptoms
 Safe, non-toxic
 Drug of choice in children
Leukotriene Inhibitors
 Montelukast
 Dose : 10mg O D
 Zafirlukast
 Zileuton
 Combined use of cetirizine and montelukast was shown
not to improve symptom control above each drug
individually in one study; but to be more effective when
combined in another.
Immuno Therapy
 First systemic desensitisation –
Noon of London (1911)
 Method of inducing tolerance to an allergen and therefore
reducing unwanted symptoms.
 Can reduce the symptoms of allergic rhinitis, offer long-
lasting reduction of symptoms (even when treatment has
stopped) and can prevent the progression of allergic
disease.
Immuno Therapy…
 Indications :
 IgE mediated disease (+ve SPT/RAST)
 Inability to avoid allergen
 Inadequacy of drug treatment
 Limited spectrum of allergens
 Patients who understood risk & limitations of treatment
Immuno Therapy…
 Contraindications
 Coexistent asthma
 Patients taking beta-blockers
 Medical/Immunological diseases
 Children below 5 years
 Pregnancy
Immuno Therapy…
 Efficacy
 50% reduction in symptoms & 80% reduction in rescue
medication requirement
 Reduction in bronchial hyper responsiveness
Immuno Therapy…
 Method : 2 phases
 Updosing phase : weekly injections of small doses of
allergen subcutaneously for 8-16 weeks
 Maintenance phase : Injections at 4-8 weeks intervals
for 3-5 years
Immuno Therapy…
 Side effects :
 Local reactions
 Trivial,require no treatment
 Systemic reaction
 In 10% of people
 Occur within 30 minutes
 In updosing phase
 Mild – rhinitis or asthma, respond to anti histamines or
inhaled broncho dilators
 Severe – general urticaria, asthma, anaphylaxis
Immuno Therapy…
 Mechanism
 Blunting of seasonal increase in allergen specific IgE
 Increase in blocking IgG antibodies
 Induce shift from Th 2 type immune response to Th 1
type response
 Inhibition of recruitment & activation of inflammatory
cells to mucosal surface
Immuno Therapy
 Novel strategies:
 Sub lingual route:
 Allergen as drops or tab. S/L
 Moderate efficacy compared to S/C route
 Conjugated to adjuvant:
 Bacterial DNA sequence
 Induce Th1 type response
ANTI-IgE ANTIBODY (OMALIZUMAB)
 Binds to circulating IgE preventing it from binding to mast
cells and causing degranulation.
 Omalizumab reduces all nasal symptoms and improves
asthma control, but has the risk of causing anaphylaxis and
is expensive.
 Administered by monthly injection.
 Currently it is recommended only for patients with severe
allergic asthma with or without rhinitis symptoms.
Surgical treatment
 Surgery cannot cure allergy but can give relief of
nasal blockage if other methods fail.
 Septal deviation
 Septoplasty/SMR
 Hypertrophied turbinate
 Turbinate reduction: SMD, cryosurgery, Laser cautery
 Turbinate resection: Partial excision, Submucosal
turbinectomy, Radical turbinectomy
 Excessive rhinorrhoea: Vidian neurectomy
Thank You

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  • 1. ALLERGIC RHINITIS Dr . Vaishnavi Sreeram
  • 2. RHINITIS  Clinical Definition : Having 2 or more symptoms of Anterior or Posterior Rhinorrhoea, sneezing, nasal blockage and/or itching of the nose during 2 or more consecutive days for more than 1 hour on most days
  • 6. OTHERS  Occupational  NARES  Hormonal  Drug induced  Irritants  Food  GERD  Ideopathic
  • 7. ALLERGIC RHINITIS  Rhinorrhoea, blocking, itching & sneezing as a result of Ig E mediated inflammation following exposure to an allergen.  10-25% population  Male predominance  Peak age – young adulthood
  • 8. ALLERGIC RHINITIS  Characterized by inflammatory changes in the nasal mucosa caused by exposure to inhaled allergens  Diagnosed when the symptoms are caused by allergen exposure leading to an IgE mediated reaction
  • 10. AETIOLOGY I. Genetics • Chromosome 5q- IL-4, IL-13 • Chromosome 11q, 13, 12q II. Family history • Allergic Rhinitis • Asthma
  • 11. AETIOLOGY contd… III. Atopy  Tendency to develop exaggerated IgE antibody response in response to one or more aero allergens  Predispose to rhinitis, asthma, eczema  AD  Gene on 11q, 13  Maternal influence  Allergen exposure to dispose to atopy
  • 12. AETIOLOGY contd… IV. Allergens  Foreign substances which are capable of provoking an IgE mediated response  Proteins  5-20 micron size  10-40 k dalton molecular weight
  • 13. Allergens - Intermittent rhinitis  Symptoms in &around a particular season when pollen of a particular plant to which the patient is sensitive is present.
  • 14. Allergens - Intermittent rhinitis  Most common grass pollen  Pollen count >50/m3 develop symptoms  Pollen count maximum in evening & night  More symptomatic
  • 15. Intermittent…  Other allergens Weeds – Rag weed,Nettle,Dock Trees-Western red cidar,ash,pine etc. Fungal spores- Aspergillus,Alternaria,Basidiospores etc.
  • 16. Allergen-persistent rhinitis  Most common cause- House dust mite  Genus –Dermatophagoides  Most common type-D.pterosynnus  Optimal growth at 15-20°C & at a relative humidity of 60 – 70%  Feed on human skin scales  Digestive enzymes-cystiene proteases  eg –Der p1- Excreted through mite faeces –dried up –become air borne
  • 17. Allergen- persistent…  Domestic pets-cats, dogs, rabbits..  Cat allergen Fel d1  Salivary protein  Preened on to fur- dried up –air borne  Remain in air for prolonged period
  • 18. Allergen- persistent…  Cockroach –a recently identified allergen
  • 19. Occupational allergens  Presence of work related symptoms with improvement during periods away from work place s/o  Flour-bakers,grain workers  Laboratory animals-guinea pigs,rats , mice-in lab workers  Wood dust-saw mill workers  Biological products enzymes  Latex –surgeons,nurses etc.  Chemicals –di iso cyanates ,polyamines
  • 20. Food Induced rhinitis  IgE mechanisms  Sensitivity to food preservatives- sulphites,benzoates,tartrazine  More common in children  Triggers- milk,egg,cheese  In adults-nuts,fish,shellfish,citrus fruits  “Pseudo allergy” –histamine containing foods like cheese,wines,poorly kept fish  Flushing, headache,rhinitis
  • 21. Drug induced rhinitis  Aspirin sensitivity –important cause  With nasal polyp& Intrinsic asthma  Other NSAIDS  Anti hypertensives-propranolol ,other beta blockers,ACE Inhibitors
  • 22. Rhinitis medicamentosa  Rebound hyperemia,nasal congestion& obstruction with tachyphylaxis occurs following prolonged use of topical vasoconstrictors  Not to use topical vasoconstrictors for >2weeks at a time
  • 23. Air pollution  More in developed countries  Life style changes,dietary modifications, Diesel exhausts ,tobacco smoke, domestic spray  Ozone  Nasal hyper reactivity- sensitivity of nasal mucosa to non specific allergens  Seen in ideopathic rhinitis  Lower level of allergen provokes symptoms
  • 24. PATHOGENESIS  IG E  Heat labile  Mol. Wt-188000  2 heavy chains(epsilon)  2 light chains(kappa or lambda)  Fc & Fab ends
  • 27. Pathogenesis contd.. (Early phase)  Preformed mediators  Histamine  Heparin  Chondroitin SO4  ECF-A  NCF-A  Newly generated mediators  PAF  PGD2  LT-B4, C4, D4  TX-A2  TNF
  • 28. Pathogenesis contd.. (Early phase)  Histamine : VD plasma exudation oedema  Heparin : Enhance phagocytosis  PGs &LTs : Vasoactive,bronchospastic  PAF : Plt aggregation, histamine& serotonin release, chemotaxis of neutrophils & eosinophils  TX A2 : Spasmogenic  TNF : Transmigration of neutrophils, eosinophils
  • 29. Late phase  Starts by 6-12 hrs  Lasts~24hrs  Cellular inflammation is characteristic  Ingress of eosinophils,basophils, mastcells, neutrophils etc.  VCAM-1, ICAM-1, E selectin  Recurrence of sneezing,rhinorrhoea, with congestion predominating.
  • 30. Eosinophils  Synthesis& release of  Cytokines –IL-3,5  MIP-1 ,TGF  PG-E1 ,PAF  ROIs  Histaminase  Cellular permeability & mucous secretion
  • 31. Endothelial cells  Release chemotactic factors,adhesion molecules  Increased expression of adhesion molecules in allergic rhinitis individuals
  • 32. Epithelial cells  Barrier & mucociliary clearance function  Expression of inflammatory mediators & adhesion molecules  More sensitive to air pollutants in allergic rhinitis
  • 33. Systemic activation  Upregulation of production & release of inflammatory cells from bone marrow  Attracted to reaction site & other parts of respiratory tract ,produce inflammatory response
  • 34. Ig E independent response  By directly inducing cytokines& chemokines  Eg . House dust mite  By mast cell degranulation  Eg morphine,codeine
  • 35. CLINICAL FEATURES -SYMPTOMS  Paroxysms of morning sneezing,nasal blockage,rhinorrhoea,  Itching eye,palate,pharynx  Stuffy nose& loss of smell due to mucosal oedema  20 symptoms- loss of taste, sinusitis,ET dysfunction
  • 36. CLINICAL FEATURES- SIGNS  Rhinoscopy  Pale oedematous nasal turbinate with thin clear secretion
  • 37. CLINICAL FEATURES -SIGNS  Dripping nose wiped off by children with hand  Thenar eminence rubbed against tip of nose with rest of hand stretched out  “ALLERGIC SALUTE”
  • 38. CLINICAL FEATURES -SIGNS  Black line across dorsum of nose due to constant upward rubbing of nose  Disappears when tip of nose pulled down  TRANSVERSE NASAL CREASE  “DARIERS LINE”
  • 39. CLINICAL FEATURES -SIGNS  ‘ALLERGIC SHINERS’  Dark areas under the eyes as a result of venous stasis in the lower orbito palpebral grooves
  • 40. CLINICAL FEATURES –SIGNS  spasm of mullers muscle venous return from skin & s/c tissue of lower eye lid oedema  ‘Bags’ under eye  Tearing, conjunctival injection, periorbital swelling
  • 41. CLINICAL FEATURES –SIGNS  ORAL CAVITY  Over riding of maxillary incisors  High arched palate  Hypertrophied lymph node on posterior pharyngeal wall- ‘cobble stone’
  • 42. CLINICAL FEATURES –SIGNS  LARYNX  Hoarseness of voice  Oedema –vocal cord
  • 43. COMPLICATIONS  C/C Sinusitis  Serous otitis media  Sleep apnoea  Dental& palatal abnormalities  Nasal polyp formation
  • 44. DIAGNOSIS  History –personal history,family history, occupational& environmental exposure dietary &drug use  Physical examination  Blood-TC&DC eosinophilia  Nasal smear  Nasal secreation collected smeared on glass slide fixed with ethanol May grunwald/ Giemsa stain eosinophil count  +ve if >25% cells are eosinophils
  • 45. DIAGNOSIS- SKIN PRICK TEST  In vivo test to demonstrate given allergen  Principle :–Allergen introduced in skin cause degranulation of mast cell with mediator release wheal & flare.  Method:- Drop of allergen extract on volar aspect of forearm, pricked in to skin  Positive control-histamine  Negative control - saline  Wheal diameter at 15 minutes  >2mm in below 5 yrs & > 3mm in adults
  • 46. DIAGNOSIS- SKIN PRICK TEST  +ve result > 2mm than –ve control  C/I:-  On anti histamines  On high dose steroids  H/o severe eczema  H/o anaphylaxis
  • 47. DIAGNOSIS - Patch test  To determine delayed type hypersensitivity  Allergen placed in skin for 48 hrs  Local reaction  Used in skin problems & food allergy
  • 48. RAST  RADIO ALLERGO SORBENT TEST  In vitro test to detect specific Ig E conc. in patient’s serum  Method:-
  • 49. RAST  Measurement of specific IgE in blood  Usually reserved for patients who require a diagnosis but where SPTs are unavailable or inappropriate.  A blood sample is taken and radio- or enzyme-labelled anti-IgE is added to the serum.  A positive result is shown by an IgE level of 0.35 kU/l or greater.  As for SPTs, a positive result may not necessarily be clinically relevant
  • 50. ADVANTAGES  Can detect picograms concentration of antibodies  No risk of allergic reaction  Results are not affected by antihistamines other drugs
  • 51.  PLASMA REACTIVE IMMUNO SORBENT TEST(PRIST)  Total IgE in plasma measured  FLUORO ALLERGO SORBENT ASSAY(FAST)  Measures antigen specific antibodies  MULTIPLE ALLERGEN SIMULTANEOUS TEST(MAST)  Test several antigens for specific antibody simultaneously
  • 52.  SERIAL ENDPOINT TITRATION (SET)  Diagnostic test to determine the amount of sensitivity to each inhalant allergen  More useful in immunotherapy
  • 53. DIAGNOSIS - Nasal allergen challenge  Gold standard of allergy diagnosis  Used in Positive history with negative SPT Prior to initiate immunotherapy if history is doubtful as in occupational allergy
  • 54. Nasal allergen challenge  Method :-  Relevant allergen obtained without any irritants  Diluent of allergen used as placebo  An allergen is applied to the nasal mucosa, or the patient exposed to an airborne allergen.  Applied in gradually increasing conc.  Monitoring of both upper & lower respiratory symptoms
  • 55. Nasal allergen challenge  Reaction is compared with placebo  Subjective:- Symptom scores, Visual analogue scale  Objective:- Sneeze count, Nasal inspiratory peak flow, Rhinomanometry, Spirometry, pulmonary peak flow  Collect nasal secretions:- Mediators, Cytokines, Cells
  • 56. Nasal allergen challenge  Disadvantages  Time consuming  Risk of inducing anaphylaxis  Require extensive laboratory facilities  Resuscitation equipment & trained staff necessary
  • 57. Treatment  Allergen Avoidance& Environmental control  Pharmacotherapy  Immunotherapy  Surgical treatment
  • 58. Allregen Avoidance & Environmental control  PRIMARY PREVENTION  Avoid smoking during pregnancy  Promote breast feeding for atleast first 3 months after birth  Reducing exposure to house dust mite
  • 59. SECONDARY PREVENTION  Avoidance of allergens House dust mite control measures  Wash bedding regularly (every 1–2 weeks) at 55– 60°C to kill mites  Wash pillows and duvets in hot water (55–60°C)  Encase pillows and mattresses with protective coverings that have a pore size of 6µm or less  Sufficient ventilation of dwellings to decrease humidity
  • 60.  Use a damp duster when dusting and cleaning surfaces  Use a good quality vacuum cleaner (if possible, one fitted with a HEPA filter)  Remove/reduce curtains and soft furnishings in the bedroom  Replace fabric-covered seating with leather or vinyl  Remove soft toys from the bedroom; wash them at 55– 60°C or freeze them (in a kitchen deep-freezer) to kill house dust mites  Exposure of mattresses, rugs and carpets to direct strong sunlight (for >3 hours) kills mites
  • 61. Pollen Avoidance measures :  Keep windows closed at peak pollen times  Wear glasses or sunglasses to help prevent pollens entering the eyes  Consider wearing a mask over nose and mouth to prevent inhalation of pollens at peak time  Use air-conditioning where possible  Install car pollen filters where possible
  • 62. Pet Allergen avoidance measures :  If possible, find another home for the pet and do not introduce new animals into the home.  If the pet is not removed from the home then: ❍ Exclude pets from bedrooms and if possible keep pets outdoors ❍ Vacuum carpets, mattresses and upholstery regularly ❍ Change clothes before going to school or work if you have had contact with any animal (e.g. horse/ cat/dog).
  • 63. Cockroach allergen avoidance:  Eradicate cockroaches with appropriate insecticidal bait  Seal cracks in floors and ceilings  Enclose all food  Do not store waste in the home  Scrub floors with water and detergent to remove allergens.
  • 64. Mould allergen avoidance:  Use dehumidifiers in the home if relative humidity is consistently high (above 50%)  Ensure heating, ventilation or air-conditioning systems are properly maintained  Use 5% ammonia solution to remove mould from bathrooms and other contaminated surfaces  Replace carpets with hard flooring and replace wallpaper with paint  Repair indoor water damage immediately.
  • 65. TREATMENT  The most widely used and effective medications to treat allergic rhinitis are oral or topical antihistamines and topical nasal steroids.  These medications aim to achieve improved symptom control and are not a cure for allergy.  Symptom control is better for patients with intermittent allergic rhinitis if they start treatment prior to exposure to the allergen to which they are sensitized.  The basic summary of recommendations for treatment is according to the ARIA guidelines
  • 66.
  • 67. Antihistamines  First-line treatment for symptoms of runny nose, sneezing and nasal and eye itching  Little effect on nasal blockage  Rapid onset of action (usually less than an hour)  Symptom reduction on a once daily dosing  Better symptomatic control when used regularly rather than on an as required basis.
  • 68. Antihistamines First generation:-  Cross BBB & interact with central histamine receptor  Sedation, psychomotor retardation, learning impairment  Chlorpheniramine: 4mg tid/qid  Diphenhydramine:25-50mg tid/qid,  Hydroxyzine :10-25mg tid/qid
  • 69. Antihistamines Second generation:-  Terfinadine -  Rapid onset(1-2hrs) & moderate duration(12-24hrs) of action  60 mg BD  S/E - QT Prolongation ECG  Ventricular arrhythmias in impaired liver function test & with Ketoconazole, Erythromycin etc.
  • 70. Antihistamines Second generation  Astemizole :-  Slow onset(2-4hrs) & long duration(2-5days) of action  Dose 10 mg OD  D/A –  Long t1/2 stop ~6 weeks before SPT  Increased appetite, weight gain  D/I with Terfinadine- VT
  • 71. Antihistamines Second generation  Loratidine  Dose 10 mg O D  Rapid onset of action  No cardiac S/E  No interaction with macrolides, antifungals
  • 72. Antihistamines Second generation  Cetrizine  Dose 10 mg OD/BID  MOA Anti histaminic effect Inhibit release of mediators from platelets Inhibit eosinophil chemotaxis  Disadvantage : Sedation at higher doses
  • 73. Antihistamines Second generation  Azelastine  Topical – as nasal spray  Adult dose –2puffs/nostril  D/A –stinging in nose, altered taste perception
  • 74. Antihistamines Second generation  Fexofenadine  Dose - 60mg BD  Mizolastine  Clemastine  Luvistine
  • 75. Topical Corticosteroids  Extremely effective in controlling nasal symptoms, eye symptoms, reduce inflammation& hyper reactivity, improve sense of smell  Intra-nasal application allows a high concentration of the active drug to be delivered to the nasal mucosa with minimal systemic absorption.  Onset of action is slow - some improvement after 6~12hrs.  Can take 2 weeks for full benefit to be noticed  Dexamethasone(.01%), Budesonide(100mcg/dose) fluticasone(.05%), Triamcinalone(.1%), Mometasone(.1%)  Lowest bioavailability with fluticasone & mometasone
  • 76. Topical corticosteroids  SideEffects :  Nasal irritation  Slight bleeding  Candida super infection  Septal perforation
  • 77. Oral steroids  Short courses are effective for  Severe peak pollen seasonal symptoms  When complete nasal blockage prevent penetration of steroid nasal spray Eg: Prednesolone 20-40 mg/day
  • 78. Decongestants Oral  Pseudoephedrine ,Phenylpropanolamine  MOA- Vasoconstriction, Reduced nasal congestion & oedema  CNS stimulation –counteract drowsiness of anti histamines
  • 79. Decongestants Topical  Phenylephrine, Xylometazoline (0.1%), Oxymetazoline (0.05%)  Dose : 2-3 drops in each nostril 8-12 hrly  D/A  Continued use cause rebound congestion
  • 80. Topical anticholinergics  Ipratropium bromide (0.03%)  Dose : 2 puffs/nostril BD or TID  Indication : Excessive watery rhinorrhoea  S/E : Excess use cause nasal drying and crusting
  • 81. Mast cell stabilisers  Sodium chromoglycate  Effective for prophylaxis of allergic rhinitis  Dose : 2% solution, one spray into each nostril 4-6 times a day before the onset of symptoms  Safe, non-toxic  Drug of choice in children
  • 82. Leukotriene Inhibitors  Montelukast  Dose : 10mg O D  Zafirlukast  Zileuton  Combined use of cetirizine and montelukast was shown not to improve symptom control above each drug individually in one study; but to be more effective when combined in another.
  • 83. Immuno Therapy  First systemic desensitisation – Noon of London (1911)  Method of inducing tolerance to an allergen and therefore reducing unwanted symptoms.  Can reduce the symptoms of allergic rhinitis, offer long- lasting reduction of symptoms (even when treatment has stopped) and can prevent the progression of allergic disease.
  • 84. Immuno Therapy…  Indications :  IgE mediated disease (+ve SPT/RAST)  Inability to avoid allergen  Inadequacy of drug treatment  Limited spectrum of allergens  Patients who understood risk & limitations of treatment
  • 85. Immuno Therapy…  Contraindications  Coexistent asthma  Patients taking beta-blockers  Medical/Immunological diseases  Children below 5 years  Pregnancy
  • 86. Immuno Therapy…  Efficacy  50% reduction in symptoms & 80% reduction in rescue medication requirement  Reduction in bronchial hyper responsiveness
  • 87. Immuno Therapy…  Method : 2 phases  Updosing phase : weekly injections of small doses of allergen subcutaneously for 8-16 weeks  Maintenance phase : Injections at 4-8 weeks intervals for 3-5 years
  • 88. Immuno Therapy…  Side effects :  Local reactions  Trivial,require no treatment  Systemic reaction  In 10% of people  Occur within 30 minutes  In updosing phase  Mild – rhinitis or asthma, respond to anti histamines or inhaled broncho dilators  Severe – general urticaria, asthma, anaphylaxis
  • 89. Immuno Therapy…  Mechanism  Blunting of seasonal increase in allergen specific IgE  Increase in blocking IgG antibodies  Induce shift from Th 2 type immune response to Th 1 type response  Inhibition of recruitment & activation of inflammatory cells to mucosal surface
  • 90. Immuno Therapy  Novel strategies:  Sub lingual route:  Allergen as drops or tab. S/L  Moderate efficacy compared to S/C route  Conjugated to adjuvant:  Bacterial DNA sequence  Induce Th1 type response
  • 91. ANTI-IgE ANTIBODY (OMALIZUMAB)  Binds to circulating IgE preventing it from binding to mast cells and causing degranulation.  Omalizumab reduces all nasal symptoms and improves asthma control, but has the risk of causing anaphylaxis and is expensive.  Administered by monthly injection.  Currently it is recommended only for patients with severe allergic asthma with or without rhinitis symptoms.
  • 92. Surgical treatment  Surgery cannot cure allergy but can give relief of nasal blockage if other methods fail.  Septal deviation  Septoplasty/SMR  Hypertrophied turbinate  Turbinate reduction: SMD, cryosurgery, Laser cautery  Turbinate resection: Partial excision, Submucosal turbinectomy, Radical turbinectomy  Excessive rhinorrhoea: Vidian neurectomy