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Allergic rhinitis 
Ramesh Parajuli MS 
Lecturer, Department of Otorhinolaryngology, Head & Neck Surgery 
Chitwan Medical College Teaching Hospital 
Bharatpur-10, Fax: 977-56-532937, Chitwan, Nepal 
drrameshparajuli@gmail.com
Definition 
“IgE mediated hypersensitivity disease of mucous membranes of 
nasal airways characterized by sneezing, watery nasal discharge , 
itching and nasal obstruction” (Durham, 1999)
Prevalence 
• Global health problem 
• Prevalence - 15% and 20% (Nathan et al.,1999) 
• Higher in pediatric age group(Wright et al.,1994) 
• Approx. 80% develop symptoms before age of 20 
(Skoner et al., 2001)
• Not a severe disorder but significantly 
alters patient’s social life 
-school performance 
-work productivity 
• Substantial cost 
Impact on quality of life
Risk factors 
1. Genetic susceptibility: 
2. Family history of atopy: e.g. asthma,eczema,hay 
fever,urticaria 
(Genes involved in atopy - loci on 5q,11q and 12q 
chromosomes) 
3. Environmental factors: 
• Pollution-climate interaction 
• Irritants 
eg. fumes, tobacco smoke, diesel exhaust, 
mosquito repellents, perfumes, scented sticks, 
domestic sprays, bleaches 
4. Exposure to allergens: 
• Seasonal : Pollen, Fungus 
• Perennial: Dust mite, domestic pets, cockroaches
5.Hygiene hypothesis 
• Increased exposure to various allergensimmune maturationhelp decrease 
the incidence of allergic diseases and asthma (Svanes C et al., 2003) 
• Early environmental exposure to infectious agents, protects against 
development of atopy (Tulic MK et al.,2003) 
• Early nursery attendance also reduces subsequent atopy (Kramer et al.,2003) 
• Lack of immune maturation (understimulated immune system) in 
infancyallergic responses (Liu A,2007)
Pathogenesis 
• Sensitization & Priming to specific antigen: 
Inhaled allergen produces specific IgE antibody 
which gets attached to mast cells 
• Subsequent exposure to same antigen: 
Allergen combines with specific IgE antibody ÂŽ 
degranulation of mast cells ÂŽ chemical mediators 
released
Acute or early phase response 
• Occurs 5–30 min after antigen exposure 
• Release of inflammatory mediators 
¡ Increased nasal gland secretion Ž runny nose 
¡ Mucosal edema & Vasodilation Ž nose block 
¡ Nerve irritation Ž sneezing & itching
Late or delayed phase response 
• Occurs 2-8 hours after antigen exposure 
• Infiltration by inflammatory cells 
(eosinophils, neutrophils, basophils, 
monocytes & CD4+ T lymphocytes) 
• Edema, congestion & thick nasal secretion 
• Sneezing & itching decreases
Symptoms 
1. Running 
2. Blocking 
3. Sneezing 
4. Itching
Signs 
Nasal crease Pale turbinate
Face: 
• Bunny nose-frequent twitching of face 
• Dennie-Morgan creases (in lower eyelid skin) 
• Allergic shiners (dark discoloration below lower 
eyelids) 
Eye: Conjunctiva is congested, increased lacrimation 
Ear: Aural fullness(ET dysfunction) 
Throat: Chronic pharyngitis, laryngitis
Types of allergic rhinitis 
• Seasonal allergic rhinitis: 
Nasal discharge and conjunctivitis (more common) 
• Perennial allergic rhinitis: 
Nasal blockage (more common), Hyposmia 
Less sneezing/nasal discharge /eye symptoms
ARIA classification= Allergic Rhinitis & its Impact on 
Asthma 
Rhinitis Rhinitis
Seasonal allergic rhinitis 
 Pollen: 
Spring (March-June) = Tree pollen 
Summer (May-August) = Grass 
Fall (August-October) = Weeds 
 Mold: 
Spores in outdoors have seasonal 
variation (reduced in winter, increased in 
summer/fall due to humidity) 
 House dust mites: 
Generally “perennial” allergen, 
but increased in damp autumn months
Perennial allergic rhinitis 
 Fungi/mold: 
Exposure peaks accompany activities 
such as harvesting & cutting grass 
 Pet dander (cats, dogs): 
up to 4 months after pet removal 
 House dust mites: 
Live in bedding & carpets 
 Cockroaches: 
Respiratory allergy 
Important allergen
Diagnosis 
1.History 
2.Physical exam 
3.Allergy diagnosis 
(I) Skin prick test (SPT) 
(II) Blood tests for allergy: Total IgE, Specific IgE 
(III) Nasal allergen challenge test
History
I. Skin prick test (SPT) 
• Rapid, efficient & cost 
effective 
• Contain multiple antigens 
(pollen, mold, dust mite, 
animal dander)
Skin Prick test 
Advantages: 
1. Cheap 
2. Immediate result 
3. Sensitive 
Contraindications: 
1. Patients on antihistamines 
2. Severe eczema 
3. Previous anaphylaxis 
4. Dermagraphism
(II) Blood tests for allergy 
1.Total IgE: 
Rarely helpful as 50% pts have IgE levels within normal range 
2.Specific IgE: 
(i) Radio-allergosorbent test (RAST) (ii)Modified RAST 
Stabilized allergen is incubated with patient’s serumany specific IgE binds to 
allergen identified by a second incubation with labelled anti-IgE.
Radio-allergosorbent test (RAST) 
Indications: 
1. When there is C/I to SPT 
2. Where SPT unavailable 
3. When SPT difficult to interpret 
Disadvantages: 
More expensive 
Delayed(takes longer) 
No more sensitive or specific to SPT
(III)Nasal allergen challenge (nasal provocation) test 
 Indication: 
- +ve history & –ive SPT 
• Subjective –symptom scores, VAS 
• Objective –sneeze count, nasal 
inspiratory peak flow , 
rhinomanometry , acoustic 
rhinometry , spirometry,pulmonary 
peak flow 
Disadvantages 
1.Time consuming 
2.Difficult 
3.Excessive lab facilities 
4.Trained staff 
5.Resuscitation equipment
Nasal endoscopy CT scan-Nose and PNS
Complications (Co-morbidities)
• Nasal symptoms -noted 80% of 
asthmatics 
• Adults-Asthma present in 22.5% of 
adults with AR, Vs 7.2% in general 
population (Laynaert, 1999 ) 
• Children-Ratio of asthmatics with AR to 
asthmatics without AR is even higher 
(Wright et al.,1996) 
• Effective treatment of allergic rhinitis 
reduces development of subsequent 
asthma (Ragab et al., 2006)
Differential diagnosis 
1.Vasomotor rhinitis (Intrinsic rhinitis/NANIPER) 
2.Sinonasal polyposis 
3.Rhinitis medicamentosa 
4.Hormonal rhinitis 
(Pregnancy, Hypothyroidism, OCP use ) 
5.CSF leak 
Take a moment to consider 
differential diagnosis
Management of allergic rhinitis 
1. Environmental control measures (Avoidance of allergens) 
2. Patient education 
3. Nasal douching 
4.Medical therapy 
5.Immunotherapy 
6.Surgery
(I) Avoidance of allergens 
• Best treatment method 
• Not always practical 
• Indoor allergens: Removing allergen from the indoor 
environment should be a primary strategy for the management 
and treatment of allergic disease 
• Outdoor allergens:
General advice 
• Avoid irritants: smoke, dust, vehicular & other atmospheric pollutants, 
• Physical factors – extreme changes in temperature can produce symptoms 
like allergic rhinitis but are non-IgE mediated responses 
• Avoid foods & drugs to which you are allergic 
• Avoid occupational irritants or change profession
Avoidance of indoor allergens
Avoidance of animal allergen 
• Remove pet animals (cats, dogs) 
from bedroom 
• Wash the pet weekly
Measures to avoid house dust mite 
• Mattress covers 
• Covers for pillows & bedding 
• Vacuuming 
• Regulation of ventilation & humidity at home 
• Liquid nitrogen 
• Acaricides 
• Protein denaturating agents- Tannic acid
Pollen avoidance measures 
• Avoid walking in open grassy spaces 
during hot, dry days 
• Keep windows closed 
• Wear facemask & sunglasses when 
moving out
(II) Patient education 
Educate patients on environmental control measures, 
which involve both the avoidance of known allergens 
(substances to which the patient has IgE-mediated 
hypersensitivity) & the avoidance of nonspecific, or 
irritant, triggers
(III) Nasal douching 
•Saline irrigation 
•Improves quality of life 
Neti Pot: Home remedy to clean nasal passages
(IV) Medical therapy
1.Antihistamines: 
Topical: Azelastine 
Systemic: Cetirizine, Levocetirizine,Fexofenadine, Loratadine, Desloratadine 
2.Nasal Decongestants: 
Topical: Oxymetazoline, Xylometazoline 
Systemic: Phenylephrine, Pseudoephedrine 
3.Mast cell stabilizers: Sodium cromoglycate nasal drop 
4.Anticholinergics: Ipratropium bromide nasal spray 
5.Corticosteroids: 
Topical :Beclomethasone,Budesonide,Mometasone,Fluticasone 
Systemic: Prednisolone 
6.Leukotriene receptor antagonists: Montelukast, Zafirlukast
Steroid 
• Most effective treatment for Allergic rhinitis(AR) 
-Topical: Nasal spray or nasal drop 
-Systemic:Oral, extremely effective 
• Reduces inflammation & consequent 
hyperreacitvityreduce nasal symptoms, eye 
symptoms, improve smell sense 
• Topical steroid when combined with antihistamines 
reduces risk of asthma exacerbation and hospitalization 
by 50% or more (Adams et al., 2002, Crystal peters et 
al., 2002) 
• Fluticasone and mometasone have low systemic 
bioavailabilitylower risk
Antihistamines 
• Adverse effects of first generation antihistamines 
“First-generation oral H1-antihistamines are not recommended when second-generation 
ones are available, due to safety concerns” 
(Allergy. 2008 Apr;63 Suppl 86:8-160)
GA2LEN- Global Allergy and Asthma European Network 
Allergy. 2010 Apr;65(4):459-66
Significance of wide therapeutic window (fexofenadine) 
Ineffective Therapeutic Window 
Maximum 
Studied dose 
(Fexo 1380 mg) 
Not tested for 
adverse effects 
Low H1-antihistamine dose High 
Minimally 
effective dose 
(Fexo 60 mg) 
Howarth PH. Advanced Studies in Medicine. 2004;4(7A):S508-512
Levocetirizine and desloratadine have some effects on nasal 
obstruction (Wilson AM, 2002)
Decongestants 
• Topical vasoconstrictor: 
-imidazoline (eg, oxymetazoline) 
• systemic (oral) vasocontrictor 
-Phenylephrine 
- Pseudoephedrine. 
• Monotherapy with vasoconstrictors has limited role 
• Oral decongestants + Antihistamineall cardinal 
symptoms of allergic rhinitis targeted
Mast cell stabilizer 
• Sodium cromoglycate inhibits degranulation of 
sensitized mast cells 
• 2% Nasal drop: Use 3 to 4 times daily limits 
compliance 
• Poorly absorbed systemically excellent safety 
record 
• Used before the onset of symptoms 
• Can be used in younger children < 2 years of age 
Ipratropium Bromide 
• Useful against nasal discharge 
• Occasionally helpful in pts with AR who do not 
respond to topical steroid(Dockhorn et al., 1999)
Antilukotrienes 
 Zafirlukast performed no better than placebo - seasonal alllergic 
rhinitis ( Pullerits T et al., 1999) 
• Montelukast clinical efficacy seasonal Allergic rhinitis 
(Chervinsky P et al., 2004) 
• Montelukast + loratadine -superior reducing day time nasal 
symptoms in seasonal Allergic rhinitis. (Meltzer EO et al., 2000) 
• Montelukast + ebastine- better symptomatic control in allergic rhinitis. 
• Montelukast -less effective than Intranasal steroid (Ratner PH et al., 
2003) 
• Leukotriene antagonist (Montelukast) doesn’t appear more effective 
than nonsedating antihistamines (Fexofenadine) (Wilson AM et al., 2004)
(V) Immunotherapy 
• Repeated administration of allergen extract 
induce state of immunological tolerance 
• Render an allergy patient less symptomatic 
when exposed to the offending antigen 
• Desensitization or Hyposensitization: 
because complete elimination of the allergic 
reaction is seldom achieved 
• Subcutaneous injection or sublingual route
Contraindications 
• Asthma(severe) 
• Autoimmune diseases 
• Beta-blockers or Anti-adrenergic medicines 
• Children less than < 5 yrs 
• Pregnancy (induction but not maintenance) 
• Efficacy: 
• Highly effective -selected patients (Grade A) 
• Treatment for 3 to 4 yrs –improvement for 3 yrs following discontinuation 
(Durham SR et al.,1999) 
• Children –seasonal rhinitis-ITX for 3 yrs-2 to 3 fold reduction –developing 
asthma (Moller et al.,2002) 
• Offers long term disease modification & prophylaxis
Side effects of Immunotherapy 
 Local reactions - trivial 
 Systemic reactions-10%-up dosing phase 
 Occasionally – severe systemic reactions-general 
urticaria , severe asthma or 
anaphylaxis
(VI) Surgery 
• Usually not indicated 
• Not last resort but complementary 
• Comorbid or complicating conditions eg 
Marked DNS, Turbinate hypertrophy, CRS
(VII) Complementary and integrative medicine(CIM) therapies 
• Honey – For seasonal AR caused by pollen 
• Chinese herbal medicine 
• Acupuncture
Recent advances 
(VIII) Human monoclonal antibody(Anti-IgE) 
• Omalizumab - recent developments in the treatment of atopic 
diseases 
 first of several monoclonal antibodies (anti IgE antibody) 
 Modulation of allergic inflammation 
 expensive for routine treatment of AR primarily indicated -severe 
asthma 
• Multiple randomized, double-blind, placebo-controlled studies 
-efficacy in seasonal and perennial AR (Vignola AM et al.,2004) 
Continued research on the molecular mechanism of 
allergic disease will inevitably generate new forms of 
therapy.
Jo tera hai woh mera hai... Jo mera hai woh tera.

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Allergic Rhinitis

  • 1. Allergic rhinitis Ramesh Parajuli MS Lecturer, Department of Otorhinolaryngology, Head & Neck Surgery Chitwan Medical College Teaching Hospital Bharatpur-10, Fax: 977-56-532937, Chitwan, Nepal drrameshparajuli@gmail.com
  • 2. Definition “IgE mediated hypersensitivity disease of mucous membranes of nasal airways characterized by sneezing, watery nasal discharge , itching and nasal obstruction” (Durham, 1999)
  • 3. Prevalence • Global health problem • Prevalence - 15% and 20% (Nathan et al.,1999) • Higher in pediatric age group(Wright et al.,1994) • Approx. 80% develop symptoms before age of 20 (Skoner et al., 2001)
  • 4. • Not a severe disorder but significantly alters patient’s social life -school performance -work productivity • Substantial cost Impact on quality of life
  • 5. Risk factors 1. Genetic susceptibility: 2. Family history of atopy: e.g. asthma,eczema,hay fever,urticaria (Genes involved in atopy - loci on 5q,11q and 12q chromosomes) 3. Environmental factors: • Pollution-climate interaction • Irritants eg. fumes, tobacco smoke, diesel exhaust, mosquito repellents, perfumes, scented sticks, domestic sprays, bleaches 4. Exposure to allergens: • Seasonal : Pollen, Fungus • Perennial: Dust mite, domestic pets, cockroaches
  • 6. 5.Hygiene hypothesis • Increased exposure to various allergensimmune maturationhelp decrease the incidence of allergic diseases and asthma (Svanes C et al., 2003) • Early environmental exposure to infectious agents, protects against development of atopy (Tulic MK et al.,2003) • Early nursery attendance also reduces subsequent atopy (Kramer et al.,2003) • Lack of immune maturation (understimulated immune system) in infancyallergic responses (Liu A,2007)
  • 7. Pathogenesis • Sensitization & Priming to specific antigen: Inhaled allergen produces specific IgE antibody which gets attached to mast cells • Subsequent exposure to same antigen: Allergen combines with specific IgE antibody ÂŽ degranulation of mast cells ÂŽ chemical mediators released
  • 8.
  • 9. Acute or early phase response • Occurs 5–30 min after antigen exposure • Release of inflammatory mediators ¡ Increased nasal gland secretion ÂŽ runny nose ¡ Mucosal edema & Vasodilation ÂŽ nose block ¡ Nerve irritation ÂŽ sneezing & itching
  • 10. Late or delayed phase response • Occurs 2-8 hours after antigen exposure • Infiltration by inflammatory cells (eosinophils, neutrophils, basophils, monocytes & CD4+ T lymphocytes) • Edema, congestion & thick nasal secretion • Sneezing & itching decreases
  • 11. Symptoms 1. Running 2. Blocking 3. Sneezing 4. Itching
  • 12. Signs Nasal crease Pale turbinate
  • 13. Face: • Bunny nose-frequent twitching of face • Dennie-Morgan creases (in lower eyelid skin) • Allergic shiners (dark discoloration below lower eyelids) Eye: Conjunctiva is congested, increased lacrimation Ear: Aural fullness(ET dysfunction) Throat: Chronic pharyngitis, laryngitis
  • 14. Types of allergic rhinitis • Seasonal allergic rhinitis: Nasal discharge and conjunctivitis (more common) • Perennial allergic rhinitis: Nasal blockage (more common), Hyposmia Less sneezing/nasal discharge /eye symptoms
  • 15. ARIA classification= Allergic Rhinitis & its Impact on Asthma Rhinitis Rhinitis
  • 16. Seasonal allergic rhinitis  Pollen: Spring (March-June) = Tree pollen Summer (May-August) = Grass Fall (August-October) = Weeds  Mold: Spores in outdoors have seasonal variation (reduced in winter, increased in summer/fall due to humidity)  House dust mites: Generally “perennial” allergen, but increased in damp autumn months
  • 17. Perennial allergic rhinitis  Fungi/mold: Exposure peaks accompany activities such as harvesting & cutting grass  Pet dander (cats, dogs): up to 4 months after pet removal  House dust mites: Live in bedding & carpets  Cockroaches: Respiratory allergy Important allergen
  • 18. Diagnosis 1.History 2.Physical exam 3.Allergy diagnosis (I) Skin prick test (SPT) (II) Blood tests for allergy: Total IgE, Specific IgE (III) Nasal allergen challenge test
  • 20. I. Skin prick test (SPT) • Rapid, efficient & cost effective • Contain multiple antigens (pollen, mold, dust mite, animal dander)
  • 21. Skin Prick test Advantages: 1. Cheap 2. Immediate result 3. Sensitive Contraindications: 1. Patients on antihistamines 2. Severe eczema 3. Previous anaphylaxis 4. Dermagraphism
  • 22. (II) Blood tests for allergy 1.Total IgE: Rarely helpful as 50% pts have IgE levels within normal range 2.Specific IgE: (i) Radio-allergosorbent test (RAST) (ii)Modified RAST Stabilized allergen is incubated with patient’s serumany specific IgE binds to allergen identified by a second incubation with labelled anti-IgE.
  • 23. Radio-allergosorbent test (RAST) Indications: 1. When there is C/I to SPT 2. Where SPT unavailable 3. When SPT difficult to interpret Disadvantages: More expensive Delayed(takes longer) No more sensitive or specific to SPT
  • 24. (III)Nasal allergen challenge (nasal provocation) test  Indication: - +ve history & –ive SPT • Subjective –symptom scores, VAS • Objective –sneeze count, nasal inspiratory peak flow , rhinomanometry , acoustic rhinometry , spirometry,pulmonary peak flow Disadvantages 1.Time consuming 2.Difficult 3.Excessive lab facilities 4.Trained staff 5.Resuscitation equipment
  • 25. Nasal endoscopy CT scan-Nose and PNS
  • 27. • Nasal symptoms -noted 80% of asthmatics • Adults-Asthma present in 22.5% of adults with AR, Vs 7.2% in general population (Laynaert, 1999 ) • Children-Ratio of asthmatics with AR to asthmatics without AR is even higher (Wright et al.,1996) • Effective treatment of allergic rhinitis reduces development of subsequent asthma (Ragab et al., 2006)
  • 28. Differential diagnosis 1.Vasomotor rhinitis (Intrinsic rhinitis/NANIPER) 2.Sinonasal polyposis 3.Rhinitis medicamentosa 4.Hormonal rhinitis (Pregnancy, Hypothyroidism, OCP use ) 5.CSF leak Take a moment to consider differential diagnosis
  • 29.
  • 30. Management of allergic rhinitis 1. Environmental control measures (Avoidance of allergens) 2. Patient education 3. Nasal douching 4.Medical therapy 5.Immunotherapy 6.Surgery
  • 31. (I) Avoidance of allergens • Best treatment method • Not always practical • Indoor allergens: Removing allergen from the indoor environment should be a primary strategy for the management and treatment of allergic disease • Outdoor allergens:
  • 32. General advice • Avoid irritants: smoke, dust, vehicular & other atmospheric pollutants, • Physical factors – extreme changes in temperature can produce symptoms like allergic rhinitis but are non-IgE mediated responses • Avoid foods & drugs to which you are allergic • Avoid occupational irritants or change profession
  • 33. Avoidance of indoor allergens
  • 34. Avoidance of animal allergen • Remove pet animals (cats, dogs) from bedroom • Wash the pet weekly
  • 35. Measures to avoid house dust mite • Mattress covers • Covers for pillows & bedding • Vacuuming • Regulation of ventilation & humidity at home • Liquid nitrogen • Acaricides • Protein denaturating agents- Tannic acid
  • 36. Pollen avoidance measures • Avoid walking in open grassy spaces during hot, dry days • Keep windows closed • Wear facemask & sunglasses when moving out
  • 37. (II) Patient education Educate patients on environmental control measures, which involve both the avoidance of known allergens (substances to which the patient has IgE-mediated hypersensitivity) & the avoidance of nonspecific, or irritant, triggers
  • 38. (III) Nasal douching •Saline irrigation •Improves quality of life Neti Pot: Home remedy to clean nasal passages
  • 40.
  • 41. 1.Antihistamines: Topical: Azelastine Systemic: Cetirizine, Levocetirizine,Fexofenadine, Loratadine, Desloratadine 2.Nasal Decongestants: Topical: Oxymetazoline, Xylometazoline Systemic: Phenylephrine, Pseudoephedrine 3.Mast cell stabilizers: Sodium cromoglycate nasal drop 4.Anticholinergics: Ipratropium bromide nasal spray 5.Corticosteroids: Topical :Beclomethasone,Budesonide,Mometasone,Fluticasone Systemic: Prednisolone 6.Leukotriene receptor antagonists: Montelukast, Zafirlukast
  • 42. Steroid • Most effective treatment for Allergic rhinitis(AR) -Topical: Nasal spray or nasal drop -Systemic:Oral, extremely effective • Reduces inflammation & consequent hyperreacitvityreduce nasal symptoms, eye symptoms, improve smell sense • Topical steroid when combined with antihistamines reduces risk of asthma exacerbation and hospitalization by 50% or more (Adams et al., 2002, Crystal peters et al., 2002) • Fluticasone and mometasone have low systemic bioavailabilitylower risk
  • 43. Antihistamines • Adverse effects of first generation antihistamines “First-generation oral H1-antihistamines are not recommended when second-generation ones are available, due to safety concerns” (Allergy. 2008 Apr;63 Suppl 86:8-160)
  • 44. GA2LEN- Global Allergy and Asthma European Network Allergy. 2010 Apr;65(4):459-66
  • 45. Significance of wide therapeutic window (fexofenadine) Ineffective Therapeutic Window Maximum Studied dose (Fexo 1380 mg) Not tested for adverse effects Low H1-antihistamine dose High Minimally effective dose (Fexo 60 mg) Howarth PH. Advanced Studies in Medicine. 2004;4(7A):S508-512
  • 46. Levocetirizine and desloratadine have some effects on nasal obstruction (Wilson AM, 2002)
  • 47. Decongestants • Topical vasoconstrictor: -imidazoline (eg, oxymetazoline) • systemic (oral) vasocontrictor -Phenylephrine - Pseudoephedrine. • Monotherapy with vasoconstrictors has limited role • Oral decongestants + Antihistamineall cardinal symptoms of allergic rhinitis targeted
  • 48. Mast cell stabilizer • Sodium cromoglycate inhibits degranulation of sensitized mast cells • 2% Nasal drop: Use 3 to 4 times daily limits compliance • Poorly absorbed systemically excellent safety record • Used before the onset of symptoms • Can be used in younger children < 2 years of age Ipratropium Bromide • Useful against nasal discharge • Occasionally helpful in pts with AR who do not respond to topical steroid(Dockhorn et al., 1999)
  • 49. Antilukotrienes  Zafirlukast performed no better than placebo - seasonal alllergic rhinitis ( Pullerits T et al., 1999) • Montelukast clinical efficacy seasonal Allergic rhinitis (Chervinsky P et al., 2004) • Montelukast + loratadine -superior reducing day time nasal symptoms in seasonal Allergic rhinitis. (Meltzer EO et al., 2000) • Montelukast + ebastine- better symptomatic control in allergic rhinitis. • Montelukast -less effective than Intranasal steroid (Ratner PH et al., 2003) • Leukotriene antagonist (Montelukast) doesn’t appear more effective than nonsedating antihistamines (Fexofenadine) (Wilson AM et al., 2004)
  • 50. (V) Immunotherapy • Repeated administration of allergen extract induce state of immunological tolerance • Render an allergy patient less symptomatic when exposed to the offending antigen • Desensitization or Hyposensitization: because complete elimination of the allergic reaction is seldom achieved • Subcutaneous injection or sublingual route
  • 51. Contraindications • Asthma(severe) • Autoimmune diseases • Beta-blockers or Anti-adrenergic medicines • Children less than < 5 yrs • Pregnancy (induction but not maintenance) • Efficacy: • Highly effective -selected patients (Grade A) • Treatment for 3 to 4 yrs –improvement for 3 yrs following discontinuation (Durham SR et al.,1999) • Children –seasonal rhinitis-ITX for 3 yrs-2 to 3 fold reduction –developing asthma (Moller et al.,2002) • Offers long term disease modification & prophylaxis
  • 52. Side effects of Immunotherapy  Local reactions - trivial  Systemic reactions-10%-up dosing phase  Occasionally – severe systemic reactions-general urticaria , severe asthma or anaphylaxis
  • 53. (VI) Surgery • Usually not indicated • Not last resort but complementary • Comorbid or complicating conditions eg Marked DNS, Turbinate hypertrophy, CRS
  • 54. (VII) Complementary and integrative medicine(CIM) therapies • Honey – For seasonal AR caused by pollen • Chinese herbal medicine • Acupuncture
  • 55. Recent advances (VIII) Human monoclonal antibody(Anti-IgE) • Omalizumab - recent developments in the treatment of atopic diseases  first of several monoclonal antibodies (anti IgE antibody)  Modulation of allergic inflammation  expensive for routine treatment of AR primarily indicated -severe asthma • Multiple randomized, double-blind, placebo-controlled studies -efficacy in seasonal and perennial AR (Vignola AM et al.,2004) Continued research on the molecular mechanism of allergic disease will inevitably generate new forms of therapy.
  • 56. Jo tera hai woh mera hai... Jo mera hai woh tera.

Editor's Notes

  1. Furthermore, the GA2 LEN (Global Allergy and Asthma European Network) task force assessed the unwanted side-effects and potential dangers of first-generation H1-antihistamines by reviewing the literature.
  2. The therapeutic window of H1 antihistamine is the dose range over which it is efficacious and also free from unwanted side effects. The lower limit of the therapeutic window is set by the lowest clinically effective dose for the disease condition whereas the upper limit is set by the highest dose tolerated without adverse effect. As an example, fexofenadine has a wide therapeutic window. It is effective at a dose of 60 mg and is free from sedation at 690 mg twice daily (1380 mg).