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![Early response
Preformed Mediators
◦ Histamine
◦ Proteases [chymase and tryptase]
Newly synthesized
◦ Prostaglandins [PGDs]
◦ Cysteinyl leukotrienes[CysLTs]
◦ Platelet activating factor
◦ Bradykinin,
◦ Ils
◦ Tumor necrosis factor-α [TNF-α]
◦ Granulocyte- macrophage colony-stimulating factor)](https://image.slidesharecdn.com/allergicrhinitis-200413125400/85/Allergic-rhinitis-15-320.jpg)
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Allergic rhinitis
- 1. Allergic Rhinitis PRESENTER: DR.SREENIVAS KAMATH
- 2. Definition: Allergic rhinitis isdefined as a symptomatic disorder of the nose induced by immunoglobulin E (IgE)-mediated inflammation due to exposure to foreign substances, referred to as allergens.
- 3. It is characterizedby 1 or more nasal symptoms 1. Pruritus 2. Sneeze 3. Discharge 4. Stuffiness
- 4. In India 20-30%of the population suffers from allergic rhinitis and/or other allergic diseases
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- 6. Predisposing factors Genetics: ◦ Studieson twins ◦ Proven Chromosomal role- 1p31 and 2q32- French studies. - 3q13.31 Demark study. ◦ Multiple gene interaction are responsible ◦ Chromosome 5,6,11,12,13 are responsible for the inflammatory process in atopy ◦ 50% of patients have family history of allergy
- 7. Early exposure •Based onhygiene hypothesis •Earlier exposure to the antigen- lesser chances of developing allergic disease in adulthood •Developed countries have higher incidence as compare to developing country
- 8. It has beensuggested that a decrease in exposure to infectious agents results in a skew in the balance between T-cell subpopulations from T helper 1 (Th1)-cell responses toward atopic Th2- cell responses, including increased production of IgE
- 9. Pollution Increase in nasalresponsiveness to environmental allergens Common outdoor pollutants include SO2, NO2, and ozone Indoor pollutants include side-stream cigarette smoke Passive smoking at young age is 3x times risk for AR
- 10. Precipitating Factor Aerobiological flora Allergenpresent in the environment House dust and dust mites Feather Tobacco smoke Industrial chemical Animal dander Nasal physiology Disturbance in nasal cycle
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- 14. Immediate (early)allergic reaction, which is characterized by rhinorrhea, obstruction, sneezing, and pruritus Cross-linking of 2 adjacent IgE molecules by antigen Release of PREFORMED and NEWLY SYNTHESISED mediators Several hours after the initialy reponse the symptoms recurs in 50% of individuals Sneezing, rhinorrhea, and CONGESTION Infiltration of inflammatory cells, including basophils, eosinophils, neutrophils, and mononuclear cells in nasal secretions An initial contact with allergen leads to the production of specific IgE molecules Interleukin (IL)-4 and IL-13 (Th2 cytokines)
- 15. Early response Preformed Mediators ◦Histamine ◦ Proteases [chymase and tryptase] Newly synthesized ◦ Prostaglandins [PGDs] ◦ Cysteinyl leukotrienes[CysLTs] ◦ Platelet activating factor ◦ Bradykinin, ◦ Ils ◦ Tumor necrosis factor-α [TNF-α] ◦ Granulocyte- macrophage colony-stimulating factor)
- 16. Cysteinyl Leukotrienes Early phase-Eosinophils, Late phase- Mast cells LTC4, LTD4, and LTE4 Unlike the other mediators- DIRECTLY STIMULATES the mucosal glands and increase the vascular permeability
- 17. Nasal Reactivity INCREASED REACTIVITYDURING SEASONS
- 18. Neural Reflexes ONE SIDEHISTAMINE TEST CAUSES CONTRALATERAL SIDE CONGESTION AND RHINORRHEA
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- 21. Intradermal dilutional test Assess thedegree of allergy Can identify the concentration at which the immunotherapy has to be started
- 23. Disadvantages of skinprick test 1. Cannot be performed in patients receiving antihistamines or who are demographics 2. Doesn’t give a quantitative results 3. Less safer than invitro tests.
- 24. Factors that increasethe skin prick response Factors that decrease the skin prick response 1 Demographism Use of antihistamines (with hold antihistamine for 1 week ) 2 Application of skin pricks too close (>2.5cm) Topical spray of azelastine within last 48hrs 3 Use of systemic betablocler Tricyclic antidepressants (amytryptyline, nortriptyline) 4 Ingestion of food which cross reacts with inhalant allergen Beta agonist- terbutaline 5 Following Pollen season due increased reactivity
- 25. RAST CAP-RAST Testing (IgECAP-RAST Test) Based on a solid-phase immunoassay in which the allergen is bound to a hydrophilic carrier polymer encased in a capsule
- 26. Approaches in aENT clinic 1 • Skin Endpoint Titration/Intradermal Dilutional Testing 2 • Skin prick test ID single allergen of interest 3 • Revised Otolaryngic Allergist Approach • Skin prick testIDT
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- 28. Antihistamines 4 types ofhistamine receptors are present
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- 30. Absence of CNSdepressant property Higher H1 selective- No anticholinergic side effects Additional antiallergic mechanism apart from histamine blockade- by acting on leukotriene
- 31. Fexofenadine Not to beused along with CYP 3A4 inhibitors ◦ Erythromycin ◦ Clarithromycin ◦ Ketoconazole ◦ Itraconazole Not safe in patients with pre existing heart conditions
- 32. Decongestant Local decongestant -Exerts the effect through α1 and α2 adrenergic receptors Oral decongestant – exert their effect by stimulating the release of nor epinephrine ◦ Pseudoephidrine ◦ Phenylephrine ORAL DECONGESTANT ALSO EXERT THEIR EFFECT ON OTHER VESSELS- CURRENT GUIDELINES STATES DON’T USE ORAL DECONGESTANT IN UNCONTROLLED HYPERTENSION.
- 33. Local decongestants- ◦ Catecholamines-Phenylephrine ◦ Imidazoline derivative- Xylometazoline and oxymetazoline
- 34. Topical Intranasal Steroids Potentdrug in reduction of inflammation in allergic rhinitis Action by reducing the pro inflammatory protiens - chemokine receptors, complements, IL-1 and IL-8 receptors, IFN-γ receptors, TNF, and TLR 2 and 4 Treatment with topical corticosteroids 1. Reduces symptoms 2. The levels of mediators, cellular infiltration during the late-phase reaction to allergen challenge 3. The priming response to antigen
- 36. Intranasal steroid formulations 1.Flunisolide 2. Beclomethasone dipropionate 3. Triamcinolone 4. Budesonide 5. Mometasone 6. Fluticasone.
- 37. Side effects ofIntranasl steroids Nasal irritation – 10% Nasal bleeding – 2% Controversial- Nasal perforation- BIOPSY AFTER PROLONGED USE DON’T SHOW THINNING OF MUCOSA NO Growth retardation
- 38. Intranasal steroid VsSecond generation Antihistamine Intranasal steroid Vs Second generation Antihistamine and Leukotriene Modulators
- 39. Systemic steroid therapy Shortcourse systemic steroid can be given for 2 weeks Total nasal obstruction Infection complicating AR
- 40. Cromolyn Sodium 4% solutionfor intranasal use Protective role thought to prevent mast cell degranulation-the exact mechanism of action not known Safe in children and pregnant Intranasal corticosteroid>Cromolyn sodium>antihistamine
- 41. Anticholinergic Ipratropium bromide inhibit parasympatheticstimulation of glandular secretion by competing for muscarinic receptors on glands.
- 42. Leukotriene Modifiers Montelukast, Zafirlukast,and Zileuton in the United States and Pranlukast in Japan Montelukast significantly improved Night-time symptoms Difficulty going to sleep Night-time awakenings Congestion on awakening Daytime symptoms Congestion, rhinorrhea, pruritus, and sneezing
- 43. Anti IgE immunoglobulin ???Not FDA approved Shown promising results in perinnial AR with asthma OMALIZUMAB
- 44. Immunotherapy Only treatment thatcan lead to a life-long tolerance Administration of aqueous extracts of allergens to an allergic patient in an incremental, dose escalation pattern to reduce the symptoms and objective evidence of allergic response to allergen exposure. Induce a state of immunologic tolerance
- 45. What immunotherapy doesto the immune system ? 1. Down modulation of target organ sensitivity to the allergen 2. A decrease in late-phase allergic response to the allergen 3. A modest reduction in allergen-specific IgE levels 4. A shift in Th1/Th2 cytokine balance in favor of Th1 (IFN-gamma) 5. Induction of Th2 cell anergy 6. Induction of regulatory T cells (commonly known as “Tregs”) that mediate allergen specific tolerance through the production of IL-10.
- 46. Mode of administration Conventionaltechnique- SHORT INCREMENTS ONCE A WEEK Modified rush (RESEARCH)- DAILY INCREMENT
- 47. Indication of immunotherapy Environmentalcontrol measures and Pharmacotherapy fail.
- 48. After immunotherapy isadministered, the patient is observed for a minimum of 30 minutes for signs of an adverse reaction, such as hives, angioedema, bronchospasm, light-headedness, or anaphylactic shock. It has been shown that 3 years of immunotherapy provides lasting benefit that can be measured as long as 6 years after stopping immunotherapy.
- 50. Reference Scott brown 8thed Ballengers 17th ed Cummins Rhinology- David kennedy