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Insights in Asthma Rhinitis link

  1. 1. Insights in Asthma Rhinitis link
  2. 2. 3
  3. 3. Asthma and allergic Rhinitis are common health problems that cause major illness and disability world wide. Both are common chronic diseases that affect the quality of life of patients and have a significant economic impact . European Respiratory Disease 2006
  4. 4. The prevalence of asthma and rhinitis varies all over the world with allergic Rhinitis being two times more prevalent than asthma. The worldwide incidence of allergic Rhinitis and asthma has been on the rise . European Respiratory Disease 2006
  5. 5. Australia asthma 18% rhinitis 25% Canada asthma 13% rhinitis 25% Sweden asthma 8% rhinitis 15% China asthma 5% rhinitis 10% Brasil asthma 10% rhinitis 22% Kenya asthma 8% rhinitis 13% ISAAC study, Lancet 1998 Worldwide prevalence
  6. 6. Using a conservative estimate, it is proposed that allergic rhinitis occurs in around 500 million people . Studies suggest that there are more than 300 million persons worldwide who are affected by asthma .
  7. 7. Slide 9 Adapted from Bousquet J et al J Allergy Clin Immunol 2001;108(suppl 5):S147–S334; Sibbald B, Rink E Thorax 1991;46:895–901; Leynaert B et al J Allergy Clin Immunol 1999;104:301–304; Brydon MJ Asthma J 1996:29–32. Up to 80% of all asthmatic patients have allergic rhinitis All asthmatic patients Epidemiological link
  8. 8. Allergic Rhinitis and Asthma frequently occur together 40% of allergic rhinitis patients have asthma . 80% of asthma patients have concomitant Rhinitis symptoms . European Respiratory Disease 2006
  9. 9. Epidemiological link Immunological link Common Triggers Common inflammatory processes Pathophysiological link Clinical links Therapeutic links Asthma rhinitis link
  10. 10. Co-Existence of Asthma and Allergic Rhinitis: A 23-Year follow- Up Study of College Students William A. Greinsner, Robert J. Settipane and Guy A. Settipane Allergy and Asthma Proc 1998
  11. 11. Allergic Rhinitis is a risk factor for asthma Allergic Rhinitis increased the risk of asthma ~3-fold 23-year follow-up of college freshmen undergoing allergy testing; data based on 738 individuals (69% male) with average age of 40 years. Adapted from Settipane RJ et al Allergy Proc 1994;15:21-25. 12 10 8 6 4 2 0 Subjects with asthma at 23- year follow- up (%) 10.5 Allergic rhinitis at baseline (n=162) 3.6 No allergic rhinitis at baseline (n=528) p<0.002
  12. 12. Rhinitis as an independent risk factor for adult- onset asthma (atopic and non-atopic) (European Community Respiratory Health Survey) Adapted from Leynaert B et al. J Allergy Clin Immunol 1999; Asthma (%) Atopic Non atopic no rhinitis, N=5198 rhinitis, N=1412 OR=11 OR=17 0 5 10 15 20 25
  13. 13. The prevalence of asthma in patients with Rhinitis varies from 10 to 40% depending on studies . Patients with moderate/severe persistent Rhinitis may be more likely to suffer from asthma than those with an intermittent and/or a milder form of the disease .
  14. 14. - 591 patients - 502 controls - allergic to pollens, mite, -epithelia 0 5 10 15 20 25 30 35 %subjects contr mild severe mild severe intermittent persistent %pazienti Prevalence of asthma (physician diagnosed) in Rhinitis Bousquet, CEA 2005
  15. 15. BHR was found in 24% to 40% of patients with active Rhinitis (In the general population the BHR prevalence is 10-20%) Di Lorenzo G. et al. “ Non-specific airway responsiveness in mono-sensitive Sicilian patients with allergic rhinitis: its relationship to total serum IgE levels and blood eosinophils during and out of the pollen season” Clin Exp Allergy 1997; 27: 1052-59 Ramsdale EH et al. “ Asymptomatic bronchial hyperresponsiveness in rhinitis” J Allergy Clin Immunol 1985; 75: 573-577 Annesi I. et al. “ Relationship of upper airways disorders to FEV1 and bronchial hyperresponsiveness in an epidemiological study” Eur Respir J 1992; 5: 1104-1110
  16. 16. Braman SS et al. “ Airway hyperresponsiveness in allergic rhinitis: a risk factor for asthma” Chest 1987; 91: 671-674 Laprise C. et al. “ Asymptomatic airway hyperresponsiveness: A three-year follow-up” Am J Respir Crit Care Med 1997; 156: 403-9 Several studies suggested that patients with allergic Rhinitis and BHR are at higher risk of developing asthma
  17. 17. Rhiniti s asthma Diseaseseverity time Togias, Allergy 1999 The current concept is that AR precedes asthma in most patients 76% asthmatic patients reported presence of Rhinitis before onset asthma.
  18. 18. The Allergy March: CHDs CHDs Atopic Dermatitis GI Distress Recurrent Otitis Media Allergic Asthma Allergic Rhinitis Food Sensitivity Inhalant Sensitivity Time (~years) Genetic Predispositio n
  19. 19. Atopic Dermatitis Food Allergy Allergic Rhinitis Allergic Childhood Asthma Adult Asthma Atopic or Allergy March Natural sequence of allergic clinical conditions appearing during a certain age period and persisting over a number of years from childhood to adulthood Atopy is the inherited tendency to develop harmful immune responses to harmless substances Allergy can affect different children in different ways
  20. 20. “ The Allergy March ” Food Allergy Atopic Eczema Allergic Rhinitis Asthma ‘ The Atopic March ’
  21. 21. 24 Asthma Predictive Index (API) Wheezing during the first 3 years of life PLUS 1 Major Criterion 2 Minor CriteriaOR  Parental history of asthma  Physician-diagnosed atopic dermatitis  Physician-diagnosed allergic Rhinitis  Wheezing unrelated to colds  Eosinophilia (4%) Castro-Rodriguez et al. Am J Respir Crit Care Med. 2000;162:1403-1406.
  22. 22. Allergic rhinitis as a predictor for wheezing onset in school-aged children. Rochat et al, JACI 2010 Cohort of 1,314 children followed from birth to 13 yrs
  23. 23. Allergic rhinitis is one of the strongest risk factors for asthma Children who suffer from asthma and concomitant allergic rhinitis tend to have : 1. a much worse quality of life 2. more difficult to control asthma 3. 2.5 times more asthma associated hospital admissions Thomas M,et al. Pediatrics 2005: 115: 129–34. Sazonov Kocevar V,et al.Allergy 2005: 60: 338–42.
  24. 24. The Proceedings of the American Thoracic Society (2009) • . Allergic asthma and Rhinitis are manifestations of the atopic syndrome and often coexist. Genetic and environmental factors are recognized as contributing factors to the development of the allergic airway syndrome. Immunological Link
  25. 25. The Proceedings of the American Thoracic Society (2009) • . The atopic syndrome is a hereditary disorder in subjects who are particularly susceptible to the development of IgE-mediated allergic reactions manifested by: 1. Infantile eczema 2. Nasal and conjunctival allergy 3. Allergic asthma The atopic syndrome
  26. 26. Allergies affect people from the early stages of their life and continue until their late adult ages
  27. 27. Th2 Th1 Th2 Balanced Th1/Th2 at ~2yr Neonatal & infant immune systems The intrauterine environment is powerfully Th2 – this imprints Th2 dominance upon the neonate Serial infections Age Immune response
  28. 28. Th1 Th2 Unbalanced Th1/Th2 Th2 dominance at ~2yr Delayed maturation of Th1 capacity Few serial infections – hygiene, small family size etc Age Immune response Longer period of time in which to make and establish Th2 responses to environmental antigens (i.e. allergens)
  29. 29. Immune System Development and the Hygiene Hypothesis Older siblings: Many infections [TH1 stimuli] TH1 No allergies Still TH2 Allergies Only child: Few infections Allergen Exposure Source: Busse WW, Lemanske RF. N Engl J Med 2001. Birth:TH2
  30. 30. The Hygiene Hypothesis
  31. 31. Allergic Rhinitis and Asthma Share Common Triggers
  32. 32. Shared Immunological Mechanisms in
  33. 33. Similar inflammatory cascade on exposure to an allergen
  34. 34. APC Th0 Th1Th2 B lymphocyte Mast cell Eosinophil Allergic Symptoms IFN  IL 4 IL 10 IL 5 IFN IL 4 IL 13 IL 9 IL 12 IL 18 IL 12 IL 18 IL 4 Allergens IgE Sensitization Phase
  35. 35. Mast cell Basophil Eosinophil Inflammatory Mediators Release Allergens Histamine - Prostaglandins – Leucotriens – Tryptase - ECP Allergic Symptoms On re-exposure
  36. 36. In many individuals, an asthma attack comprises immediate (mainly bronchospasm) and delayed (inflammatory reaction) phases 0 2 4 6 8 Time (hours) 1.0 1.5 2.0 2.5 3.0 FEV1(lires)  Inhalation of grass pollen Early phase (bronchospasm) Late phase (inflammation)
  37. 37. • . Allergic Rhinitis and asthma share similar inflammatory processes Common triggers Similar inflammatory cascade on exposure to allergen Similar pattern of early- and late-phase responses Infiltration by the same inflammatory cells (e.g.eosinophils) Several potential connecting pathways including systemic transmission of inflammatory mediators
  38. 38. Eosinophils in airway mucosa are regarded as the hallmark of allergic Rhinitis and asthma . Eosinophilic inflammation has been found in the lower airways of allergic Rhinitis patients without asthma and in the upper airways of asthmatic patients without nasal complaints .
  39. 39. Bronchial biopsioes after Specific provocation in patients with rhinitis or asthma Crimi E et al, JAP 2001 ASTHMA RHINITIS ALONE Same inflammation
  40. 40. Nasal allergen challenge Increases bronchial reactivity Induces bronchial inflammation Littell NT, Changes in airways resistance following nasal provocation. Am Rev Respir Dis 1990 Corren J Changes in bronchial responsiveness following nasal provocation with allergens. JACI 1992 Small P ET AL The effects of allergen-induced nasal provocation on pulmonary function in patients with perennial allergic rhinitis. Am J Rhinol 1989
  41. 41. Bronchial endoscopic challenge With allergen Induces nasal inflammation
  42. 42. Togias A Allergy 1999;54(suppl 57):94.. Aspiration of Inflammatory Material Oral breathing Nasopharyngo-bronchial reflex Systemic Propagation of Nasal Inflammation Mechanisms of pathologic relationships between upper and lower airways.
  43. 43. AllergicRhinitis and asthma are manifestations of one syndrome, in 2 parts of the respiratory tract , the upper and lower airways. At the low end of the severity spectrum, Rhinitis may occur alone , in the middle range of the spectrum, Rhinitis and AHR may be present and, at the high end, Rhinitis and asthma may both be present. . Togias A, J Allergy Clin Immunol Jun2003
  44. 44. Chronic Allergic Inflammatory Airway Syndrome Allergic Rhinitis Allergic rhinitis + Bronchial Hyperreactivity Allergic Rhinitis + Asthma
  45. 45. The allergic Rhinitis and asthma frequently co-exist leading to the concept that these seemingly separate disorders are manifestations of the same disease expressed to a greater or lesser extent in either the upper or the lower airways. Togias A, J Allergy Clin Immunol Jun2003
  46. 46. The nose-lung interaction in allergic rhinitis and asthma: united airways disease G.Passalacqua, G.Ciprandi & G.W.Canonica 2004 Asthma and Rhinitis as different Aspects of a sinlge disorder In some patients Rhinitis predominates and asthma is undiagnosed or sub-clinical, in others it is reversed, while in many both are clinically expressed .
  47. 47. Clinical links
  48. 48. Influence of comorbid conditions on asthma Boulet LP, ERJ 2009
  49. 49. Cruz, Allergy 2008
  50. 50. Adams et al. J.A.C.I. 2002 Treatment of Rhinitis reduces emergency visits for asthma Crystal-Peters, JACI 2002 Fuhlbrigge, Curr Opin Allergy Immunol 2003 Baena-Cagnani et al, Int Arch Allergy Immunol 2003 Nelson HS, JACI 2003
  51. 51. No. of GP visits (Mean) No. of SAß2A prescriptions % Hospitalizations 1.4 0.5 Children with Asthma (n=7.643) Children with Asthma + Allergic Rhinitis (n=1.879) <0,0001 3.4 4.4 0 3 5 4 2 1 <0,001 1.8 2.3 <0,001 per patient / year
  52. 52. • therapeutic Therapeutic aspects
  53. 53. Those patients whose allergic rhinitis was severe or poorly controlled had worse asthma control and tended to have more persistent asthma than those with mild or well controlled rhinitis. In addition, bronchial hyperresponsiveness can be present in patients with allergic rhinitis without clinical evidence of asthma ARIA 2008
  54. 54. Prompt and effective treatment of nasal disease can have a marked effect on preventing the development of asthma, and on existing asthma symptoms. The World Allergy Organization IAACI, 2003 Treatment of rhinitis has the potential to reduce asthma symptoms to such an extent that treatment with asthma medications may be unnecessary in some patients. Curr Opin Allergy Clin Immunol 2003
  55. 55. The recommended clinical approach is to manage the two disorders discretely but simultaneously. You should treat each disease separately; that even though it's 1 disease, you can't just treat the nose and take care of the asthma,or treat the asthma and take care of the nose. Each one has to be treated appropriately.
  56. 56. 71
  57. 57. Airway inflammation Airflow obstruction Bronchial hyperresponsiveness Symptoms Asthma Pathophysiology The tip of the iceberg
  58. 58. Asthma, irrespective of the severity, is a chronic inflammatory disorder of the airways. Airway inflammation is associated with: ● Airway hyperresponsiveness ● Airflow limitation ● Respiratory symptoms. Definition of Asthma
  59. 59. Controllers vs Relievers Controllers = medications taken daily on a long-term basis to keep asthma under clinical control  due to antiinflammatory effects Relievers = medications used on an as-needed basis that act quickly to reverse bronchoconstriction and relieve its symptoms
  60. 60. Asthma therapy Controllers  Inhaled corticosteroids  Inhaled long-acting b2- agonists  leukotriene modifiers  SR theophyllines  Anti-IgE Relievers  Inhaled short-acting B2 agonists
  61. 61. 77 • Inhaled corticosteroids are the recommended & most effective preventer drug for adults and children with asthma , for achieving overall treatment goals.
  62. 62. 78
  63. 63. 79
  64. 64. 80 ICS usage as a preventer therapy should be explained to the parents in simple, plain terms.
  65. 65. 81 Pharmacokinetics of Inhaled corticosteroids
  66. 66. 82 1. Oropharyngeal candidiasis 2. Hoarseness 3. Coughing To reduce the potential for adverse affects:  Use the lowest dose necessary to maintain control.  Administer with spacers/holding chambers.  Advise patients to (Rinse with water , gargle and spit out) after inhalation. Local side effects
  67. 67. 83
  68. 68. Problems with inhaler technique are common in clinical practice & can lead to poor asthma control All patients should be trained in technique & trainers should be competent with the inhalation technique Assess inhaler technique
  69. 69. Invest the time to train each patient in proper inhaler technique Recheck inhaler technique on each revisit Assess inhaler technique
  70. 70. 89 Fate of inhaled drugs – Good Technique Swallowed GI tract Deposited in lung Lungs Metabolism or absorption from the lung Liver Oral bioavailability Absorption from gut First-pass metabolism Systemic Circulation Mouth pharynx mucociliary clearance 80% 20% Schematic representation of potential dose distribution A Guide to Aerosol Delivery Devices for Respiratory Therapists. American Association for Respiratory Care. 1st Edition. Page 1. Webpage: http://www.aarc.org/education/aerosol_devices/ Adapted from Barnes et al. AJRCCM 1998;157:S1-S53
  71. 71. 90 Fate of inhaled drugs – Good Technique Swallowed GI tract Deposited in lung Lungs Metabolism or absorption from the lung Liver Oral bioavailability Absorption from gut First-pass metabolism Systemic Circulation Mouth pharynx mucociliary clearance 80% 20% Schematic representation of potential dose distribution A Guide to Aerosol Delivery Devices for Respiratory Therapists. American Association for Respiratory Care. 1st Edition. Page 1. Webpage: http://www.aarc.org/education/aerosol_devices/ Adapted from Barnes et al. AJRCCM 1998;157:S1-S53 Swallowed GI tract Deposited in lung Lungs Metabolism or absorption from the lung Liver Oral bioavailability Absorption from gut First-pass metabolism Systemic Circulation Mouth pharynx mucociliary clearance 95% 5% Schematic representation of potential dose distributionAdapted from Barnes et al. AJRCCM 1998;157:S1-S53 A Guide to Aerosol Delivery Devices for Respiratory Therapists. American Association for Respiratory Care. 1st Edition. Page 1. Webpage: http://www.aarc.org/education/aerosol_devices/ Fate of inhaled drugs – Poor Technique
  72. 72. Treatment Options for adult Patients Not Controlled on Iow dose ICS Patients not controlled on inhaled steroids (ICS) Increase the dose of inhaled steroid Add leukotriene receptor antagonists Add long-acting beta2-agonists Add SR theophylline
  73. 73. UPDATED 2016
  74. 74. GINA 2017, Box 3-5, Step 5 (8/8) Other controller options RELIEVER STEP 1 STEP 2 STEP 3 STEP 4 STEP 5 Low dose ICS Consider low dose ICS Leukotriene receptor antagonists (LTRA) Low dose theophylline* Med/high dose ICS Low dose ICS+LTRA (or + theoph*) As-needed short-acting beta2-agonist (SABA) Low dose ICS/LABA** Med/high ICS/LABA PREFERRED CONTROLLER CHOICE UPDATED 2017 *Not for children <12 years **For children 6-11 years, the preferred Step 3 treatment is medium dose ICS #For patients prescribed BDP/formoterol or BUD/ formoterol maintenance and reliever therapy  Tiotropium by mist inhaler is an add-on treatment for patients ≥12 years with a history of exacerbations Refer for add-on treatment e.g. tiotropium,* anti-IgE, anti-IL5* As-needed SABA or low dose ICS/formoterol# Add tiotropium* High dose ICS + LTRA (or + theoph*) Add low dose OCS
  75. 75. Stepwise management
  76. 76. Asthma Control Test (ACT)
  77. 77. Asthma Control Test (ACT)
  78. 78. Allergic rhinitis
  79. 79. Allergic rhinitis (AR) is the most common chronic disease in childhood is often ignored, misdiagnosed and/or mistreated. Undertreated AR impairs quality of life, exacerbates asthma and is a major factor in asthma development.
  80. 80. Allergic rhinitis (AR) is an under-recognised inflammatory condition of the nasal mucosa, caused by IgE-mediated early-phase and late-phase hypersensitivity responses, usually to inhalant allergens, similar to those in allergic asthma. Allergic rhinitis is caused by an IgE-mediated reaction to specific seasonal , perennial or episodic aeroallergens.
  81. 81. ALLERGIC RHINITIS • In relation to symptom frequency classified as : Intermittent Vs. Persistent • In relation to Severity classified as : Mild Vs. Moderate/severe • In relation to allergen exposure classified as: Perineal Vs Seasonal Vs Episodic
  82. 82. Perennial AR is typically caused by sensitization to indoor allergens such as dust mites, mold and animal dander (Symptoms are present throughout the year) Seasonal AR is most often due to sensitization to pollen allergens (Symptoms appear in or around a particular season). Episodic AR results from sporadic exposures to aeroallergens that are not typically encountered, such as visiting a farm or home with animal allergens that an individual would not typically encounter
  83. 83. Symptoms of Allergic rhinitis (AR) is characterized by one or more symptoms including Nasal congestion,rhinorrhea, sneezing and itching on consecutive days . •
  84. 84. Looking for Allergic rhinitis in Primary Care Setting
  85. 85. Minimal persistent inflammation is also Present in patients with seasonal allergic rhinitis V. Ricca, M.Landi, P.Ferrero, A.Bairo, C.Tazzer,G.W.Canonica and G.Ciprandi gw111199 J.A.C.I. 2001
  86. 86. Concept of "minimal persistent inflammation" Threshold level for symptoms 0,1 1 10 100 0 2 4 6 8 10 12 Months miteallergen(µg/gofdust) Minimal persistent inflammation Symptoms inflammation Ciprandi et al, J Allergy Clin Immunol 1996
  87. 87. Stimulus The concept of Minimal Persistent inflammation Symptoms Symptom threshold INFLAMMATION
  88. 88. Instead of considering allergic rhinitis as a disease of acute symptoms, it needs to be understood as a chronic inflammatory disease. Even in the absence of symptoms, continuous exposure to low levels of allergen results in an inflammatory infiltration and ICAM-1 expression, which is known as "minimal persistent inflammation" (MPI).
  89. 89. The concept of minimal persistent inflammation suggests a different approach to therapy in which symptoms can be considered the “tip of the iceberg” of the allergic reaction with inflammation and hyper-responsiveness representing the submerged iceberg Therefore, any optimal therapeutic strategy for AR should focus on minimizing inflammatory phenomena rather than only on alleviating acute symptoms.
  90. 90. Therapeutic implications The intranasal corticosteroids (INCSs) are the current first-line therapy for moderate to severe cases of seasonal and perennial AR Regular persistent use of INCSs has been effective in reducing all symptoms nasal congestion, rhinorrhoea, sneezing, and nasal itching in both adults and children.
  91. 91. INCS are the most effective drug In A.R. ICS are the milestone asthma treatment • ICS+INCS in the same UAD patients???????
  92. 92. Simplified AR Treatment Algorithm Small and Kim. AACI Nov 2011. Treatments can be used individually or in any combination Allergen avoidance Allergen immunotherapy (SCIT/SLIT) Oral or intranasal antihistamines Leukotriene receptor antagonists Intranasal corticosteroids
  93. 93. Recognized as the most effective agent for symptom control in allergic rhinitis, are currently recommended as first-line therapy for patients with moderate-to- severe symptoms or those with nasal congestion as the dominant complaint. The onset of action ranges from 3 to 36 hours after the first dose, and continuous use is more effective than intermittent use. The intranasal corticosteroids
  94. 94. No single product is recommended over another, as studies have shown comparable efficacy among products. In the control of nasal symptoms, intranasal steroids have shown superior efficacy compared with oral antihistamines; however, intranasal antihistamines have a faster onset of action The intranasal corticosteroids
  95. 95. Concerns over stunted growth in children precipitated several clinical trials; reduced growth was seen with budesonide and beclomethasone, but not with fluticasone furoate, triamcinolone acetonide, mometasone furoate, or fluticasone propionate. Accordingly, for pediatric patients, guidelines recommend using those agents not shown to reduce growth. The intranasal corticosteroids
  96. 96. The intranasal corticosteroids • The most common side effects of INS are a result of local irritation and include dryness, burning, stinging, blood tinged secretions, and epistaxis. • The incidence of epistaxis with different preparations ranges from 4% to 8% over short treatment periods ranging from 2 to 12 weeks with no differences between placebo and active therapy.
  97. 97. The intranasal corticosteroids • Epistaxis can be minimized with proper INS positioning and administration, generally pointed away from the septum within each side of the nose. • Septal perforations, although rare, have been reported. • Biopsy specimens from the nasal mucosa of patients with perennial rhinitis who have been treated with INS continuously for 1 to 5 years showed no evidence of atrophy
  98. 98. The intranasal corticosteroids • Studies in adults and children evaluating the effects of INS on the hypothalamic-pituitary axis using morning cortisol concentrations, cosyntropin stimulation, and 24- hour urinary free cortisol excretion show no adverse effects • Studies with INS given over several months have failed to show development of posterior subcapsular cataracts, significant increases in intraocular pressure, or glaucoma.
  99. 99. 133 Pharmacological management of AR
  100. 100. Oral Leukotriene receptor Antagonists (LTRAs) • Leukotriene Receptor Antagonists, are No longer recommended as primary therapy in allergic rhinitis, only are reserved for combination therapy • LTRA (montelukast) was found to be either equally effective or less effective than oral antihistamines, and it was less efficacious than intranasal steroids. • Because this agent treats both allergic rhinitis and asthma, a patient with both conditions is the best candidate .
  101. 101. Immunotherapy • Immunotherapy is the only proven treatment for AR that has the potential to change the natural history of the disease. • It must be emphasized that demonstration of IgE- mediated allergy based on history and confirmed by specific allergy testing (skin or in vitro) is a prerequisite for all forms of immunotherapy, both SLIT and SCIT. • The typical duration of treatment for either form of immunotherapy is several years, typically 3 to 5 years.
  102. 102. Immunotherapy • With a clear patient history, diagnosis can be made without further tests. However, if in doubt, looking for the likely IgE molecules by skin prick or blood test can be helpful, although this should be guided by history, rather than performed in a random fashion. • Positive tests do not always indicate clinical disease, a positive test to an allergen with no pertinence to patient’s history has no relevance for diagnosis and might result in over-diagnosis . • Testing should always be considered in the context of the possible clinical benefit, which can be from allergen avoidance, if the patient is able and willing tocomply, allergen specific immunotherapy.
  103. 103. Immunotherapy • Patients on SIT should be monitored on a regular basis for effectiveness based on clinical parameters such as symptoms and medication use; • Typically, positive benefits of immunotherapy on AR symptoms appear from several weeks to 1 year after initiation of therapy.
  104. 104. Immunotherapy • Due to the potential for serious reactions, current practice guidelines indicate that SCIT should not be used in patients with severe, uncontrolled asthma . • SCIT should be administered in a physician’s office where serious reactions can be promptly recognized, and the patient should be observed for 30 minutes after injection.
  105. 105. 147
  106. 106. Pediatric rhinitis : Position paper of the European Academy of Allergy and Clinical Immunology. Allergy 2013
  107. 107. The Rhinitis Control Assessment Test (RCAT)
  108. 108. The Rhinitis Control Assessment Test (RCAT)
  109. 109. Scores Total scores > 24 indicate good disease control Score of the upper airway: controlled if score is > 8 Score of the lower airway : controlled if score is > 16
  110. 110. Treating comorbid rhinitis & asthma Upper airway treatment options Lower airway treatment options Nasal steroids Inhaled steroids Antihistamines Upper and lower airway treatment options Leukotriene receptor antagonists Anti-IgE Immunotherapy
  111. 111. “Allergic rhinitis and asthma are chronic inflammatory disorders that have been linked epidemiologically, immunologically , pathophysiologically, and therapeutically as “one airway disease.” Final Remarks
  112. 112. Final Remarks 1-Patients with persistent Rhinitis should be evaluated for asthma 2-Patients with persistent asthma should be evaluated for Rhinitis 3-A combined strategy should be used in the treatment of upper and lower airways
  113. 113. 157