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Childhood allergies & their progression

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  • Here is a graphic representation of the Allergy March. Taken in isolation, each of these five conditions seems unrelated, but as the ovals and lines illustrate, they can be tied to allergic sensitivities and inflammation, beginning with foods and shifting to inhalants. Although these illnesses often follow the progression of the March, allergy sensitivities may emerge with symptoms of any one of the five conditions, and may involve more than one illness at a time. This progression can commence early. Family history can predispose a child to allergy, and atopy can emerge soon after birth—in fact, IgE may be detected in children as young as 3 months. And in some young patients, allergic asthma may emerge by the age of 3 or 4. 1 That’s why it’s critical that we work to recognize and treat underlying atopy, which can alter or arrest the march toward pediatric asthma. Understanding the allergic sensitivities in these diseases allows us to provide solid, evidence-based avoidance and treatment plans to treat the cause as well as the symptoms. Now, let’s take a look at each of these conditions to get a sense of prevalence and the specific role atopy plays for each. ETAC ® Study Group. Pediatr Allergy Immunol . 1998;9:116-124.
  • The prevalence of current eczema, allergic rhinitis, and asthma estimated from compiled data over the age span of birth to 70 years, incorporating studies from 1980 to 2008. Prevalence data used to generate these figures were from studies that used questionnaire data from developed countries. including the United States. Western Europe, and the United Kingdom Allergy Asthma Immunol 2009;103:282-9
  • The Children’s Respiratory Study showed that the presence of physician-diagnosed allergic rhinitis in infancy was independently associated with a doubling of the risk of developing asthma by 11 years of age. In adults, allergic rhinitis as a risk factor for asthma was shown in a 23-year follow-up of college students. Significantly more (10.5%) of the students originally diagnosed with allergic rhinitis went on to develop asthma compared with 3.6% of those who did not have rhinitis. Allergy 2003: 58: 691–706 When examining the temporal relationship between rhinitis and asthma, several studies demonstrate that rhinitis in infancy or childhood is associated with the development of asthma later in life. "S,% In the Tasmanian Asthma Study, childhood allergic rhinitis (present by 7 years of age) increased the likelihood of both new-onset asthma and having asthma persist from childhood into middle ageP3 The Tucson Children's Respiratory Study found that rhinitis in the first year of life was associated with more respiratory symptoms and the diagnosis of asthma at 6 years of age. Allergy Asthma Immunol 2009;103:282-9 Thus, as suggested by the ARIA document, a spirometry should be performed, also in absence of overt asthmatic symptoms, in patients with moderate-severe persistent allergic rhinitis with these risk factors to prematurely detect the possible presence of severe BHR. Allergy. 2010 Feb 4
  • Characteristic symptoms of allergic rhinitis are shown in this slide. In addition, AR is associated with ear fullness and popping, itchy throat, and pressure over the cheeks and forehead. Malaise, weakness, and fatigue may also be present. When not all the typical rhinitis symptoms are expressed, the diagnosis is more difficult to make. Distinct temporal patterns of symptom production may aid diagnosis. SAR symptoms typically appear during a defined season. In contrast, indoor allergens responsible for PAR are present in the environment throughout the year. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Impairment of quality of life is seen in adults and children. Patients might also have sleep disorders, emotional problems, and impairment in activities and social functioning. Poorly controlled symptoms of AR might contribute to sleep loss or disturbance. Moreover, H1-antihistamines with sedative properties can increase functional disturbances in patients with AR. AR affects school and work.2 Although several economic analyses of AR have been published, there are relatively few cost-of-illness studies. The economic effect of AR is often underestimated because the direct costs of the disease are lower than those of a number of other chronic illnesses. However, the indirect costs are substantial. Ref: Unmet needs in severe chronic upper airway disease (SCUAD). Bousquet J, Bachert C, Canonica GW, Casale TB, Cruz AA, Lockey RJ, Zuberbier T; Extended Global Allergy and Asthma European Network, World Allergy Organization and Allergic Rhinitis and its Impact on Asthma Study Group. J Allergy Clin Immunol. 2009 Sep;124(3):428-33. Allergic rhinitis is the most prevalent chronic allergic disease in children (948). Although it is not life-threatening, it can have a significantly detrimental effect on a childs QOL, and it may exacerbate a number of common co-morbidities, including asthma and sinusitis (2169). There are many different causes of rhinitis in children and approximately 50% are induced by allergy (2170). Allergic and nonallergic rhinitis are often difficult to differentiate based on symptoms. Ref ARIA 2008. Allergy 2008: 63 (Suppl. 86): 8–160 88% of pediatric patients with AR are estimated to experience difficulty sleeping. during childhood and adolescence, sleep-disordered breathing has been associated with an increased frequency of learning performance disorders, behavioral disorders, and attention deficit disorders. AR has also been demonstrated to adversely affect childhood learning and decrease cognitive functioning. J Allergy Clin Immunol 2009;124:S43-70
  • An association between allergic rhinitis and conditions including asthma, sinusitis, nasal polyposis, and conjunctivitis has been observed. Although the link may be predominantly an allergic one, nonallergic factors may also play a role. Spector SL. Overview of comorbid associations of allergic rhinitis. J Allergy Clin Immunol . 1997;99(2 suppl):S773-S780.
  • Data was collected at two French centres participating in the European Community Respiratory Health Survey (ECRHS) were analysed to assess p resence of concurrent allergic rhinitis and asthma. Asthma defined as one or more asthma attacks in the preceding 12 months or positive response to metachloline challenge. Patients were considered to have allergic rhinitis if they responded positively to one or two questions regarding rhinitis symptoms. Reference Leynaert et al. Am J Respir Crit Care Med 2000; 162: 1391-1396
  • Diagnosis of allergic rhinitis requires a detailed and accurate history. As symptoms of allergic and nonallergic rhinitis are often similar, the patient should be asked about specific symptoms and symptom patterns, including onset, progression, severity, relationship to seasons, etc. Personal and family histories of allergic disease are also important. Physical examination should focus on the nose, eyes, and ears, but should also include examination of the lungs and skin. The patient should be observed for mouth breathing, repeated nose wiggling, wiping, and pushing – the allergic salute – a nasal crease, “allergic shiners” (a darkening of the infraorbital skin resulting from venous dilation and indicative of chronic nasal congestion, particularly in children), and related eye symptoms. Determination of specific IgE, preferably by skin testing, is indicated to provide evidence of an allergic basis for the patient’s symptoms, to confirm or exclude suspected causes of symptoms or to assess the sensitivity to a specific allergen for avoidance measures and/or allergen immunotherapy. Nasal smears for eosinophils are not necessary for routine use in diagnosing AR. Although CT and MRI are not indicated for the evaluation of patients with uncomplicated rhinitis, they may be useful with suspected complications or comorbidities such as nasal polylposis and/or concomitant sinusitis. Standard radiographs are generally not indicated because of the availability of preferred procedures. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Atopic individuals respond to allergen exposure by producing allergen-specific IgE. IgE antibodies bind to IgE receptors on mast cells throughout the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the allergen binds to and crosslinks IgE on the mast cell surface, resulting in activation and release of inflammatory mediators. Nasal mast cells release histamine, prostaglandins, leukotrienes, PAF, and bradykinin, among other mediators. These result in the signs and symptoms of allergic rhinitis. Tissue eosinophilia is also a feature of allergic rhinitis, and eosinophil-derived mediators are associated with nasal epithelial injury and desquamation, subepithelial fibrosis, and hyperresponsiveness. The allergic nasal response consists of an immediate phase, which peaks at 15 to 30 minutes after allergen exposure and corresponds to mast cell degranulation and mediator release, and a late phase, which peaks at 6 to 12 hours after exposure and corresponds to infiltration of the nasal tissues by eosinophils, basophils, and other inflammatory cells. Patients with allergic rhinitis usually have similar inflammatory changes in the linings of the paranasal sinuses.  
  • There are 4 general principles of allergy management, as shown on this slide: Avoid factors that cause symptoms Use appropriate treatments. The goal of pharmacotherapy is to alleviate and prevent symptoms. Palliative treatment—nasal lavage and mist inhalation—may also be helpful Evaluate for immunotherapy Educate and follow up. Use appropriate patient education materials Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Environmental controls are first-line therapies and need to be tailored to the individual patient's exposures and sensitivities. Unfortunately, environmental controls are not always practical or effective, and supplemental medical management may be required. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Allergic rhinitis is caused by an immunoglobulin E (IgE)-mediated reaction of the nasal mucosa to one or more allergens. In seasonal allergic rhinitis (SAR), symptoms are periodic and correlate with seasonal variations in airborne allergens. Common allergens that cause SAR include grass, tree, and weed pollens, and fungal (mold) spores in certain climates. Perennial allergic rhinitis (PAR) is an IgE-mediated reaction to allergens that show little or no seasonal variation. Typically these allergens are found indoors and include house-dust mite, animal dander, cockroach, and mold. However, pollen that is prevalent perennially can also cause PAR. SAR and PAR often coexist in the same individual. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Clinical Effects of Leukotrienes Leukotrienes Increase vascular permeability Increase mucus production and secretion Neuronal stimulation Smooth muscle constriction and proliferation Production, adhesion, migration and survival of inflammatory cells (eosinophils) Modulate generation of inflammatory mediators like cytokines, chemokines, growth factors 1 Several studies have demonstrated that CysLT levels in nasal fluids are increased in patients with AR. CysLTs are released from inflammatory cells that participate in AR. Administration of CysLTs reproduces the symptoms of AR. 2 Clinically, they have been found to cause rhinorrhea, nasal congestion, pruritus and sneezing. 2 References Van Hoecke H, Vandenbulcke L , Van Cauwenberge P. Histamine and leukotriene receptor antagonism in the treatment of allergic rhinitis: An update. Drugs. 2007;67(18):2717–2726. 2. Peters-Golden M, Gleasonw MM, Togiasz A. Cysteinyl leukotrienes: Multi-functional mediators in allergic rhinitis. Clin Exper Aller. 2006;36:689–703.
  • Decongestants The vasoconstriction caused by decongestants reduces swelling and is effective in nasal obstruction, however, nasal pruritis, and rhinorrhea are not controlled. A rebound congestion after 10 days of intranasal administration has made this unfavorable for use in AR. Oral decongestants are also associated with many adverse side-effects. 1,2 Leukotriene Modifiers Interference with the synthesis or activity of leukotrienes B4 and C4 (LTB4 and LTC4) or inhibition of chemokine production reduces eosinophilic inflammation. 3 Cysteinyl leukotrienes (CysLTs) LTC4, LTD4 and LTE4 activate of two receptors (CysLT-1 and CysLT-2) in inflammatory cells, esinophils and mast cells. CysLT levels are increased in the late phase causing mucus production and LTRAs are more effective in treating asthma. LTRAs are highly specific to CysLT-1 receptors. They block CysLT-1 receptors on target cells thereby reduce inflammatory response, mucous secretion and tissue edema. By this, the patient is relieved of congestion, sneezing and rhinorrhea. Table: Eight studies compared oral leukotriene receptor antagonists with placebo. The following outcomes were analyzed: daytime and nighttime nasal symptoms, rhinoconjunctivitis quality of life, and eye symptoms (mean change from baseline or absolute values). Pooled analysis showed that oral leukotriene receptor antagonists significantly reduced daytime and nighttime nasal symptoms and eye symptoms compared with placebo. Also, leukotriene receptor antagonists produced significantly greater improvement compared with placebo in the quality-of-life overall score. 4 There is an obvious need for an integrated disease management for AR and asthmatic symptoms since the same eosinophilic inflammation is observed in both these upper and lower airway disorders . They share a common shared inflammatory pathway, histamine and leukotrienes as common, crucial inflammatory mediators. While histamine causes relief of upper airway AR symptoms, leukotrienes are more effective in treating lower airway asthma symptoms. 3 References 1.Allergic rhinitis and its impact on asthma (ARIA). Eur J Aller Clin Immun. 2008;63(S86). 2. Luskin AT, Scherger JE, Pollart SM. Beyond the nose: The systemic inflammatory effects of allergic rhinitis. Hosp Phy .2004;13–22. 3.Van Hoecke H, Vandenbulcke L , Van Cauwenberge P. Histamine and leukotriene receptor antagonism in the treatment of allergic rhinitis: An update. Drugs. 2007; 67(18):2717–2726. Table Reference 4.Rodrigo GJ, Yanez A. The role of antileukotriene therapy in seasonal allergic rhinitis: a systematic review of randomized trials. Ann Allergy Asthma Immunol. 2006;96:779–786.
  • Decongestants The vasoconstriction caused by decongestants reduces swelling and is effective in nasal obstruction, however, nasal pruritis, and rhinorrhea are not controlled. A rebound congestion after 10 days of intranasal administration has made this unfavorable for use in AR. Oral decongestants are also associated with many adverse side-effects. 1,2 Leukotriene Modifiers Interference with the synthesis or activity of leukotrienes B4 and C4 (LTB4 and LTC4) or inhibition of chemokine production reduces eosinophilic inflammation. 3 Cysteinyl leukotrienes (CysLTs) LTC4, LTD4 and LTE4 activate of two receptors (CysLT-1 and CysLT-2) in inflammatory cells, esinophils and mast cells. CysLT levels are increased in the late phase causing mucus production and LTRAs are more effective in treating asthma. LTRAs are highly specific to CysLT-1 receptors. They block CysLT-1 receptors on target cells thereby reduce inflammatory response, mucous secretion and tissue edema. By this, the patient is relieved of congestion, sneezing and rhinorrhea. Table: Eight studies compared oral leukotriene receptor antagonists with placebo. The following outcomes were analyzed: daytime and nighttime nasal symptoms, rhinoconjunctivitis quality of life, and eye symptoms (mean change from baseline or absolute values). Pooled analysis showed that oral leukotriene receptor antagonists significantly reduced daytime and nighttime nasal symptoms and eye symptoms compared with placebo. Also, leukotriene receptor antagonists produced significantly greater improvement compared with placebo in the quality-of-life overall score. 4 There is an obvious need for an integrated disease management for AR and asthmatic symptoms since the same eosinophilic inflammation is observed in both these upper and lower airway disorders . They share a common shared inflammatory pathway, histamine and leukotrienes as common, crucial inflammatory mediators. While histamine causes relief of upper airway AR symptoms, leukotrienes are more effective in treating lower airway asthma symptoms. 3 References 1.Allergic rhinitis and its impact on asthma (ARIA). Eur J Aller Clin Immun. 2008;63(S86). 2. Luskin AT, Scherger JE, Pollart SM. Beyond the nose: The systemic inflammatory effects of allergic rhinitis. Hosp Phy .2004;13–22. 3.Van Hoecke H, Vandenbulcke L , Van Cauwenberge P. Histamine and leukotriene receptor antagonism in the treatment of allergic rhinitis: An update. Drugs. 2007; 67(18):2717–2726. Table Reference 4.Rodrigo GJ, Yanez A. The role of antileukotriene therapy in seasonal allergic rhinitis: a systematic review of randomized trials. Ann Allergy Asthma Immunol. 2006;96:779–786.
  • Intranasal corticosteroids are the most effective medication class in controlling the symptoms of AR. They are effective in controlling the four major symptoms of AR: sneezing, itching, rhinorrhea, and nasal congestion. Intranasal corticosteroids have minimal local side effects. Intranasal corticosteroids may provide significant relief of SAR when used on an as-needed basis, though when used in this manner they may not be as effective as when used on a continuous basis. 1 Patient preference should be taken into consideration when prescribing intranasal corticosteroids, as it affects compliance. 2 In addition, patients should be taught proper administration of intranasal corticosteroids, to help avert rare nasal septal perforations. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84. Brunton SA, Fromer LM. Treatment options for the management of perennial allergic rhinitis, with a focus on intranasal corticosteroids. South Med J . 2007;100(7):701-708.
  • Proper administration of intranasal corticosteroids includes following a series of steps. First, the patient should clear their nose, then shake the spray bottle. Tilting their head forward approximately 30 degrees, 1 the patient should use the correct axis of insertion and be sure to direct the spray away from the septum to minimize the risk of septal perforation. 2 The patient should then fully depress spray nozzle and alternate nostrils with each puff. 1 Loh CY, et al. Chao SS, Chan YH, Wang DY. A clinical survey on compliance in the treatment of rhinitis using nasal steroids. Allergy. 2004;59(11):1168-1172. Brunton SA, Fromer LM. Treatment options for the management of perennial allergic rhinitis, with a focus on intranasal corticosteroids. South Med J .  2007;100(7):701-708.
  • Cromolyn sodium, a topical mast cell stabilizer, blocks the early- and late-phase nasal allergic response, minimizing nasal pruritus, sneezing, and rhinorrhea. It does not improve ocular symptoms. Cromolyn sodium is not as effective in treating the symptoms of AR as intranasal corticosteroids. Side effects are generally minor and include sneezing and burning. 1 Leukotriene-receptor antagonists are antagonists of cysteinyl leukotrienes  chemical mediators of airway inflammation. The biologic effects of cysteinyl leukotrienes include increased mucus secretion and vascular permeability. Antileukotrienes act as receptor antagonists to prevent leukotriene-mediated inflammation. 2 Intranasal anticholinergics provide relief from excessive rhinorrhea not controlled by other medications. They do not relieve nasal congestion, pruritus, or sneezing, and they are not well absorbed from the nasal mucosa. Common local side effects are dose related, and include nasal dryness and bloody nasal discharge. 1 Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84. Aprile A, Lucarelli S, Vagnucci B, Frediani T. The use of antileukotrienes in paediatrics. Eur Rev Med Pharmacologic Sci. 2001;5:53-57.
  • Immunotherapy, also known as hyposensitization, requires sequential subcutaneous introduction of increasing dosages of specific allergens to which the patient is sensitive. Although the mechanism of action is currently unknown, it has been hypothesized that immunotherapy shifts the immune response to allergens from a TH2-mediated to a TH1-mediated response. Immunotherapy has been demonstrated to be effective in clinical studies in children with AR, allergic conjunctivitis, allergic asthma, and/or hypersensitivity to stinging insects. Moreover, early intervention with immunotherapy may modify the course of the disease. Immunotherapy should be used in combination with pharmacotherapy, because few patients respond completely to immunotherapy alone. The benefits of immunotherapy must be weighed against potential risks, including anaphylaxis. Sublingual immunotherapy is not currently approved by the FDA for use in the US. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol . 2008;122(2 suppl):S1-S84.
  • Transcript

    • 1. Childhood allergies and their progression  Dr. Vinod Gandhi MD, DNB [ Pediatrics ] Director Colours Children hospital Dhantoli;Nagpur
    • 2. Question 1 Jagdish is a 6 year old boy with a runny, stuffy nose for the last 2-3 weeks. You notice that he is sniffing and that he keeps rubbing his nose with the palm of his hand. What is the likely diagnosis? 1. Upper respiratory infection 2. Allergic rhinitis 3. Acute sinusitis 4. Acute otitis media
    • 3. Prevalence & burden Globally, AR affects about 4 out of 10 children In India, an increased incidence is seen –AR increased from 22.5% to 27.5% between 1994 to 1999 –3 out of 4 asthmatic children are associated with AR & 3 out of 10 AR children have co-morbid asthma
    • 4. Risk Factors for Allergic Rhinitis  Family history of allergy is single most important factor predisposing a child to development of allergic disease Development of allergic diseases in atopic –50% with one parent having atopy –66% with both parents having atopy – individuals is due to 85% have similar allergy like parents  •Other Risk Factors –small family size Environmental Environmental Genes Genes –early use of antibiotics factors factors –western lifestyle –dietary factors Gene–environment Gene–environment interactions interactions –passive smoke exposure –Atopic dermatitis –High serum IgE levels at 6 years of age
    • 5. Allergy can affect different children in different ways Food Allergy Atopic Dermatitis Allergic RhinitisAtopic or Allergy MarchNatural sequence of allergic clinical conditions Allergic Childhood Asthmaappearing during a certain age period and persistingover a number of years from childhood toadulthood Adult AsthmaAtopy is the inherited tendency to develop harmfulimmune responses to harmless substances
    • 6. The Allergy March Food Sensitivity Recurrent Atopic Food URIs? Allergic Allergic Dermatitis Allergy Rhinitis AsthmaGeneticPredisposition Inhalant Sensitivity Time (~years)
    • 7. Prevalence of eczema, AR and asthma Allergy Asthma Immunol 2009;103:282-9
    • 8. Physiology of the Nose  The nose is the “air conditioner” to the lower airways  Humidifies  Warms  Filters out particles  Olfaction  Phonation  Source of Nitric Oxide
    • 9. Impact of upper airway on lower airway  Children Respiratory Study  allergic rhinitis in infancy associated with a doubling of the risk of developing asthma by 11 years of age  Tasmanian Asthma Study  childhood allergic rhinitis (7 years of age) increased the likelihood of both new-onset asthma and having asthma persist from childhood into middle age  Tucson Childrens Respiratory Study  rhinitis in the first year of life associated with more respiratory symptoms and the diagnosis of asthma at 6 years of age Allergy 2003: 58: 691–706; Allergy Asthma Immunol 2009;103:282-9
    • 10. Symptoms of Allergic Rhinitis4 major symptoms Repetitive sneezing Itching of eyes, nose, ears, throat Watery rhinorrhea Nasal congestion2 or more of symptoms > than 1 hr for most of days is Allergic Rhinitis Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84.
    • 11. Question no 2  What is likely to be the most troublesome symptom for this patient? 1. Sneezing 2. Runny nose 3. Itchy eyes 4. Nasal congestion
    • 12. Question no 2  What is likely to be the most troublesome symptom for this patient? 1. . 2. Runny nose 3. . 4. Nasal congestion
    • 13. Impact on Quality of life in children  Sleep disorders  88% experience difficulty in sleeping  Learning performance disorders  Behavioral disorders  Attention deficit disorders  Emotional problems  Impairment in activities and social functioning  Decrease cognitive functioning J Allergy Clin Immunol. 2009 Sep;124(3):428-33, Allergy 2008: 63 (Suppl. 86): 8–160; J Allergy Clin Immunol 2009;124:S43-70
    • 14. Comorbid Disorders Eustachian Conjunctivitis Tube Dysfunction Sleep Allergic Nasal Apnea Polyposis Rhinitis Asthma Sinusitis Spector SL. J Allergy Clin Immunol. 1997;99(2 suppl):S773-S780.
    • 15. AR, Sinusitis, Asthma: The link Common Triggers and PathophysiologyAnatomy/ Physiology Same mediators• Upper and lower airways are contiguous • IgE• Functional linkage – nose vs mouth breathing • Histamine• Similar histology(epithelial, neural, vascular) • Cytokines • LeukotrienesSame triggers• HDM, pollen, pet dander, moulds, fungi Same drugs Allergic • Anti IgE ?Same cells Rhinitis • Steroids(ICS/ INS)• Mast cells • Antihistamines ?• Eosinophils • Antileukotrienes ? Asthma Sinusitis J Allergy Clin Immunol 2001;108:S147-336.
    • 16. Most patients with asthma have rhinitis  Approximately 80% of patients with asthma have rhinitis Rhinitis alone Rhinitis + asthma Asthma alone Adapted from The Workshop Expert Panel. Management of Allergic Rhinitis and its Impact on Asthma (ARIA) Pocket Guide. A Pocket Guide for Physicians and Nurses. 2001; Bousquet J and the ARIA Workshop Group J Allergy Clin Immunol 2001;108(5):S147-S334; Sibbald B, Rink E Thorax 1991;46:895-901; Leynaert B et al Am J Respir Crit Care Med 2000;162:1391-1396.
    • 17. Effects of Treatment of Allergic Rhinitison Asthma Rarely does one have a wheeze without a sneeze AR and Asthma are two related conditions linked by 1 common airway Treatment of AR with INS improves both asthma symptoms & PFT. Numerous studies confirm -Successful treatment of AR can improve Asthma symptoms significantly and decrease their impact
    • 18. Physical Examination • Nose  External deformity, nasal polyps, nasal crease • Eyes  Conjunctivitis, allergic shiners • Ears  Abnormalities of tympanic membranes, eustachian tube dysfunction • Mouth  Mouth breathing, malocclusion • Chest  Bilateral and expiratory wheezing • Skin  Eczema, skin dryness Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84.
    • 19. General Appearance Allergic shiners Lower eyelid edema venous stasis  Allergic crease Nose may have a Allergic salute lateral crease Rubbing nose in an upward direction  Allergic gape Dennie’s Lines constant mouth breathing, frequent Creases in lower eyelid (Mueller’s snoring muscle spasm)  Darrier`sline Allergic lashes A horizontal crease Long,silky,full eye lashes above tip of nose
    • 20. Diagnosis of Allergic RhinitisSigns of atopy and recurrent or persistent rhinitis
    • 21. Diagnostic Testing  Skin Testing  SPT rapid (30 minutes) and relatively inexpensive  Antihistamines may interfere  Can’t do for certain skin diseases  Blood testing  No risk to patient  No interference by drugs  Somewhat more expensive per test  Delay in obtaining results
    • 22. Question no 3  What is the first think you recommend for this patient? 1. Drug therapy 2. Allergy shots 3. Environmental control 4. Do nothing, he will get over it.
    • 23. Treatment of Allergic Rhinitis Allergen Avoidance Drug therapy Immunotherapy Patient Education Bousquet J, et al. J Allergy Clin Immunol. 2001;108(suppl):S147- S334.
    • 24. Principles of treatment  Patient education  Environmental control measures [ Identify and avoid the triggers]  Drug therapy [ Immediate & long term treatment ]  Immunotherapy
    • 25. Environmental Control Allergens  Dust mites [ 50%]  Pollens [7.5 %] (Casuarina, Acalypha, Cassia, Ageratum, Salvadora, Ricinus, Albizia lebbeck and Artemisia)  Animal dander [ 5 %]  Mold spores  Cockroach droppings [ 25%] Irritants  Smoke  Fumes: environmental and occupational  Perfumes  Strong odors Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84. Sing AB, Kumar P. Indian Journal of Clinical Biochemistry, 2004, 19 (2) 190-
    • 26. Environmental control measures Irritants :  Smoke Control ETS, fumes from agarbattis,stove, fire wood, cow dung  Fine dust Avoid chalk, sprays, talcs  Strong odors Do not use strong perfumes  Mosquito repellent mats & coils Mosquito nets, long clothing
    • 27. Environmental control measures Allergens :  Dust mite antigen / Cockroach antigen • Wash / Airtight covers to beddings • Remove carpets / upholstery / any clutter • Cotton sheets rather than woolens. • Expose mattresses to sunlight • Wash soft toys, HEPA filters, Vaccum clean • Keep kitchen surfaces clean & dry. Covering food items.
    • 28. Environmental control measures Allergens :  Molds and spores • Attend to damp walls / leakages • Clean air-conditioner filters monthly  Pollen Avoid flowers/perfumes indoors • Stay indoors during harvesting season  Animal dander (pets) If possible avoid • Bathe pets weekly, keep outdoors
    • 29. US Classification of Allergic Rhinitis(AR ) Immunoglobulin E (IgE)-mediated reaction to allergens Seasonal allergic rhinitis (SAR)  Symptoms periodic and correlate with seasonal variations in airborne allergens SAR 20%  Typical allergens: grass, tree, and weed pollens; PAR 40% Ragweed fungal (mold) spores in certain climates Combination of SAR and PAR Perennial allergic rhinitis (PAR) 40%  Symptoms persistent, the result of exposure to perennial environmental allergens  Typical allergens: dust mites, molds, animal Dust mite allergens, certain occupational allergens, pollen prevalent perennially  Patients can have both SAR and PAR Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84.
    • 30. ARIA ClassificationIntermittent Persistent. < 4 days per week . ≥ 4 days per week. or < 4 weeks . and ≥ 4 weeksMild Moderate-severe one or more items normal sleep . abnormal sleep& no impairment of daily . impairment of daily activities, sport, leisure activities, sport, leisure& normal work and . abnormal work and school school . troublesome symptoms& no troublesome symptomsin untreated patients
    • 31. Question no 4 Jagdish has these symptoms each year December through March and August through October. He has milder symptoms year-round When he is sick he is not able to sleep, he misses school and he is miserable What classification of rhinitis does he have now? 1. Mild intermittent 2. Mild persistent 3. Moderate intermittent 4. Moderate persistent
    • 32. Back to the patient Medication History  Jagdish tried a first-generation antihistamine/ decongestant several times for colds, but that made him sleepy.  For that reason, he hasn’t taken any medications yet for his current problem  He has not used any nose sprays and does not like the idea of spraying something into his nose. Family History  Jagdish’s brother and father both have hay fever
    • 33. Question no 5 He now reports having sneezing, runny nose, congested nose, itchy nose and itchy watery eyes. Which drug treatment do you recommend initially? 1. Second generation H1-antihistamine 2. Leukotriene modifier 3. Nasal steroid 4. Oral decongestant
    • 34. Question no 5 He now reports having sneezing, runny nose, congested nose, itchy nose and itchy watery eyes. Which drug treatment do you recommend initially? 1. Second generation H1-antihistamine 2. . 3. . 4. Oral decongestant
    • 35. Medications for allergic rhinitis sneezing rhinorrhea nasal nasal eye obstruction itch symptomsH1-antihistamines oral +++ +++ 0 to + +++ ++ intranasal ++ +++ + ++ 0 intraocular 0 0 0 0 +++Corticosteroids +++ +++ ++ ++ +Chromones intranasal + + + + 0 intraocular 0 0 0 0 ++Decongestants intranasal 0 0 ++ 0 0 oral 0 0 + 0 0Anti-cholinergics 0 +++ 0 0 0Anti-leukotrienes + ++ ++ ? ++
    • 36. Antihistamines First generation  Second generation  Alkylamines  Primary agents  Chlorpheniramine (Avil)  loratadine (Alaspan)  Brompheniramine  terfenadine (Terfed)*  Ethanolamines  astemizole (Stemiz)*  Clemastine (Taviest)  Metabolites  Diphenhydramine (Benadryl)  cetirizine (Zyrtec)  Piperazines  desloratadine (Clarinex)  Hydroxyzine ( Atarax)  fexofenadine (Allegra)  Piperadines  tecastemizole (?)*  Cyproheptadine ( Cypon )  Single Isomer  levocetirizine (Xyzal) *Not available
    • 37. Antihistamines (AHs) 1st line therapy for mild AR (Sneezers) Negligibly effective against Nasal congestion (Blockers) Only new generation H1 antihistamines are recommended 1st gen. antihistamines (though effective) -not recommended Long-term use (12-18 months) with 2nd generation AHs is safe Desloratadine, Fexofenadine & Loratadine are devoid of sedation in objective studies Levocetirizine & Cetirizine are less sedating than 1st generation AHs
    • 38. Antihistamines Age wise dose Cetrizine 6 months to < 2 years 6 –12 mth –2.5 mg OD 12 –23mth –2.5 mg OD or BD 2 to 5 years: 2.5mg OD/ BD or 5 mg OD 6 to 11 years: 5 -10 mg OD > 12 years: 5 or 10 mg OD Levocetrizine 6 months to 5 years: 1.25 mg OD 6 to 11 years: 2.5 mg OD > 12 years: 5 mg OD Fexofenadine 6 months to 2 years: 15 mg BD 2 yrs –11yrs : 30mg BD > 12 years: 60mg BD or 180 mg OD Loratadine 2 to 5 years: 2.5 mg 6 -11yrs : 5 mg OD >12 yrs : 10mg OD Desloratadine 6 to 11 months: 1 mg OD 12 months to 5 years: 1.25 mg OD 6 to 11 years: 2.5 mg OD > 12 years: 5 mg OD
    • 39. Leukotriene Modifiers Montelukast Sodium  Approved for both Allergic Rhinitis & Asthma  Very useful in AR patients with co-morbid or Asthma patients with co-morbid AR  Fixed dose combinations (FDCs) of LTRA + AH widely available -not recommended  Allergic Rhinitis dosing - –6 months to 5 yrs : 4mg OD –6 to 14 yrs : 5mg OD –> 15yrs : 10 mg OD Recommended Minimum for 3 months Clin and Exper All, 2006;36:689–703, Drugs. 2007; 67(18):2717–2726.
    • 40. Leukotriene Modifiers  Interfere with the synthesis or activity of CystLTs  LTRAs are highly specific to CystLT1 receptors  Reduce inflammation following allergen challenge  Decrease mucus production  Effective in controlling symptoms of AR Drugs. 2007; 67(18):2717–2726., Ann Allergy Asthma Immunol. 2006;96:779–786
    • 41. Oral Decongestants  Alpha adrenergic agonists [Ephedrine, Phenylephrine, Phenylpropanolamine]  Cause vasoconstriction and reduce swelling  Relieves nasal obstruction  Rebound congestion  Adverse effects ; Not recommended  Systemic side effects Drugs. 2007; 67(18):2717–2726., Ann Allergy Asthma Immunol. 2006;96:779–786
    • 42. Intranasal Corticosteroids 1st line therapy for moderate-severe AR (Blockers) Effective against all symptoms of AR incl. Congestion, Sneezing, Itching (nasal), Rhinorrhea, & Eye symptoms Most efficacious medication available for Allergic Rhinitis Onset of action -5-7 hours of dosing Maximum efficacy require up to 2 weeks 100% appropriate for nasal blockers Quality of life score improvement with INS better than oral & topical H1 antihistamines Recommended continuously for 3 months Therapy failure is often due to poor compliance or technique 1. Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84. 2. Brunton SA, Fromer LM. South Med J. 2007;100(7):701-708.
    • 43. Nasal corticosteroids Age (years) Drug Good safety data >4 Mometasone Yes Fluticasone Yes >5 Flunisolide - Dexamethasone - >6 Triamcinolone - Beclomethasone - > 12 Budesonide Yes Betamethasone -
    • 44. Intranasal Corticosteroids:Proper Technique for Use • Clear the nose1 • Shake the spray bottle • Tilt head ~30° forward • Use correct axis of insertion – Direct spray away from the septum to minimize risk of septal perforation2 • Fully depress spray nozzle1 • Breath gently • Alternate nostrils with each puff 1. Loh CY, et al. Allergy. 2004;59(11):1168-1172. 2. Brunton SA, Fromer LM. South Med J. 2007;100(7):701-708.
    • 45. Other Drug Treatments• Mast cell stabilizers1  Not as effective as intranasal corticosteroids  Prevent and relieve AR symptoms  Side effects include sneezing, burning• Intranasal anticholinergics [ only > 5 yrs ]  Provide relief from watery nasal discharge not controlled by other medications  Side effects include nasal dryness, bloody nasal discharge 1. Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84. 2. Nathan RA. Ann Allergy Asthma Immunol. 2003;90(2):182-191.
    • 46. Immunotherapy  Desensitization or Specific Immunotherapy  Also called ‘allergy vaccination or shots’ -only therapeutic option that modifies underlying cause of allergy & not just symptoms of allergy  Demonstrated short-term & long-term clinical benefits and sustained effect after treatment completion  Different types of immunotherapy : subcutaneous & Sublingual [ SLIT ] Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 suppl):S1-S84.
    • 47. 2 weeks later Jagdish comes back to your clinic He did well with your initial recommendation of an H- 1 antihistamine Now his symptoms are much worse. What do you recommend? 1. Add a nasal corticosteroid 2. Add a leukotriene receptor blocker 3. Add an oral decongestant 4. Add an oral corticosteroid
    • 48. Treatment of allergic rhinitis (ARIA)Allergic Rhinitis and its Impact on Asthma moderate severe mild persistent moderate persistent severe mild intermittent intermittent intra-nasal steroid local chromone Oral or local non-sedative H1-blocker Leukotriene Receptor Blockers (2007 update) intra-nasal decongestant (<10 days) or oral decongestant allergen and irritant avoidance immunotherapy
    • 49. Conclusions  Allergic Rhinitis is a significant global health condition  It can lead to significant comorbidity and poor quality of life  It often progresses to asthma  Diagnosis includes  History  Physical exam  Allergy testing
    • 50. Conclusions  Treatment includes  Education  Avoidance  Medications  Allergen immunotherapy  No person with Allergic Rhinitis should suffer from their condition
    • 51.  THANK YOU Dr.Vinod Gandhi MD, DNB [Ped] Dhantoli, Nagpur -12 # 09373107243 drgandhi_ngp@rediffmail.com drgandhi8012@gmail.comwww.colourschildrenhospital.com