Allergic rhinitis, which affects between 10-40% of the global population and up to 40% of children in the USA (Liu et al., 2010), is a common disabling inflammatory disease of the nasal airways characterized by typical nasal symptoms such as itching, sneezing, rhinorrhoea and airway constriction (Kim et al., 2010).
Extant research has found nasal constriction to be the most dominant symptom resulting from allergic inflammation, and is indeed deemed as a critical symptom in patients presenting with allergic rhinitis (Hellings & Fokkens, 2006; Liu et al., 2010).
In the case scenario, the 4-year old patient has been diagnosed with IgE mediated allergic rhinitis, implying that the infection has an immunologic basis since IgE stands for immunoglobulin E (Burns, 2012; Hellings & Fokkens, 2006).
Recent mechanistic studies have shown that the symptoms of allergic rhinitis “…result as a consequence of allergen-induced release and/or synthesis of a variety of pro-inflammatory mediators (including histamine, cytokines, arachidonic acid metabolites, chemokines, adhesion molecules, etc) from a variety of inflammatory cells (particularly mast cells, eosinophils and T-lymphocytes)” (Liu et al., 2010 p. 1150).
Following from this juxtaposition of facts, the family needs to know that the patient may be having a hereditary condition known as Atopy, which is characterized by excessive production of antibody immunoglobulin E (IgE) in response to specific allergens (e.g., house dust, mite droppings, animal dander and certain types of pollen) that are undisruptive to most individuals (Hellings & Fokkens, 2006; Liu et al., 2010).
In terms of effect, extant literature demonstrates that once IgE is released it circulates around the body and binds itself to specific receptors such as nasal mast cells, leading to symptoms associated with asthma or allergic rhinitis (Burns, 2012).
This view is reinforced by Liu et al (2010), who argue that the production of high levels of allergen-specific IgE in certain individuals adversely interacts with inflammatory cells found in the respiratory and upper airways, particularly the nasal mast cell and eosinophils, leading to symptoms associated with asthma and allergic rhinitis.
The production of IgE is positively correlated to exposure of the mentioned allergens. The development of symptoms in patients with mild or persistent allergic rhinitis follows a similar pattern. The first step is the sensitization of the individual when nasal mast cells, eosinophils and other inflammatory cells found in the respiratory and upper airways become coated with IgE.
On re-exposure the mast cells and other cells release inflammatory mediators such as histamine, cytokines, arachidonic acid metabolites and chemokines (Burns, 2012). These mediators are responsible for the symptoms relevant to the affected organ, including sneezing, mucus production, itching and nasal constriction in allergic rhinitis, and coughing, chest tightness, wheezing and dyspnoea in asthma (Hellings & Fokkens, 2006).
The family needs to have the information regarding the management of allergic rhinitis. Extant literature demonstrates that “…reducing inflammation is a crucial aspect of managing these conditions, which explains the importance of corticosteroids in the treatment of patients with asthma and allergic rhinitis” (Burns, 2012, p. 43).
Many treatment and management guidelines recommend allergen avoidance to prevent allergic rhinitis, but this is not a comprehensive treatment strategy because the condition is triggered by many different allergens and it may be difficult to identify the specific causative agent.
The main pharmacological interventions for allergic rhinitis, according to recent evidence, include: nasal decongestants, antihistamines (topical or systematic), intranasal corticosteroids, leukotriene receptor antagonists, and specialized immunotherapy (Burns, 2012; Kim et al., 2010; Liu et al., 2010).
References
Burns, D. (2012). Management of patients with asthma and allergic rhinitis. Nursing Standard, 26(32), 41-46.
Hellings, P.W., & Fokkens, W.J. (2006). Allergic rhinitis and its impact on otorhinolaryngology. Allergy, 61(6), 656-664.
Kim, T.H., Lee, J.Y., Lee, H.M., Lee, S.H., Cho, W.S., Ju, H…Lee, S.H. (2010). Remodeling of nasal mucosa in mild and severe persistent allergic rhinitis with special reference to the distribution of collagen, proteoglycans, and lymphatic vessels. Clinical & Experimental Allergy, 40(12), 1742-1754.
Liu, F., Zhang, J., Liu, Y., Zhang, N., Holtappels, G., Lin, P., & Bachert, C. (2010). Inflammatory profiles in nasal mucosa of patients with persistent vs. intermittent allergic rhinitis. Allergy, 65(9), 1149-1157.