Systemic corticosteroids have been found efficacious in the management of both rhinitis and asthma, but as a result of its side effect profile, systemic corticosteroid therapy is only used in severe refractory cases. They can be given in cases of rhinitis medicamentosa to provide some relief while discontinuing decongestants.

Oral antihistamines have proven to be efficacious in controlling symptoms of sneezing, itching, rhinorrhea, and ocular symptoms, while not having much affect on nasal congestion [95]. They function by inhibiting the release of preformed mediators from mast cells and basophils, as well as inhibiting the expression of cell adhesion molecules, recruitment and survival of eosinophils, and downregulation of transcription factors that are responsible for the production of pro-inflammatory cytokines and adhesion proteins [95–99]. Older H₁ antihistamines are referred to as first-generation antihistamines and are known for having more pronounced sedative and anticholinergic side effects, when compared to the newer second-generation antihistamines [95] (see Table 10.2).

Second-generation antihistamines are lipophobic and are recognized by P-glycoprotein efflux pump expressed on the luminal surface of the vascular endothelial cells, making for poor central nervous system penetration as compared to the first-generation antihistamines and subsequently less sedative side effects [95, 99]. In light of the decreased anticholinergic properties of the second-generation antihistamines, they are not as efficacious in the treatment of rhinorrhea [100]. Some H₁ antihistamines may cause QT prolongation, and in fact, astemizole and terfenadine have been taken off the market due to the risk of torsade de pointes [95, 101]. Antihistamines have proven efficacious in controlling the nasal and ocular symptoms of AR as well as aiding in asthma control [102]. The onset of action is between 1 and 3 h and the duration of action is at least 24 h.

H₁ antihistamines come in the form of a nasal spray and an ophthalmic solution as well. In light of the difference in the pharmacokinetics, these drugs are dosed twice a day as opposed to once daily. Nasal antihistamines such as azelastine significantly reduce rhinorrhea, but do have sedative properties.

Anticholinergic medications, such as ipratropium bromide, have been shown efficacious in the management of rhinorrhea but have no effect on nasal congestion or sneezing. They work by blocking the muscarinic receptors of the nasal seromucinous glands, effectively decreasing glandular secretion [83, 103].

Chromones such as nedocromil are mast cell stabilizers with anti-inflammatory properties [83, 103]. Although chromones have been shown to improve symptoms in AR, studies comparing chromones to intranasal steroids have shown superior symptom control with intranasal steroids, and they are therefore not as commonly used [104, 105].

Decongestant is a broad term that refers to either oral or nasal medications that act on adrenergic receptors located on the precapillary and postcapillary blood vessels of the nasal mucosa with resultant vasoconstriction. This results in decreased blood flow and has been shown to significantly decrease nasal airway resistance (NAR) and significantly increase in peak nasal inspiratory flow (PNIF) [83, 106, 107]. They have a relatively quick onset of action. Decongestants when used in combination with nasal steroids or antihistamines have been shown to improve symptom control when compared with either treatment modality alone [108, 109]. Importantly, use of topical nasal decongestants are not recommended beyond 7–10 days as it may lead to rebound swelling of the nasal mucosa and worsening of nasal congestion, referred to as rhinitis medicamentosa. Decongestants should be avoided in children less than 1 year of age, elderly, and pregnancy. They should be avoided in hypertensive patients, patients with cardiac conditions, hyperthyroidism, prostate hypertrophy, glaucoma, and psychiatric disorders, and in patients on beta-blocker or MAO inhibitor [83].

Leukotrienes are inflammatory mediators formed from the breakdown of arachidonic acid by mast cells, basophils, eosinophils, monocytes/macrophages, dendritic cells, and T lymphocytes [110]. Cysteinyl leukotrienes (CysLTs) refer to LTC₄, LTD₄, and LTE₄. Inhibitors of the 5-lipoxygenase pathways such as zileuton block the production of CysLTs, and leukotriene receptor antagonist, montelukast and zafirlukast, block the end organ effects of CysLTs. CysLTs have been shown to increase vascular permeability and nasal mucosal blood flow and significantly increase NAR [111, 112]. Montelukast has proven to be effective in the treatment of both nasal and ocular symptoms with comparable results to antihistamines [113]. When used in combination, montelukast and antihistamines have been shown to provide better symptom control than either used independently [114].

Omalizumab is a monoclonal anti-IgE antibody, which binds free circulating IgE. This reduces the amount of IgE available to bind to high affinity receptors on mast cells and therefore leads to a decrease in degranulation and the release of the preformed mediators responsible for the symptoms of AR [115]. Omalizumab has been shown to be efficacious in both the treatment of AR and allergic asthma, resulting in improvements in AR and asthma symptoms, as well as a decreased number of asthma exacerbations [116]. Omalizumab when used in combination with subcutaneous immunotherapy (SCIT) has shown to decrease the risk of anaphylaxis fivefold, allowing for a more rapid and higher regimen of immunotherapy to safely be administered and therefore decreased duration of treatment [117].

Immunotherapy is the only treatment modality that has been shown to alter the natural course of AR. In cases of severe persistent AR, not adequately controlled by pharmacologic means, or in patients with adverse reactions to allergy medications, allergen-specific immunotherapy may be indicated. Immunotherapy results in the production of allergen-specific T-regulatory cells. This suppresses the T-cell response to allergen and is referred to as T-cell tolerance [118, 119]. The Th2 polarized immune response is suppressed [120]. Allergen-specific IgG molecules are produced with a subsequent decrease in IgE. In addition, there is a decrease in the number of mast cells, basophils, and eosinophils [118].

Immunotherapy can be performed through subcutaneous injection and sublingual application. Treatment with subcutaneous immunotherapy requires repeat injections of allergen extract in an office or hospital setting. It has been estimated that there is a 0.1 % chance of developing a systemic reaction [46]. The risk is not insignificant, and immunotherapy should be administered by experienced personnel and in a properly equipped setting. Therapy lasts an average of 3–5 years and is marked by an initial “buildup phase” in which increasing doses of allergen are administered, followed by a “maintenance phase” [83].

Sublingual immunotherapy has been shown to be an effective and safe treatment option [121]. Unlike injection therapy only, the initial dose of sublingual immunotherapy needs to be administered in the office. The side effects are generally confined to gastrointestinal symptoms and respiratory symptoms such as wheezing.

Both SCIT and sublingual immunotherapy (SLIT) have shown to significantly improve symptoms, quality of life scores, and medication scores in multiple studies [122–126]. These improvements are sustained after therapy is discontinued. Durham et al. [126] performed a randomized, double-blind, placebo-controlled trial in which he was able to demonstrate that patients who had received 3–4 years of immunotherapy for grass pollen allergy had persistent improvements in symptoms and a decreased use of medications for 3 years after cessation of the immunotherapy. Use of immunotherapy in patients with AR may prevent the development of asthma. In a randomized controlled trial by Moller et al. [15], the use of immunotherapy to birch and/or timothy pollen in children with AR was shown to significantly prevent the development of asthma at 3 years.

Allergic rhinitis is one of the most common chronic diseases worldwide. While it is not a life-threatening condition, its impact on quality of life is substantial. AR is comorbid with a variety of other disease processes and is not only associated with but is a risk factor for the development of asthma [6–10]. Many treatment options exist and should be tailored to the individual. It has been shown that early and aggressive therapy of rhinitis may be preventative in development of asthma.