9 Allergy and Chronic Rhinosinusitis

Traditional perspectives on the pathophysiology of chronic rhinosinusitis (CRS) focus on a cycle of anatomic obstruction, osteomeatal occlusion, stasis of mucosal secretions, and bacterial infection. Recognizing that this paradigm may be overly simplistic, applying only to a segment of patients with CRS, our understanding of the pathogenesis of CRS has evolved in recent years to focus on other chronic inflammatory processes. Although a specific cause effect correlation between allergy and CRS is not established, epidemiologic data do support a relationship between allergic rhinitis and rhinosinusitis.1,2 Further, there has been increasing support for the concept of the “unified airway,” a model of respiratory disease that connects inflammatory disease in the upper and lower airways and regards the entire respiratory tract, from the sinonasal mucosa to the lungs, as an integrated system influenced by both local and systemic inflammatory mediators.³ Krouse et al allege that upper airway inflammatory diseases, such as allergic rhinitis and sinusitis, and lower airway inflammatory disease, such as asthma, often coexist, and physicians should approach these diseases as a spectrum of inflammatory disorders. Studies have shown that interventions directed at one airway disease process often prove beneficial to other airspace inflammatory processes. For example, studies have demonstrated an improvement in asthma control with treatment of allergic rhinitis. Based on this same reasoning, improved control of allergic rhinitis in the patient suffering from CRS may be an important component of the overall treatment strategy.

Mechanisms

Allergic rhinitis is characterized by an immunoglobulin (Ig) E-mediated, type 1 hypersensitivity reaction. When this type 1 hypersensitivity reaction occurs in response to an inhaled antigen, mast cells degranulate and release preformed mediators including histamine, tryptase, and cytokines including interleukin (IL)-5. These cytokines then act as chemoattractants and stimulate migration of other inflammatory mediators including neutrophils, eosinophils, T lymphocytes, and macrophages.⁴ This migration of additional mediators is associated with the late-phase allergic response, occurring hours after initial antigen exposure; this late-phase response is believed to correlate with the more chronic nature of inflammatory disease, as is seen in CRS.

A critical player in this late-phase allergic response is the eosinophil that releases additional tissue-damaging mediators including peroxidases and major basic protein. Eosinophilia is considered central to the allergic response and is a common feature in other airway inflammatory disorders including asthma and many subsets of CRS. In fact, tissue samples of sinus mucosa of adults with CRS have shown high levels of both IL-5 and eosinophils.⁵ High levels of IL-5 and eosinophils are also seen in the polypoid tissue in patients with chronic rhinosinusitis with nasal polyposis (CRSwNP). Although nasal polyposis (NP) is not always associated with atopy, the predominance of IL-5 and eosinophils in polypoid tissue argue for a relationship with mast cell pathophysiology. Many therapies for CRS are now directed at these chronic inflammatory pathways, and allergic disease is regarded as an inflammatory factor that should be considered in the evaluation and management of the patient with CRS.

Allergy Diagnostics

Patient history and physical examination lie at the core of allergy diagnosis. In fact, the vast majority of patients with allergic rhinitis do not require confirmatory diagnostic testing. If a patient is poorly controlled with medical therapy, if a patient desires to implement environmental controls, and/or if a firm diagnosis of allergy will influence treatment including consideration of immunotherapy, then allergy diagnostic testing is reasonable. Options for allergy testing can be classified as either in vivo or ex vivo. The gold standard for allergy testing is in vivo challenge. Typically reserved for experimental situations, select antigens can be administered to the bronchial, nasal, or conjunctival tissues and clinical manifestations are observed.

A more accessible and similarly reliable tissue to test is the skin. The skin harbors tissue mast cells. When these cells are sensitized to a particular antigen, they will degranulate, and the skin will develop a wheal and flare reaction (Fig. 9.1). Such skin tests can be administered via either epicutaneous prick tests or intradermal tests.⁶ It is important to highlight the fact that any in vivo challenge carries a risk of severe, life-threatening allergic reaction and such testing should be performed in a clinical setting prepared to manage anaphylaxis. An alternative to skin testing is the in vitro testing modality of allergen-specific serum IgE testing. All in vitro testing modalities are premised on measurement and quantification of antigen-specific IgE in the patient’s serum. In vitro testing has been shown to correlate well with skin testing and offers a safety advantage with no risk of anaphylaxis. An in-depth discussion regarding the selection and application of allergy testing techniques is beyond the scope of this chapter.

Figure 9.1 Skin prick testing. Figure shows typical skin responses to prick testing. The white arrow shows a negative prick test. The black arrowhead shows the whealing response associated with a positive skin test. The black arrow shows the erythema (flare) associated with skin testing.

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