2016 Section 5 Green Book

Stachler

by many inciting events, such as exercise, allergen or irritant exposure, change in weather, or viral respiratory infection. The symptoms and airflow limitation can resolve and re- spond to medications, or may be very subtle and not be noticed for some time. Episodic flare-ups can occur, which can be life threatening. Asthma is associated with airway hyperresponsiveness to direct or indirect stimuli. In some cases, a complex process is initiated involving inflamma- tory mediators, eosinophils, mast cells, T lymphocytes, neu- trophils, and epithelial cells. Chronicity of the condition, if it occurs, leads to advanced disease and airway remodeling. This may lead to irreversible pulmonary mucosal changes. These changes, inflammation with ensuing airway obstruc- tion, can result in the classic symptoms of wheezing, chest tightness, coughing, and breathlessness. 8 Clinicians need to focus primarily on the inflammatory component of the dis- ease to prevent the chronic changes that can occur, while treating the reversible increased bronchial reactivity. Un- controlled asthma or suboptimal management may result in the chronic changes the clinician is trying to avoid. Asthma has been noted to be closely related to AR. Corren, 9 in 1997, reviewed this relationship and found that 78% of asthmatics have nasal symptoms. Thirty-eight percent (38%) of patients with rhinitis (AR and non-AR) will have asthma. His data also suggests that rhinitis often precedes the development of asthma. Other authors 10,11 have shown a 3-fold increase in asthma over a 20-year period in allergic patients when compared to nonallergic controls. Guerra et al.’s study 10 also showed that patients with higher serum immunoglobulin E (IgE) levels at the onset of the study had a 5-fold increase in their risk of developing asthma. Shaaban et al., 12 in a longitudinal population-based study noted that the presence of AR increases the relative risk for asthma to 3.53 (95% confidence interval [CI], 2.11 to 5.91). The relative risk for asthma in patients with non- AR was 2.71 (95% CI, 1.64 to 4.46). AR clearly is often discovered concurrently with asthma, and predisposes one to develop asthma over time. Asthmatic Nordic children with AR had a higher risk of hospital readmissions and more hospital days per year com- pared to asthmatic patients without rhinitis. 13 Nasal symp- toms have been associated with asthma. Patients with nasal complaints (congestion, itching, and rhinorrhea), should be carefully evaluated for asthma. Bronchial hyperactivity has been demonstrated in patients with AR who were unaware of their pulmonary condition. 14,15 Clinicians, otolaryngol- ogists, pulmonologists, and primary care physicians need to consider asthma on a more regular basis when evaluating patients with severe nasal complaints. AR has been shown to worsen the overall prognosis of asthma. 16 Those who have asthma and AR have more se- vere lower respiratory disease and account for more costs Relationships between asthma and upper airway disease

TABLE 1. Similar histopathologic findings in CRS and asthma

Mucosal edema Vasodilation Cellular (eosinophil and lymphocyte) infiltration Major basic protein deposition Thickening of the basement membrane Hyperplasia of the goblet cells Mucous gland hypertrophy Angiogenesis

Collagen deposition Epithelial damage Subepithelial fibrosis CRS = chronic rhinosinusitis.

to the healthcare system. Tight control of the AR leads to improved asthma control and vice versa. 16–18 Chronic rhinosinusitis, histopathologically, appears simi- lar to asthma. 19 The nasal mucosa remodels and thickens in a similar manner seen with chronic changes in the bronchial mucosa. Under the microscope the findings are nearly indis- tinguishable (Fig. 1). Remodeling is due to mucosal edema, submucosal gland and bronchial smooth muscle hypertro- phy, collagen deposition, basement membrane thickening, and subepithelial fibrosis in the lamina reticularis (Table 1). The only finding that is different is the mucosal thickening is not as noted in the nose in rhinitis as it is in the bronchial airway in asthma patients. Nasal polyposis is associated with rhinitis and asthma. It is one of the diagnostic criteria for allergic fungal rhinosinusitis. 20 Aspirin-sensitive respiratory disease is an- other condition with a strong association of polyps, rhinos- inusitis, and asthma. It occurs when one has an allergy to aspirin or other nonsteroidal anti-inflammatory agents. As- pirin ingestion leads to an intense inflammatory response of the upper and lower airways, exacerbations of rhinosinusi- tis, and asthma (Samter’s triad). 21 Awad et al. 22 reported that aspirin-intolerant asthmatics had statistically superior asthma outcomes with endoscopic sinus surgery for chronic rhinosinusitis compared to aspirin-tolerant sinus surgery patients. Chronic rhinosinusitis patients with asthma have a higher rhinosinusitis severity score (Lund-Mackay score) than nonasthmatic patients and more nasal polyps regardless of atopic status, indicative of a strong relationship between chronic rhinosinusitis severity and chronic airway inflam- matory diseases, asthma, and nasal polyps. 23 Asthmatic pa- tients with coexistent symptomatic chronic sinusitis have greater asthmatic severities requiring more aggressive man- agement to gain control of the condition. 24–31 Both medical and surgical treatment of chronic rhinosinusitis has been

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