Epidemiologic relationships

The relationship between allergic rhinitis and asthma has been appreciated for many years. It is known that, among patients diagnosed with allergic rhinitis, the likelihood of developing asthma during a 20-year period is 3 times greater among allergic individuals than in their nonallergic counterparts. In addition, about one-third of patients with rhinitis have concurrent asthma at the time of their rhinitis diagnosis, whereas more than 80% of patients with asthma have active rhinitis, either allergic or nonallergic. Furthermore, the presence of rhinitis not only predicts the concurrence of clinically significant asthma but also is associated with the degree of bronchial hyperreactivity among patients not yet diagnosed with asthma. There seems to be an ongoing persistent inflammation in patients with allergic rhinitis and asthma, even in the absence of currently active disease.

In addition, there is a consistent relationship noted among patients with asthma and those with chronic rhinosinusitis (CRS). Although the prevalence of asthma in the general community is estimated at about 7%, among patients with CRS, the prevalence increases to about 20%. The prevalence continues to increase to 42% among patients with CRS undergoing sinus surgery, and, among patients with CRS with polyps and those with asthma, to a prevalence of more than 50%. Successful medical and surgical treatment of CRS is associated with improvement in patient symptoms and quality of life, as well as improved level of asthma control. Not only is surgery thought to improve nasal respiration among patients with CRS, but to decrease the load of immunoactive tissue, with subsequent reduction in propagation of inflammation to the lower airways.

Pathophysiologic mechanisms and clinical airway disease

Pathophysiologic mechanisms that are involved in rhinitis, CRS, and asthma are similar and interrelated. Two areas are important to consider among patients being considered for rhinoplasty surgery:

• 1.
  

  Impairment in nasal respiration

  
  
• 2.
  

  Shared inflammation.

Sufficient nasal respiration is thought to be vital physiologically in sustaining maximal pulmonary function, especially among patients with bronchial hyperreactivity and asthma. In a classic study, when patients with asthma were allowed to breathe either with their noses obstructed or open, obstruction of the nose was associated with a decline in pulmonary function and worsening bronchospasm when these patients increased their exercise activity. Nasal obstruction inhibits the conditioning of inspired air by the nasal turbinates, and seems to contribute to lower respiratory symptoms and the development of asthma. With the increase in ventilatory rate during exercise, greater volumes of cold dry air with higher amounts of particulate matter are delivered to the lungs; interference with nasal breathing, as with nasal obstruction, inhibit the nose’s ability to filter and condition inspired air, contributing to lower airway inflammation and bronchospasm.

The effect of nasal obstruction on the mechanics of breathing and lower airway resistance was extensively studied by Ogura and colleagues in the 1960s, who noted that total nasal obstruction increases pulmonary resistance, and postulated a reflex mechanism controlling bronchial smooth muscle physiology. This effect of nasal obstruction on increased pulmonary resistance and bronchoconstriction has also been noted with the use of packs placed during nasal surgery. There is increased risk for these effects on pulmonary physiology among patients with asthma, who have decreased pulmonary reserve, increased bronchial hyperreactivity, and increased epithelial inflammation.

In addition to the adverse effects of nasal obstruction on lower airway mechanics and function, there is a prominent role for shared inflammatory processes across both the upper and lower respiratory systems. The inflammatory cascade in the airway is initiated in allergic patients with deposition of allergen on the mucosa, usually first in the nose. Both early-phase and late-phase responses are then initiated in susceptible individuals. Allergic responses involve the degranulation of mast cells on cross-linking of adjacent immunoglobulin-E (IgE) molecules, resulting in the release of histamine and other inflammatory mediators into the local tissues. Other stimulatory and regulatory responses are also initiated, including the recruitment of T-helper 2 (Th2) cells, as well as late-phase mediators, especially eosinophils, proinflammatory cytokines, and leukotrienes, sustaining the allergic response and promoting persistent inflammation.

In addition to the inflammatory changes seen in allergic disease, common pathophysiologic mechanisms are noted in both CRS and asthma. In each of these diseases, as well as in allergic rhinitis, the primary effector cell is the eosinophil. In both CRS and asthma, progressive inflammatory changes occur in the epithelium over time, involving elements of basement membrane thickening, goblet cell hyperplasia, cellular infiltration, and mucus hypersecretion. The coexistence of asthma and CRS seems to be associated with worse pathophysiologic mucosal changes in both the sinuses and the lungs than is seen with either disease alone. Although remodeling is seen in both patients with CRS and those with asthma, the degree of remodeling seems to be less in the nose than in the lung. However, the generalized presence of inflammatory mediators throughout the respiratory tract shows that communication occurs between portions of the respiratory system on both a cellular and a mediator level.

The interactive effects of nasal inflammation and lower airway physiology have been shown clinically in several studies. Several articles have shown that direct nasal antigen or irritant challenge can result in a significant increase in bronchial hyperreactivity. In addition, the severity of asthma symptoms worsens directly with increasing rhinitis, supporting the role of nasal inflammation in exacerbating lower airway disease. Furthermore, treatment of allergic rhinitis with topical intranasal corticosteroids is associated with decrease in asthma symptoms and improvement in objective indices of pulmonary function. In addition, both medical and surgical management of CRS have been shown to decrease asthma symptoms and to decrease inflammatory mediators in the lower airway.

In addition to direct effects with medical and surgical management, treatment of allergic rhinitis with subcutaneous immunotherapy has been shown to not only improve rhinitis symptoms, but to also downregulate systemic inflammatory mediators and reduce asthma symptoms. Because concurrent disease in both the upper and lower airways is common, immunomodulatory therapy can promote system-wide beneficial effects, not only in the reduction of rhinitis symptoms but in the improvement of asthma symptoms and asthma control.

An evaluation of these various clinical studies confirms the close association of the upper and lower airway in health and disease. Shared inflammatory processes are at the core of this respiratory interdependence, and factors that increase symptoms in one portion of the airway generally result in increased disease throughout the airway. Direct influences on the nasal airway, including nasal congestion and nasal obstruction, can further exacerbate these symptoms, contributing to not only nasal disease but to worsening asthma symptoms as well.

Pathophysiologic mechanisms and clinical airway disease

Pathophysiologic mechanisms that are involved in rhinitis, CRS, and asthma are similar and interrelated. Two areas are important to consider among patients being considered for rhinoplasty surgery:

• 1.
  

  Impairment in nasal respiration

  
  
• 2.
  

  Shared inflammation.

Sufficient nasal respiration is thought to be vital physiologically in sustaining maximal pulmonary function, especially among patients with bronchial hyperreactivity and asthma. In a classic study, when patients with asthma were allowed to breathe either with their noses obstructed or open, obstruction of the nose was associated with a decline in pulmonary function and worsening bronchospasm when these patients increased their exercise activity. Nasal obstruction inhibits the conditioning of inspired air by the nasal turbinates, and seems to contribute to lower respiratory symptoms and the development of asthma. With the increase in ventilatory rate during exercise, greater volumes of cold dry air with higher amounts of particulate matter are delivered to the lungs; interference with nasal breathing, as with nasal obstruction, inhibit the nose’s ability to filter and condition inspired air, contributing to lower airway inflammation and bronchospasm.

The effect of nasal obstruction on the mechanics of breathing and lower airway resistance was extensively studied by Ogura and colleagues in the 1960s, who noted that total nasal obstruction increases pulmonary resistance, and postulated a reflex mechanism controlling bronchial smooth muscle physiology. This effect of nasal obstruction on increased pulmonary resistance and bronchoconstriction has also been noted with the use of packs placed during nasal surgery. There is increased risk for these effects on pulmonary physiology among patients with asthma, who have decreased pulmonary reserve, increased bronchial hyperreactivity, and increased epithelial inflammation.

In addition to the adverse effects of nasal obstruction on lower airway mechanics and function, there is a prominent role for shared inflammatory processes across both the upper and lower respiratory systems. The inflammatory cascade in the airway is initiated in allergic patients with deposition of allergen on the mucosa, usually first in the nose. Both early-phase and late-phase responses are then initiated in susceptible individuals. Allergic responses involve the degranulation of mast cells on cross-linking of adjacent immunoglobulin-E (IgE) molecules, resulting in the release of histamine and other inflammatory mediators into the local tissues. Other stimulatory and regulatory responses are also initiated, including the recruitment of T-helper 2 (Th2) cells, as well as late-phase mediators, especially eosinophils, proinflammatory cytokines, and leukotrienes, sustaining the allergic response and promoting persistent inflammation.

In addition to the inflammatory changes seen in allergic disease, common pathophysiologic mechanisms are noted in both CRS and asthma. In each of these diseases, as well as in allergic rhinitis, the primary effector cell is the eosinophil. In both CRS and asthma, progressive inflammatory changes occur in the epithelium over time, involving elements of basement membrane thickening, goblet cell hyperplasia, cellular infiltration, and mucus hypersecretion. The coexistence of asthma and CRS seems to be associated with worse pathophysiologic mucosal changes in both the sinuses and the lungs than is seen with either disease alone. Although remodeling is seen in both patients with CRS and those with asthma, the degree of remodeling seems to be less in the nose than in the lung. However, the generalized presence of inflammatory mediators throughout the respiratory tract shows that communication occurs between portions of the respiratory system on both a cellular and a mediator level.

The interactive effects of nasal inflammation and lower airway physiology have been shown clinically in several studies. Several articles have shown that direct nasal antigen or irritant challenge can result in a significant increase in bronchial hyperreactivity. In addition, the severity of asthma symptoms worsens directly with increasing rhinitis, supporting the role of nasal inflammation in exacerbating lower airway disease. Furthermore, treatment of allergic rhinitis with topical intranasal corticosteroids is associated with decrease in asthma symptoms and improvement in objective indices of pulmonary function. In addition, both medical and surgical management of CRS have been shown to decrease asthma symptoms and to decrease inflammatory mediators in the lower airway.

In addition to direct effects with medical and surgical management, treatment of allergic rhinitis with subcutaneous immunotherapy has been shown to not only improve rhinitis symptoms, but to also downregulate systemic inflammatory mediators and reduce asthma symptoms. Because concurrent disease in both the upper and lower airways is common, immunomodulatory therapy can promote system-wide beneficial effects, not only in the reduction of rhinitis symptoms but in the improvement of asthma symptoms and asthma control.

An evaluation of these various clinical studies confirms the close association of the upper and lower airway in health and disease. Shared inflammatory processes are at the core of this respiratory interdependence, and factors that increase symptoms in one portion of the airway generally result in increased disease throughout the airway. Direct influences on the nasal airway, including nasal congestion and nasal obstruction, can further exacerbate these symptoms, contributing to not only nasal disease but to worsening asthma symptoms as well.