The effect of CPAP on the nasal airway is relatively unexplored

Future Directions

The effect of CPAP

Several theories have tried to explain the relationship between SDB and nasal obstruction. Of these, the following theories are most credible: (1) the switch from nasal to oronasal breathing (due to nasal obstruction) causes loss of nasal airflow resulting in decreased nasal receptor-derived stimulation of ventilation and changes in phasic activity leading to decreased upper airway patency; and (2) the increased nasal airway resistance (due to nasal obstruction) generates an increased negative inspiratory force/pressure causing turbulence in the relaxed soft tissues and upper airway collapse (retropharyngeal) resulting in upper airway obstruction and SDB.

These hypotheses are based on a few studies that have used varying methods and small numbers of study subjects and therefore require further confirmation. If this is found to be true, technologies and treatments aimed at facilitation of nasal breathing should be explored further in the context of SDB. In the interim, use of topical nasal steroids in patients with SDB and preferential use of nasal CPAP in treatment may be reasonable.

Longitudinal studies in children with nasal obstruction are required to determine the risk factors for SDB, including the relationship of nasal obstruction to structural abnormalities of the face and upper airway. It is possible that certain congenital variations in facial structures are deleterious to nasal breathing and exacerbated by nasal obstruction from other causes. Knowledge of these factors could be useful in preventing the development of SDB.

The effect of CPAP on the nasal airway is relatively unexplored. Anecdotally, it appears that CPAP may increase nasal inflammation and, in some, promote vasomotor rhinitis. It is possible this may lead to decreased adherence to treatment. This is another area in need of further research.


Hemopoietic Processes as Targets of Therapy

While intranasal steroids can improve lower airway hyperresponsiveness, a greater benefit is seen in patients with both allergic rhinitis and asthma if topical steroids are delivered to both sites of inflam-mation. Of less remarkable but still significant clinical benefit, working through a different pathway, montelukast, a specific leukotriene receptor antagonist (LTRA), has been shown to reduce allergic rhinitis and asthma symptoms. Cysteinyl leuko-trienes (CysLTs) are potent receptor agonist mediators capable of inducing cell recruitment and bronchospasm, increased vascular permeability, and nasal airway resistance. Hemopoietic Processes as Targets of Therapy

Table 1—Effects of Several Antiallergic Treatment Options on Hemopoietic Processes and Eosinophils

Treatment Sputum






Antihistamine Uncertain Reduce/no effect Reduce
LTRA Reduce Reduce Reduce
Topical steroid Reduce Reduce Reduce
Systemic steroid Reduce Reduce Uncertain

Montelukast antagonizes these effects and thus attenuates the allergen-induced early and late asthmatic responses. It also reduces sputum eosinophilia following allergen challenge. Since CysLT receptors are expressed on hemopoietic progenitors, antagonism with montelukast may attenuate tissue eosinophilia via a systemic antiinflammatory effect (see below).

Hemopoietic Processes as Targets of Therapy

Modulation of Eosinophil Differentiation by CS

Hemopoietic mechanisms can be targeted by antiallergic therapies (Table 1). For example, topical treatment with CS can affect the hemopoietic response by abrogation of cytokine production by airways tissues, reduction in peripheral blood Eo/B progenitors, and decreases in BM myeloid progenitors (in a canine asthma model). Most likely, inhaled CS in these models exert their effects on the marrow progenitor response indirectly by interfering with cytokines elaborated from the inflamed tissue, which can then act systemically on the BM. However, a direct effect on progenitors cannot be excluded because there is evidence that, both in vitro and in vivo, low systemic levels of CS (10~9 mol/L) can block differentiation of the Eo/B progenitor in humans and of the myeloid progenitor in dogs.