FIGURE 14–1. Multiple factors contributing to the pathogenesis of CRS.

• It is unclear whether bacteria cause CRS due to a classic infectious process versus an inflammatory process.

Allergy

• Theorized that allergies result in inflammation that can eventually progress to CRS

• Higher incidence exists of developing both acute and chronic rhinosinusitis in patients with a diagnosis of allergic rhinitis although direct causal link is unclear.

• Incidence of allergies in patients with CRSwNP approximates that of the general population.

• Allergies can exacerbate sinonasal symptoms in patients with CRS.

Immunology

• Increased risk of infection in patients with compromised immune system

• 8% to 63% prevalence of immunodeficiency in patients with refractory sinusitis

• Immune function evaluation should be considered in patients with recurrent and severe sinus infections who have failed aggressive medical management, especially if they have a history of pulmonary infections and/or a family history of primary immunodeficiencies.

• Primary immunodeficiencies (PIDs)

1. Intrinsic defect in the host immune system that increases host susceptibility to bacterial infection (B cell deficiency), intracellular pathogens/opportunistic infections/fungi (T cell dysfunction), sinopulmonary infections and autoimmune disorders (complement deficiencies), and abscess formation (phagocytic disorders)

– Disorders of the adaptive immune system include antibody deficiencies (congenital agammaglobulinemia, selective IgA deficiency, IgG subclass deficiencies), T cell disorders (severe combined immunodeficiency), and combined B and T cell disorders (common variable immunodeficiency)

– Disorders of the innate immune system include complement deficiencies and phagocytic disorders

• Secondary immunodeficiencies

Host Genetics

• Evidence of familial patterns and cases of concordant disease in monozygotic twins suggest a genetic basis of CRS.

• Family history of CRS more common in patients with CRSwNP.

1. Correlation between a positive family history of nasal polyps and the severity of sinonasal disease in the affected patient

• Association with asthma and allergic rhinitis infer genetic predisposition.

• Multiple single nuclear polymorphisms associated with inflammatory mediators that increase the risk of CRS have been found in CRS patients.

• Genetic alterations that result in loss of the T2R38 bitter taste receptor function are associated with increased rates of gram-negative related CRSsNP.

1. Bitter taste receptors identify quorum-sensing molecules secreted by gram-negative bacteria and contribute to innate immune function.

• CRS is associated with genetic syndromes.

1. Kartagener syndrome/primary ciliary dyskinesia (PCD)

– Impaired ciliary motility results in decreased mucus clearance and recurrent upper and lower airway infections.

– Multiple genes for dynein arms and microtubule binding have been identified in PCD; mutations in these genes are likely responsible for the almost 100% rate of CRS in patients with PCD.

2. Cystic fibrosis (CF)

– Thickened secretions result in decreased mucociliary clearance, infection, and inflammation.

– Viscous mucus may also cause a local hypoxia that could be associated with biofilm formation.

– Higher prevalence of CRS is found in CF mutation gene carriers than those who are not carriers of the gene.

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