Nasal Polyps: Pathogenesis and Treatment Implications

Clinical presentation and diagnosis

When discussing trends in clinical presentation, the diversity of patients with NPs must always be respected, and broad generalizations should be avoided. Nevertheless, trends in clinical complaints have been shown when comparing patients with CRS with polyps with those without evidence of polyps. Patients with NPs are more likely to complain of a constellation of symptoms, including diminished olfaction, headache, and postnasal drip.³ In addition, symptoms are more likely to be described as

Imaging for Nasal Polyps

It is undeniable that computed tomographic (CT) imaging has become an essential tool for the diagnosis and surgical management of sinusitis. Classically, CT scans of sinuses in patients with NP are described as possessing polypoid masses associated with partial or complete opacification of paranasal sinuses with infundibulum widening.⁸ With respect to its use as a diagnostic tool, CT imaging's major weakness lies in its inability to differentiate polyps from mucous and other soft tissue masses.

Chronic Rhinosinusitis and Nasal Polyp

The largest proportion of patients with NP has a diagnosis of CRS. CRS affects about 30 million Americans, imparting an annual medical cost of $2.4 billion. Societal effects are further compounded by sick days, lost work hours, and other indirect costs.⁹ To standardize a formerly amorphous clinical diagnosis, CRS criteria have been set forth. A diagnosis of CRS requires a symptom duration longer than 12 weeks with 2 of the following symptoms: facial pain/pressure, hyposmia/anosmia, nasal

Pathogenesis

In attempting to understand pathogenesis in nasal polyposis, it must be remembered that this subject represents a topic in flux. To date, there exists no delineated pathway that can clearly explain the journey from insult to tissue change. The current understanding is instead limited to comprehending and elucidating differing inflammatory promoters and pathways. Much as in the mastery of any sport, it is essential to understand the roles of the key players before tackling overall strategy. It

Eosinophilic and noneosinophilic nasal polyposis

It has been well accepted that not all patients with CRS that form NPs demonstrate T_H2 eosinophilic-dominant pathology.27, 28 New emphasis on noneosinophilic nasal polyposis has emerged primarily from Asian research groups. It is notable that 80% of Western patients with CRSwNP demonstrate tissue eosinophilia compared with less than 35% of Korean patients.²⁹ To examine the possible differences in Western and Eastern nasal polyposis, Zhang and colleagues³⁰ compared Chinese patients with CRSwNP

Staphylococcus aureus enterotoxin

S aureus enterotoxin (SAE) has been suggested as a possible instigating and/or modifying factor in nasal polyposis. As in other superantigen reactions, SAE acts to nonspecifically activate T cells by binding the major histocompatibility II complex.³² The unregulated upregulation results in an increase of T_H2-biased proinflammatory cytokine levels.³³ This outcome is enhanced by S aureus colonization, with 60% of patients with CRSwNP demonstrating colonization compared with 33% in controls.³⁴ The

Aspirin-Exacerbated Respiratory Disease

A small portion of patients with NPs and CRS are classified as having AERD, also known as Samter triad or aspirin triad. These patients present with the classic Samter triad with aspirin sensitivity, polyposis, and asthma. An additional near-universal feature of these patients is hyperplastic eosinophilic sinusitis.³⁶ The increased tissue eosinophilia, infiltrating mast cells producing histamine, and increased levels of cysteinyl leukotrienes secondary to overexpression of leukotriene C₄

Cystic Fibrosis

CF is a rare autosomal recessive genetic disorder affecting approximately 1 in every 2500 people. All patients with CF develop chronic sinusitis, but of these patients, 7% to 48% demonstrate NPs (CF-NP).⁴⁰ CF-NP stands out from other NP groups by way of its obvious phenotype and diagnosis. Defects of ciliary clearance in these patients create an environment in which bacterial colonization, particularly with Pseudomonas aeruginosa, is a virtual constant.⁴¹ The resultant neutrophilic response to

Summary points: Nasal Polyps

• 1.

  CRS is the most common cause for NPs, but not all NPs are created equally.

• 2.

  Patients with asthma and CRS represent clinical examples of the unified airway. As such, these patients benefit from treatment aimed at control of T_H2-driven eosinophilic inflammation.

• 3.

  NPs are not a uniquely T_H2-driven process. Recent research has demonstrated a clear pathogenic role for T_H1- and T_H17-driven processes.

• 4.

  Future research in understanding the development of NPs will dictate the proper medical management of NPs.