Nasal Polyps

Nasal polyps are benign growths of the sinus lining — soft, pale, grape-like masses that develop when the mucosa of the nose and sinuses becomes chronically inflamed and begins to prolapse into the nasal cavity. They are not tumours, not infections, and not dangerous in the sense of being malignant. What they are is persistent. Left untreated, they grow, block the nose, destroy the sense of smell, and in patients with comorbid asthma, make the lower airway harder to control as well.

The understanding of what drives nasal polyps has changed substantially over the past decade. For many years, the cause was described in clinical literature as “unknown.” This is no longer an accurate statement. The inflammatory biology is now well characterised — nasal polyps are the product of a type 2 eosinophilic inflammatory process driven by specific cytokines, the same cytokines that underlie severe asthma and atopic dermatitis. That biological understanding has led directly to a new class of treatments — monoclonal antibodies targeting these pathways — two of which are now PBS-listed in Australia and have meaningfully changed the management of severe, recurrent polyp disease.

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1. Definition and Terminology

The clinical syndrome of bilateral nasal polyps arising in the context of chronic sinonasal inflammation is formally designated chronic rhinosinusitis with nasal polyps (CRSwNP). This term distinguishes polyp-associated disease from chronic rhinosinusitis without nasal polyps (CRSsNP), which follows a different inflammatory course and has different treatment implications. The EPOS 2020 (European Position Paper on Rhinosinusitis and Nasal Polyps) criteria define chronic rhinosinusitis as sinonasal inflammation persisting for 12 weeks or more, characterised by two or more of: nasal blockage or congestion, nasal discharge, facial pain or pressure, and reduction or loss of smell — with objective confirmation on endoscopy or CT imaging.

The term eosinophilic CRS (eCRS) has been proposed as a more inclusive designation, capturing patients in whom type 2 eosinophilic inflammation is present regardless of whether visible polyps have yet formed. Histologically, eCRS is defined by the presence of more than 10 eosinophils per high-power field (HPF) on tissue examination, or more than 20% eosinophils in the total inflammatory cell count. In clinical practice, a threshold of 27% eosinophils in tissue has been found to predict polyp recurrence after surgery with 96.7% sensitivity and 92.5% specificity.

Unilateral polyps, antrochoanal polyps (arising from the maxillary sinus in children and young adults), and polyps associated with specific conditions such as cystic fibrosis, primary ciliary dyskinesia, or inverted papilloma are distinct clinical entities and are addressed separately in the classification section below.

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2. Epidemiology

Chronic rhinosinusitis affects roughly 10–12% of the global population by self-report — though physician-diagnosed CRS is closer to 2–4% of adults, which reflects the large number of people who put up with blocked noses and poor sleep for years before seeking assessment. Of those with CRS, approximately 25–30% have nasal polyps. That puts CRSwNP prevalence at around 1–4% of the adult population in Western countries — a surprisingly large number for a condition that most people have barely heard of.

CRSwNP is more prevalent in men than in women by a ratio of approximately 1.5:1. Prevalence increases with age, peaking in the sixth to eighth decades of life. The average age at diagnosis is approximately 42 years, indicating that polyp disease is typically a lifelong condition requiring decades of specialist management. Higher prevalence is recorded in urban compared with rural populations, consistent with the environmental contributions to type 2 inflammatory disease.

Comorbidity patterns are clinically important. Asthma is present in approximately 30–48% of CRSwNP patients. Aspirin-exacerbated respiratory disease (AERD, or Samter’s triad) occurs in up to 26% of patients with both CRSwNP and asthma. Among patients undergoing endoscopic sinus surgery for CRS, AERD prevalence has been reported as high as 33% in some series. Allergic rhinitis coexists in a proportion of patients, though the relationship between allergy and polyp formation is weak — most patients with allergic rhinitis do not develop polyps, and many polyp patients are non-atopic.

In Asian populations, CRSwNP was historically characterised by a predominantly neutrophilic rather than eosinophilic inflammatory infiltrate — a fundamentally different endotype. Over the past two decades, however, a marked shift toward eosinophilic disease has been documented across multiple Asian countries, with prevalence of eosinophilic nasal polyps in South Korean series increasing from 24% to 51% over a 17-year period. Similar trends have been observed in Japan, China, and Thailand, and are thought to reflect the adoption of a Western lifestyle and its associated environmental exposures.

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3. Pathophysiology

The pathophysiology of eosinophilic CRSwNP centres on a self-amplifying type 2 inflammatory loop initiated at the level of the sinonasal epithelium and sustained by a cascade of cytokine-driven cellular interactions. The process can be understood in three phases: epithelial barrier disruption, innate immune activation, and adaptive immune amplification.

Epithelial Barrier Dysfunction

The sinonasal epithelium functions as the primary structural and immunological barrier between the external environment and the mucosal immune system. In CRSwNP, this barrier is compromised by a combination of genetic predisposition, environmental exposures, and the downstream effects of type 2 cytokines themselves. IL-4 and IL-13 drive epithelial-to-mesenchymal transition (EMT), in which epithelial cells lose structural integrity and transform into migratory mesenchymal-like cells — directly worsening barrier function and contributing to the persistence of inflammation. Impaired mucociliary clearance, resulting from ciliary damage and goblet cell hyperplasia, further compromises the epithelium’s capacity to clear pathogens and allergens, facilitating biofilm formation and chronic microbial colonisation.

Innate Immune Activation — Alarmins and ILC2s

When the damaged sinonasal epithelium is exposed to environmental triggers — including allergens, pollutants, microorganisms, and proteases — it releases a family of innate cytokines known as alarmins: IL-25 (also called IL-17E), IL-33, and thymic stromal lymphopoietin (TSLP). These alarmins activate innate lymphoid cells type 2 (ILC2s) — a population of innate immune effector cells residing in sinonasal mucosa that are present in 100-fold higher concentrations in nasal polyp tissue than in healthy controls. Activated ILC2s rapidly produce large quantities of IL-4, IL-5, and IL-13, initiating the type 2 inflammatory cascade without requiring prior antigen sensitisation. This alarmin-ILC2 axis represents the innate arm of polyp inflammation and helps explain why CRSwNP can develop in the absence of demonstrable allergy.

Adaptive Immune Amplification — Th2 Cytokines and Eosinophilia

The innate cytokine environment created by activated ILC2s promotes polarisation of naive T cells toward the Th2 phenotype, establishing the adaptive arm of inflammation. The resulting Th2/ILC2 synergy creates a self-amplifying cytokine loop in which IL-4, IL-5, and IL-13 are produced in escalating quantities:

• IL-4 and IL-13 activate the shared IL-4Rα/STAT6 signalling pathway, inducing IgE production by B cells, promoting goblet cell hyperplasia (with consequent mucus hypersecretion), causing ciliary dysfunction, and driving epithelial barrier deterioration — perpetuating the cycle of damage.
• IL-5 is the principal regulator of eosinophil biology: it drives eosinophil maturation in the bone marrow, directs their migration to inflamed tissue, and prolongs their survival at the inflammatory site. Elevated tissue and serum IL-5 levels correlate positively with CRSwNP recurrence after surgery.
• IL-13 upregulates MUC5AC gene expression in goblet cells, driving mucus plug formation and activating fibroblasts — contributing to the oedematous, fibrotic stroma characteristic of established polyp tissue.
• IgE, produced under IL-4/IL-13 drive, mediates local sensitisation of mast cells and basophils, amplifying inflammatory mediator release and sustaining tissue eosinophilia.

The accumulated eosinophils within polyp tissue are not passive bystanders — they are active inflammatory effectors. On activation, eosinophils degranulate, releasing major basic protein, eosinophil cationic protein (ECP), eosinophil peroxidase, and eosinophil-derived neurotoxin. These granule proteins are directly cytotoxic to the epithelium, perpetuating the barrier disruption that initiated the cascade. Eosinophils also produce cysteinyl leukotrienes, prostaglandins, and reactive oxygen species, contributing to the oedema and remodelling that give polyp tissue its characteristic macroscopic appearance.

The result is a structural transformation of the sinus mucosa: an oedematous, eosinophil-infiltrated stroma with a thickened basement membrane, goblet cell hyperplasia, subepithelial fibrosis, and — in established disease — visible polyp formation as the swollen mucosa herniates through the sinus ostia into the nasal cavity.

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4. Classification and Endotypes

Classification of nasal polyps has evolved from simple phenotypic description (polyps present or absent) toward mechanistic endotyping based on the predominant inflammatory pathway. This shift has clinical implications because endotype determines prognosis, recurrence risk, and the most appropriate biological therapy.

Endotyping in clinical practice is informed by tissue histology from surgery, blood eosinophil count, total serum IgE, specific IgE to mould allergens, CT imaging characteristics, and the clinical history — particularly NSAID sensitivity, asthma, and atopy.

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5. Clinical Features

The symptoms of CRSwNP arise from two mechanisms: mechanical obstruction of the nasal passages and sinuses by the polyp tissue itself, and the functional consequences of the chronic mucosal inflammation. Symptom severity does not always correlate with polyp size — small polyps involving the olfactory cleft can produce complete anosmia, while large polyps predominantly obstructing the nasal floor may preserve smell.

Quality of life impairment in CRSwNP is comparable to that seen in moderate-to-severe asthma and congestive heart failure in validated disease burden studies. The SNOT-22 (Sino-Nasal Outcome Test) questionnaire is the standard patient-reported outcome measure used to quantify symptom burden and track treatment response in clinical practice.

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6. Diagnosis

Nasal Endoscopy

The cornerstone of diagnosis. A rigid endoscope (typically 0° or 30°, 4mm diameter) is passed through the nostril under topical anaesthesia as an outpatient procedure. Nasal polyps appear as smooth, pale, semi-translucent, grape-like masses arising most commonly from the middle meatus — the region lateral to the middle turbinate through which the anterior ethmoid sinuses, maxillary sinus, and frontal sinus drain. The endoscopic nasal polyp score (NPS) grades each side 0–4 based on polyp extent, giving a total bilateral score of 0–8. A score of ≥4/8 in the context of persistent symptoms is the threshold for defining severe CRSwNP eligible for advanced treatment including biological therapy.

CT Imaging

CT of the paranasal sinuses (fine-cut coronal reconstruction) is performed in all patients being considered for surgery or biological therapy. CT provides the surgical roadmap — identifying the distribution of disease, anatomical variants that affect surgical approach, the relationship of the sinuses to critical structures (orbit, optic nerve, internal carotid artery, skull base), and the extent of mucosal thickening and polyp burden. The Lund-Mackay CT scoring system quantifies disease extent across six sinus groups bilaterally on a 0–2 scale, with a maximum score of 24. CT scanning should be performed at baseline when the patient is clinically stable, not during an acute infective exacerbation.

CT findings that should prompt further investigation include unilateral disease, bony erosion or expansion, intracranial or orbital extension, and atypical-density mucin — any of which may indicate AFRS, inverted papilloma, or sinonasal malignancy rather than simple inflammatory polyposis.

Histopathology

Tissue submitted from endoscopic sinus surgery is examined histologically to confirm the inflammatory endotype. Eosinophilic CRSwNP is defined by tissue eosinophilia >10/HPF or >20% of inflammatory cells. The histological report guides biological therapy selection, prognosis, and the intensity of post-operative medical management.

Blood Tests

Peripheral blood eosinophil count and total serum IgE are obtained when biological therapy is being considered. Blood eosinophilia ≥250 cells/μL and total IgE >100 IU/mL are supporting criteria for type 2 inflammation and contribute to PBS biological therapy eligibility assessment. Specific IgE to mould allergens (Alternaria, Aspergillus, Cladosporium) is relevant when AFRS is suspected. Sweat chloride testing or CFTR gene mutation analysis is indicated when cystic fibrosis is a diagnostic consideration.

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7. Medical Treatment

Medical management is first-line treatment for CRSwNP and continues indefinitely after surgery. The goal is to suppress the underlying type 2 inflammatory process, reduce polyp burden, relieve symptoms, and minimise the frequency and severity of acute exacerbations.

Intranasal Corticosteroids (INCS)

The foundation of medical management. Topical corticosteroids — fluticasone furoate, mometasone furoate, budesonide — suppress local mucosal inflammation with minimal systemic absorption. Standard nasal sprays are effective for mild-to-moderate disease. High-volume budesonide nasal rinse — dissolving budesonide respules (0.5mg/2mL) into a 240mL saline rinse — delivers corticosteroid directly to the sinus mucosa through surgically opened drainage pathways and is the preferred topical corticosteroid delivery method post-operatively. Penetration to the ethmoid sinuses with standard sprays is limited by intact anatomical barriers; after FESS, topical delivery improves dramatically. Consistent long-term use is required — INCS are not a short-course treatment.

Saline Nasal Irrigation

High-volume isotonic or hypertonic saline irrigation (240mL, using a squeeze bottle such as NeilMed Sinus Rinse or a neti pot) improves mucociliary clearance, physically removes mucus crusts and inflammatory debris, reduces mucosal oedema, and importantly, improves the distribution and penetration of subsequently applied topical corticosteroids. It is an inexpensive, safe, and highly effective adjunct that should be performed consistently — typically once or twice daily. When used as a vehicle for budesonide (see above), the saline rinse becomes a drug delivery system rather than merely a mechanical flush.

Oral Corticosteroids (OCS)

Short courses of systemic prednisolone produce rapid and dramatic polyp shrinkage and symptom relief — anosmia in particular often recovers within days of starting oral steroids. A typical course is prednisolone 40–50mg daily for 5–7 days. OCS are valuable for pre-operative polyp debulking (improving surgical conditions and reducing intraoperative bleeding), as rescue treatment during acute exacerbations, and as a diagnostic tool to confirm steroid-responsive disease. They are not appropriate for long-term continuous use due to systemic effects including adrenal suppression, bone density reduction, glycaemic disturbance, and cataract formation. Cumulative OCS exposure exceeding 500mg prednisolone equivalent per 12 months is a PBS eligibility criterion for biological therapy in Australia.

Leukotriene Receptor Antagonists

Montelukast and related agents block the CysLT1 receptor, reducing the pro-inflammatory effect of cysteinyl leukotrienes on the sinonasal mucosa. Evidence of benefit in CRSwNP is modest, and their primary role is as an adjunct in patients with AERD, where dysregulated leukotriene production is a central pathophysiological mechanism. In patients with both CRSwNP and asthma, leukotriene antagonists may provide incremental benefit to both conditions.

Antibiotics

Antibiotics are appropriate for acute bacterial exacerbations of CRS superimposed on established polyp disease, guided by symptom characteristics (purulent discharge, facial pain, fever). Long-term prophylactic low-dose macrolide therapy (azithromycin, roxithromycin) has immunomodulatory properties independent of antimicrobial activity — reducing neutrophil-driven inflammation and biofilm formation — and may be considered in patients with recurrent acute infective episodes or in non-eosinophilic CRSwNP where type 2-targeted therapies are less appropriate.

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8. Biological Therapies

Biological therapies — monoclonal antibodies targeting specific cytokines or their receptors in the type 2 inflammatory cascade — represent the most significant advance in the management of severe CRSwNP in the past decade. Three biologics have TGA registration for CRSwNP in Australia, two of which are currently PBS-listed.

Dupilumab in Detail

Dupilumab is the most thoroughly studied and, based on current evidence, most efficacious biological therapy for CRSwNP. The phase 3 SINUS-24 and SINUS-52 trials demonstrated significant reductions in nasal polyp score, nasal congestion, and requirement for systemic steroids and rescue surgery compared with placebo. Biomarker analysis confirms that dupilumab reduces concentrations of type 2 inflammatory mediators including eotaxin-3, periostin, ECP, and IL-5 in nasal secretions, and total IgE in blood. Notably, dupilumab produces rapid improvement in sense of smell — an effect that appears to occur through mechanisms beyond simple airflow improvement, consistent with the direct roles of IL-4 and IL-13 on olfactory receptor function demonstrated in preclinical studies.

The EVEREST trial (2025) — the first head-to-head comparison of dupilumab and omalizumab in patients with severe CRSwNP and coexisting asthma — found dupilumab superior on all primary and secondary efficacy endpoints at 24 weeks, including nasal polyp score, smell (UPSIT), nasal congestion, and quality of life. Dupilumab also addresses comorbid asthma and atopic dermatitis in patients with these coexisting type 2 inflammatory conditions.

PBS Eligibility in Australia

In Australia, dupilumab is PBS-listed for CRSwNP in adults. To qualify, patients must generally have documented bilateral nasal polyps, persistent symptoms despite adequate topical corticosteroid use, and either prior sinus surgery or a documented contraindication to surgery, along with evidence of type 2 inflammation (elevated blood eosinophils, total IgE, or tissue eosinophilia). Cumulative OCS exposure and quality of life impairment also contribute to eligibility assessment. The specific restriction criteria are set by the Pharmaceutical Benefits Advisory Committee (PBAC) and can be confirmed at consultation.

Mepolizumab has been PBS-listed for adults (≥18 years) with severe, eosinophilic CRSwNP that is recurrent post-surgery since 1 April 2023 — the first PBS-listed monoclonal antibody for this indication in Australia. Phase 3 trial data showed patients treated with mepolizumab were 57% less likely to require further surgery compared with controls.

Prescribing of PBS biological therapies for CRSwNP requires authority approval and must be initiated by a relevant specialist (otolaryngologist, respiratory physician, or clinical immunologist/allergist). Dr Roth’s practice can initiate applications for eligible patients.

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9. Surgical Treatment — Functional Endoscopic Sinus Surgery (FESS)

Surgery is indicated when polyp burden is causing significant mechanical obstruction or sinus blockage despite optimised medical management, when recurrent acute infective exacerbations are occurring, or when medical therapy (including a course of oral steroids) has not produced adequate symptom control. The decision is made on clinical grounds and is not determined solely by polyp size or CT score.

Goals and Principles

The surgical goal is not cure — it is surgical optimisation of the sinonasal anatomy to facilitate effective ongoing medical management. By removing the polyp bulk and opening the natural sinus drainage pathways (particularly the ethmoids, maxillary ostia, frontal recess, and sphenoid), FESS creates an environment in which topical corticosteroids, saline irrigation, and — where used — biological therapies can reach the sinus mucosa directly rather than being blocked by obstructing tissue. The inflammatory tendency that drives polyp regrowth is not removed by surgery; without post-operative medical management, recurrence is the rule.

Technique

FESS is performed entirely through the nostrils under general anaesthesia — there are no external incisions and no skin scars. Rigid endoscopes (typically 0° and 30°) provide illuminated, magnified visualisation of the sinus anatomy. Powered microdebrider instruments remove polyp tissue with precision while preserving healthy mucosa. Image-guided navigation — a CT-based intraoperative tracking system that maps instrument position to a pre-operative CT in real time — is used for complex revision cases, high-risk anatomy (proximity to orbit or skull base), and bilateral pan-sinusitis to improve safety and completeness of dissection.

The extent of surgery is individualised based on CT distribution: limited anterior ethmoidectomy with middle meatal antrostomy for restricted disease, through to complete bilateral dissection including sphenoidotomy, frontal sinusotomy, and total ethmoidectomy for pan-sinusitis with extensive polyp burden. Dr Roth completed his fellowship training in advanced rhinology and endoscopic sinus surgery at the Midwest Sinus Center at Rush University Medical Center in Chicago under Professor Bruce Tan, and performs more than 300 nasal and sinus procedures per year.

Medicare and Private Health Insurance

FESS for CRSwNP is a functional surgical procedure and attracts Medicare rebates under the relevant MBS item numbers for endoscopic sinus surgery. This is distinct from cosmetic surgery. Private health insurance may contribute to hospital and anaesthetist fees depending on your level of cover. A full itemised estimate with applicable MBS item numbers is provided at consultation.

Recovery

FESS for nasal polyps is performed as a same-day or overnight procedure. Post-operative management typically includes: 48–72 hours of rest with head elevation; commencement of saline nasal rinse on day 2–3 post-operatively; commencement of budesonide nasal rinse at 2–4 weeks; avoidance of nose-blowing for 2 weeks; and a return to light work within 1–2 weeks. Nasal crusting, altered smell (often temporarily worse before improving), and mild epistaxis are expected in the first 2–4 weeks. Endoscopic review is arranged at 2–3 weeks to remove crusting and assess healing.

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10. Recurrence and Long-Term Management

Recurrence is the defining clinical challenge of CRSwNP. In the absence of ongoing medical management, polyps recur in the majority of patients after surgery — approximately 40% of patients report polyp recurrence within 18 months of FESS, and 80% have inadequately controlled symptoms within 3–5 years. In the GA2LEN European database, 59% of patients who had undergone surgery subsequently required revision surgery, with nearly 23% experiencing four or more revision procedures.

Recurrence risk is stratified by endotype. Eosinophilic CRSwNP — and particularly AERD — carries the highest recurrence risk. Tissue eosinophilia >27% of inflammatory cells predicts recurrence with 96.7% sensitivity. Comorbid asthma, bilateral pan-sinusitis on CT, and high NPS at the time of surgery are additional risk factors.

The objective of long-term management is to maintain the post-operative surgical anatomy — keeping the sinuses open, the mucosa healthy, and the eosinophilic inflammatory burden suppressed — through a combination of:

• Budesonide nasal rinse (ongoing, at least once daily) — the most effective topical anti-inflammatory measure available post-operatively
• Regular endoscopic surveillance — typically at 3, 6, and 12 months post-operatively, then annually — to identify and treat early recurrence before it becomes symptomatic or requires revision surgery
• Biological therapy in eligible patients — dupilumab and mepolizumab substantially reduce recurrence rates and the requirement for further surgery
• Allergen immunotherapy where relevant sensitisation is identified and allergy is a contributing factor
• NSAID avoidance in patients with AERD, with aspirin desensitisation considered in appropriate candidates

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11. AERD — Aspirin-Exacerbated Respiratory Disease (Samter’s Triad)

AERD, also known as Samter’s triad or Widal’s triad, is a distinct and severe clinical phenotype defined by the co-occurrence of CRSwNP, asthma, and hypersensitivity to aspirin and other NSAIDs that inhibit the cyclooxygenase-1 (COX-1) enzyme. The triad was first described by Widal, Abrami, and Lermoyez in 1922 and further characterised by immunologist Max Samter in 1968.

AERD affects approximately 0.3–2.5% of the general population, rising to approximately 7% of asthmatic adults, 15% of those with severe asthma, and up to 40% of those with both asthma and nasal polyps. Among patients undergoing sinus surgery for CRS, AERD has been identified in up to 33% of cases, suggesting significant under-diagnosis in the community.

The pathophysiology of AERD involves a constitutive dysregulation of the arachidonic acid metabolic pathway. COX-1 inhibition by aspirin or NSAIDs reduces prostaglandin E2 (PGE2) production. In healthy individuals, PGE2 provides a tonic inhibitory signal that limits mast cell degranulation and leukotriene production. In AERD patients, baseline PGE2 levels are already reduced, and COX-1 inhibition removes this inhibitory brake — triggering a massive surge in cysteinyl leukotriene release from mast cells and eosinophils. The result is bronchoconstriction, rhinorrhoea, nasal congestion, and in severe cases, urticaria and angio-oedema, typically within 30–180 minutes of NSAID ingestion.

AERD-associated nasal polyps are characteristically more extensive, more rapidly recurrent after surgery, and more refractory to conventional medical management than non-AERD CRSwNP. Management includes strict NSAID avoidance (substituting paracetamol or COX-2-selective inhibitors where analgesia is required), leukotriene receptor antagonists, and biological therapy — dupilumab and mepolizumab have both shown efficacy in AERD patients. Aspirin desensitisation, performed under careful medical supervision by an allergist, can reduce the hyperresponsiveness to aspirin and may improve asthma and sinonasal symptoms in selected patients, and is particularly relevant when aspirin is needed for cardiovascular disease.

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12. Relationship to Asthma — The United Airway Concept

CRSwNP and asthma are not independent diseases that happen to coexist — they are anatomically separated manifestations of the same underlying systemic type 2 eosinophilic inflammatory process, a concept captured in the united airway model. The correlation between sinonasal and lower airway inflammatory profiles in biopsy studies is statistically significant, and the extent of CT sinus disease correlates with lower airway eosinophilia and exhaled nitric oxide levels in patients with coexisting asthma.

Clinically, this relationship has several important implications:

• Patients with CRSwNP and asthma have more severe sinonasal disease, worse quality of life, higher polyp recurrence rates, and are more difficult to treat both medically and surgically than polyp patients without asthma
• Asthma in the context of nasal polyposis is harder to control, more prone to exacerbations, and more likely to be characterised by fixed airflow obstruction
• Effective treatment of CRSwNP — through surgery, topical steroids, and biological therapy — can produce measurable improvement in lower airway control and asthma exacerbation frequency
• Biological therapies that target the shared type 2 pathway (particularly dupilumab) address both conditions simultaneously, offering a compelling advantage in patients with the combined phenotype

This systemic view of type 2 airway disease also extends to atopic dermatitis, eosinophilic oesophagitis, and chronic otitis media with effusion — conditions that share the same IL-4/IL-13-driven inflammatory pathway and may coexist in the same patient. Dupilumab has TGA approval for multiple type 2 inflammatory conditions and, in eligible patients, may address several simultaneously.

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13. Frequently Asked Questions

Common questions about nasal polyps answered by Dr Jason Roth, fellowship-trained rhinologist and Specialist Otolaryngologist, Sydney.

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