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Nasal polyp

Nasal polyps are benign, noncancerous growths that form as soft, teardrop- or grape-like swellings on the lining of the nasal passages or sinuses, typically resulting from chronic inflammation of the sinonasal mucosa.^[1] They are most commonly associated with chronic rhinosinusitis (CRS), affecting approximately 2-4% of the general population, though up to 25-30% of CRS patients develop them, with higher prevalence among adults aged 40-60 and a male predominance (about 62%).^[2] These growths can be unilateral or bilateral, often linked to type 2 inflammatory pathways involving eosinophils, and are exacerbated by factors such as allergies, asthma, aspirin sensitivity, cystic fibrosis, or recurrent infections.^[3]^[2] Small nasal polyps may cause no symptoms and go unnoticed, but larger ones can obstruct nasal airflow, leading to common complaints including persistent nasal congestion, runny nose, postnasal drip, reduced or lost sense of smell (hyposmia or anosmia), facial pressure or pain, snoring, and headaches.^[1]^[4] In severe cases, they may contribute to complications like worsened asthma control, sleep disturbances, or secondary infections, and unilateral polyps warrant evaluation to exclude rare malignancies.^[2] Diagnosis typically involves a clinical history, nasal endoscopy to visualize the grayish, movable masses, and imaging such as CT scans to assess extent and rule out other conditions.^[4]^[5] Treatment focuses on reducing inflammation and managing underlying causes, starting with intranasal corticosteroid sprays, saline irrigations, or short courses of oral corticosteroids to shrink polyps; antihistamines or antibiotics may address allergic or infectious triggers.^[3] For refractory cases, biologic therapies like dupilumab (targeting IL-4 and IL-13 pathways), omalizumab, mepolizumab, or the recently approved tezepelumab (as of October 2025) or endoscopic sinus surgery (e.g., polypectomy or functional endoscopic sinus surgery) can provide relief, though recurrence rates are high, often exceeding 50% within years without ongoing management.^[2]^[5]^[6] Preventive strategies include avoiding allergens, maintaining nasal hygiene, and treating comorbidities like asthma to minimize regrowth and improve quality of life.^[3]

Overview

Definition

Nasal polyps are benign, inflammatory, and hyperplastic outgrowths of the sinonasal mucosa, characterized by their soft, painless, and noncancerous nature.^[2] They most commonly arise in the context of chronic rhinosinusitis (CRS), particularly chronic rhinosinusitis with nasal polyposis (CRSwNP), a condition involving persistent inflammation of the nasal passages and sinuses lasting more than 12 weeks.^[2]^[7] In CRSwNP, these growths develop due to ongoing mucosal irritation and swelling, affecting approximately 25% to 30% of patients with chronic rhinosinusitis.^[2] Anatomically, nasal polyps primarily originate in the nasal cavity or paranasal sinuses, often presenting as bilateral and multiple lesions.^[2] Antrochoanal polyps emerge from the maxillary sinus and extend into the nasal cavity, typically unilaterally, while ethmoidal polyps arise from the ethmoid sinuses and protrude into the nasal cavity through the middle meatus or sphenoethmoid recess.^[2] These locations contribute to their role in obstructing nasal airflow, though they remain confined to the sinonasal region without invading surrounding tissues.^[1] Visually, nasal polyps exhibit a grape-like or pedunculated appearance, forming as soft, edematous projections from the inflamed mucosa that may appear as teardrop-shaped or hanging grape clusters.^[7]^[8] They are often described as smooth, mobile, grey, and semi-translucent masses, reflecting the underlying edematous and hyperplastic changes in the sinonasal lining.^[2]

Types

Nasal polyps are primarily classified into two main types based on their anatomical origin and clinical presentation: antrochoanal polyps and ethmoidal polyps.^[2] Antrochoanal polyps are solitary, unilateral lesions that originate from the mucosa of the maxillary sinus, extending through the ostium into the nasal cavity and often reaching the choana.^[9] They are more prevalent in children and young adults, typically presenting with nasal obstruction on one side.^[2] In contrast, ethmoidal polyps are multiple and bilateral, arising from the ethmoid sinuses and protruding into the nasal cavity through the middle meatus; they are characteristically associated with chronic rhinosinusitis with nasal polyposis (CRSwNP) in adults.^[2] These polyps often lead to more extensive bilateral symptoms compared to the unilateral nature of antrochoanal types.^[2] Other less common variants include sphenochoanal polyps, which rarely originate from the sphenoid sinus and extend to the choana.^[2] Additionally, certain conditions such as inverted papilloma can mimic nasal polyps due to their polypoid appearance and location in the sinonasal tract, though they represent a distinct neoplastic entity requiring differentiation.^[10]

Clinical presentation

Symptoms

Nasal polyps most commonly manifest as nasal obstruction or congestion, which affects a significant majority of patients and frequently leads to chronic mouth breathing due to impaired airflow through the nasal passages.^[1]^[3]^[5] Another primary symptom is anosmia or hyposmia, characterized by a reduced or complete loss of the sense of smell, which often accompanies a diminished sense of taste as smell plays a key role in flavor perception.^[1]^[2]^[5] Secondary symptoms include rhinorrhea, typically involving thick nasal discharge, and postnasal drip, where mucus accumulates in the throat, potentially causing irritation.^[1]^[2] Patients may also experience facial pressure or pain, headache, snoring due to obstructed breathing, and sleep disturbances such as fragmented sleep or increased risk of sleep apnea.^[5]^[3]^[1]^[11] These symptoms can substantially impair quality of life, with anosmia leading to reduced appetite and altered eating habits, as well as emotional effects like frustration from diminished sensory enjoyment.^[12]^[13]^[14] In untreated cases, symptoms are typically chronic, persisting for more than 12 weeks, and may progressively worsen, exacerbating nasal blockage and associated discomfort over time.^[5]^[15]^[3]

Signs

Nasal endoscopy typically reveals pale, edematous, polypoid masses originating in the middle meatus, often appearing as bilateral, mobile, smooth, grey, and semi-translucent growths that obstruct the nasal passages.^[2]^[16] These findings confirm the presence of polyps and their extent, distinguishing them from other nasal pathologies during clinical examination.^[17] Anterior rhinoscopy may demonstrate bilateral pale swellings within the nasal cavity, accompanied by mucoid secretions, while coexisting septal deviation can further exacerbate obstruction by narrowing the nasal airways.^[18]^[16] Observable associated signs include chronic mouth breathing due to nasal obstruction and a nasal quality to the voice from altered resonance, particularly in prolonged cases.^[2] In severe pediatric instances, extensive polyposis can lead to facial deformity characterized by broadening of the nasal bridge and increased intercanthal distance, known as "frog face."^[19] These signs often correlate with patient-reported symptoms such as nasal congestion.^[20] The Lund-Kennedy endoscopic scoring system assesses polyp size and extent during examination, grading polyps from 0 (absent) to 2 (extending beyond the middle meatus), alongside edema and discharge, to quantify disease severity.^[21]^[22]

Causes and risk factors

Etiology

Nasal polyps primarily develop as a consequence of chronic inflammation stemming from recurrent rhinosinusitis, a condition characterized by persistent mucosal swelling and edema in the sinonasal cavities. This inflammatory process disrupts normal tissue architecture, leading to the outgrowth of benign, pedunculated lesions that protrude into the nasal passages.^[2] Key initiating factors include an impaired epithelial barrier in the sinonasal mucosa, which reduces mucociliary clearance and increases permeability to environmental antigens and microbes, thereby perpetuating immune activation. Microbial dysbiosis further drives this pathology, with an imbalance in the nasal microbiome—often involving overcolonization by opportunistic pathogens—exacerbating barrier dysfunction and inflammatory cascades.^[20] Genetic predispositions contribute in specific subsets, notably mutations in the CFTR gene underlying cystic fibrosis, which impair chloride transport and mucociliary function, leading to viscous secretions that foster polyp formation; such mutations are implicated in approximately 20% of pediatric cases of chronic rhinosinusitis with nasal polyps associated with systemic genetic disorders.^[23] Environmental triggers such as asthma and allergic rhinitis heighten susceptibility by amplifying type 2 inflammatory responses in the airways, while aspirin-exacerbated respiratory disease (AERD, or Samter's triad) uniquely combines aspirin sensitivity with nasal polyposis and asthma to intensify mucosal inflammation.^[1] Infectious elements, particularly bacterial biofilms produced by Staphylococcus aureus, play a critical role by shielding bacteria from host defenses and antibiotics, while S. aureus-derived superantigens stimulate excessive T-cell activation and eosinophil recruitment, promoting the chronic inflammation essential for polyp persistence. Recent case reports and studies as of 2025 also suggest that viral infections, such as SARS-CoV-2 (COVID-19), may contribute to polyp development by triggering Th2-skewed immune responses in susceptible individuals.^[24]^[25]

Associated conditions

Nasal polyps are frequently comorbid with respiratory conditions, particularly asthma and chronic obstructive pulmonary disease (COPD). Asthma co-occurs in 20-60% of patients with chronic rhinosinusitis with nasal polyps (CRSwNP), contributing to a multifactorial disease burden that affects airway management.^[26] Similarly, the presence of nasal polyps is associated with an elevated prevalence of COPD, often complicating lower airway function in affected individuals.^[27] Allergic and immune disorders also show strong links to nasal polyps. Aspirin-exacerbated respiratory disease (AERD), characterized by sensitivity to aspirin and nonsteroidal anti-inflammatory drugs alongside asthma and nasal polyps, affects approximately 10% of patients with CRSwNP.^[28] Eosinophilic granulomatosis with polyangiitis (EGPA), a systemic vasculitis, commonly presents with nasal polyps as an early manifestation, occurring in a significant proportion of cases and highlighting shared eosinophilic inflammation pathways.^[29] Genetic and systemic conditions further increase susceptibility to nasal polyps. In cystic fibrosis (CF), nasal polyposis has a high prevalence ranging from 6% to 48%, driven by mucociliary clearance defects that promote chronic sinonasal disease.^[30] Primary ciliary dyskinesia (PCD), another ciliopathy, is associated with nasal polyps in about 15% of cases, though less frequently than in CF, with sinonasal involvement persisting across age groups.^[31] Other comorbidities include gastroesophageal reflux disease (GERD) and immune deficiencies. GERD elevates the risk of chronic rhinosinusitis, including cases with nasal polyps, through potential mechanisms of acid-related mucosal irritation.^[32] Immune deficiencies, such as primary immunodeficiencies, heighten susceptibility to CRSwNP by impairing host defenses against sinonasal pathogens.^[33] These associated conditions can collectively exacerbate nasal obstruction and respiratory symptoms, underscoring the need for integrated management.

Pathophysiology

Inflammatory mechanisms

Nasal polyps are characterized by a predominantly Th2-skewed immune response, where CD4+ T helper 2 (Th2) cells and type 2 innate lymphoid cells (ILC2s) orchestrate chronic inflammation through the production of key cytokines such as interleukin-4 (IL-4), IL-5, and IL-13.^[34] These cytokines drive the recruitment and activation of eosinophils, with IL-5 specifically promoting eosinophil maturation, survival, and infiltration into nasal tissues, while IL-4 and IL-13 stimulate B-cell class switching to immunoglobulin E (IgE), amplifying allergic hypersensitivity and local immune responses.^[35] This Th2-dominated milieu sustains a cycle of eosinophil degranulation, releasing cytotoxic proteins like major basic protein and eosinophil cationic protein, which further exacerbate tissue damage and inflammation.^[34] Epithelial dysfunction plays a central role in perpetuating this inflammatory environment, marked by impaired barrier integrity and increased susceptibility to environmental triggers. Type 2 cytokines, particularly IL-4 and IL-13, downregulate tight junction proteins such as zonula occludens-1 (ZO-1) and occludin in nasal epithelial cells, leading to reduced barrier function and heightened permeability that allows allergens and pathogens to penetrate and provoke ongoing immune activation.^[34] Additionally, IL-13 induces epithelial-mesenchymal transition (EMT) markers like vimentin and promotes mucus hypersecretion via MUC5AC overexpression, while impairing mucociliary clearance through ciliary dysfunction, thereby trapping inflammatory mediators and fostering chronicity.^[35] T-cells and macrophages are integral to maintaining this inflammatory cascade, with Th2 cells serving as primary cytokine producers that recruit and polarize other immune effectors. Th2 cells, through IL-4 and IL-13, not only enhance eosinophil and IgE responses but also upregulate programmed death-ligand 1 (PD-L1) on epithelial cells, dysregulating immune checkpoints and intensifying Th2 dominance.^[34] Concurrently, alternatively activated M2 macrophages, induced by IL-4/IL-13 signaling, contribute by secreting chemokines like CCL24 (eotaxin-2), which further amplifies eosinophil chemotaxis, and by promoting tissue remodeling through profibrotic factors, thus sustaining the inflammatory loop without resolution.^[34] Nasal polyps exhibit distinct inflammatory endotypes, primarily eosinophilic (type 2-high) and noneosinophilic (type 2-low), differentiated by their cytokine profiles and biomarker expression. The eosinophilic endotype, prevalent in Western populations and associated with comorbid asthma, features elevated Th2 cytokines (IL-4, IL-5, IL-13), high tissue eosinophil counts (≥10 per high-power field), increased IgE, eosinophil cationic protein (ECP), and periostin, reflecting robust eosinophil-driven inflammation and epithelial remodeling.^[36] In contrast, the noneosinophilic endotype shows diminished IL-5 and IL-13 but upregulated IL-17A, IL-6, and IL-23, with neutrophil predominance, lower eosinophil infiltration, and biomarkers like calgranulin C (S100A12) and resistin, indicating a mixed Th1/Th17-mediated response with less pronounced type 2 features.^[36] These endotypic differences underscore heterogeneous inflammatory pathways, influencing disease severity and therapeutic responses.^[36]

Polyp formation

Nasal polyp formation begins with chronic inflammation of the sinonasal mucosa, which initiates structural changes leading to the development of polypoid tissue.^[37] A key early feature is stromal edema, where fluid accumulation in the submucosal connective tissue causes tissue expansion and the formation of pseudocysts filled with plasma proteins such as albumin.^[37] This edema may include hyperplasia of seromucinous glands in some cases, which can increase mucus production and contribute to the outpouching of the inflamed mucosa into polypoid structures.^[38] The resulting pseudocysts and edematous stroma provide the mechanical basis for the polyp's soft, pedunculated growth, protruding from the sinus or nasal lining.^[2] As formation progresses, angiogenesis promotes increased vascularity within the polypoid tissue, supporting nutrient supply to the expanding mass and facilitating further inflammation.^[37] Concurrently, fibrosis develops through extracellular matrix remodeling, involving deposition of collagen and fibronectin that partially stabilizes the structure while maintaining its pliability.^[39] These vascular and fibrotic changes help sustain the polyp's viability despite its reliance on the host mucosa for attachment.^[40] Mucosal remodeling further characterizes polyp development, featuring goblet cell hyperplasia that enhances mucus secretion and contributes to obstruction.^[39] Squamous metaplasia may occur in response to chronic irritation, altering the respiratory epithelium to a more protective squamous type, while basement membrane thickening strengthens the epithelial-stromal interface but impairs normal barrier function.^[37] These adaptations reflect the tissue's attempt to cope with ongoing stress. The overall progression follows a model from chronic sinusitis to polypoid degeneration, where persistent mucosal inflammation leads to localized tissue weakening and protrusion.^[2] Altered airflow patterns and anatomical factors exacerbate this by promoting uneven pressure distribution, favoring polyp growth in specific sites like the ethmoid and maxillary sinuses.^[37]

Diagnosis

Clinical evaluation

The clinical evaluation of nasal polyps commences with a detailed medical history to determine the duration and characteristics of symptoms, which typically include nasal obstruction, rhinorrhea, postnasal drip, and hyposmia or anosmia persisting for at least 12 weeks, fulfilling the diagnostic criteria for chronic rhinosinusitis with nasal polyps (CRSwNP).^[41] Inquiry should focus on associated comorbidities such as asthma, allergic rhinitis, or aspirin-exacerbated respiratory disease (AERD, formerly Samter's triad), as these are present in up to 40% of CRSwNP cases and influence disease severity.^[2] Medication history, particularly the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or aspirin, is essential, given the heightened risk of AERD exacerbation in sensitive patients.^[42] Additionally, environmental exposures like smoking or occupational irritants, along with prior sinonasal surgeries or family history of cystic fibrosis (especially in children), must be documented to guide differential considerations.^[42] Physical examination follows, beginning with anterior rhinoscopy using a nasal speculum and light source to inspect for visible polyps, which appear as pale, edematous, and glistening masses in the nasal cavity.^[2] Nasal endoscopy, performed with a flexible or rigid endoscope, is the cornerstone of evaluation, enabling precise visualization of polyp location, typically in the middle meatus or sphenoethmoidal recess, and assessment of bilateral versus unilateral involvement.^[41] This procedure confirms the diagnosis in most cases and allows grading of polyp extent using the modified Lund-Kennedy endoscopy score, which rates polyp size (0-2), edema (0-2), and discharge (0-2) per side on a 0-12 scale, providing a standardized measure of disease burden with a minimal important difference of 3 points.^[41] To quantify symptom impact, validated patient-reported outcome measures are employed, such as the 22-item Sino-Nasal Outcome Test (SNOT-22), a questionnaire evaluating sinonasal symptoms, ear/facial discomfort, sleep, and psychological effects on a 0-5 Likert scale per item (total 0-110), with a minimal clinically important difference of 8.9-12 points.^[2] This tool establishes baseline severity and tracks longitudinal changes, aiding in personalized management decisions.^[41] Certain findings raise red flags requiring heightened suspicion, including unilateral polyps, which occur in fewer than 5% of CRSwNP cases and may indicate malignancy, inverted papilloma, or unilateral antrochoanal polyps, necessitating prompt specialist referral.^[2] Other concerning features encompass profuse epistaxis, severe unilateral facial pain, or cranial nerve involvement, which deviate from typical bilateral, painless CRSwNP presentations and warrant exclusion of neoplastic or infectious etiologies.^[43]

Imaging

Computed tomography (CT) scanning serves as the gold standard for imaging nasal polyps, providing detailed visualization of polyp opacification within the paranasal sinuses and aiding in the assessment of disease extent.^[44] On CT, nasal polyps appear as soft tissue density masses causing opacification, often leading to obstruction of the ostiomeatal complex and involvement of multiple sinuses such as the ethmoids and maxillary sinuses.^[2] The Lund-Mackay scoring system is commonly applied to quantify severity on coronal CT scans, assigning scores of 0 (no opacification), 1 (partial opacification), or 2 (complete opacification) to each sinus group, with the ostiomeatal complex scored as 0 (patent) or 2 (obstructed), yielding a total possible score of 0-24; higher scores indicate greater disease burden and correlate with surgical outcomes.^[44] Magnetic resonance imaging (MRI) complements CT by offering superior soft tissue differentiation, which is particularly useful when fungal sinusitis or neoplastic processes are suspected, as it can distinguish polyps from more aggressive lesions based on signal characteristics like T2 hyperintensity.^[44] MRI is less routinely used due to its limitations but provides value in evaluating complications such as orbital or intracranial extension.^[2] Indications for imaging primarily include preoperative mapping to delineate polyp distribution and sinus involvement, especially for functional endoscopic sinus surgery planning, and to assess ostiomeatal complex obstruction that contributes to polyp persistence.^[44] Imaging findings often correlate with endoscopic observations, confirming the extent of mucosal disease.^[2] Limitations of CT include radiation exposure, estimated at approximately 0.86 mSv per scan, which may be a concern for repeated imaging, while MRI is hindered by higher costs and longer acquisition times, making it less practical for routine evaluation.^[44]

Histopathology

Nasal polyps exhibit characteristic microscopic features on histopathological examination, including edematous stroma rich in a mixed inflammatory infiltrate, with eosinophils being the predominant cell type. This eosinophilic inflammation is a hallmark of chronic rhinosinusitis with nasal polyps (CRSwNP), often showing elevated levels of tissue eosinophils (≥10 per high-power field), plasma cells, macrophages, and markers such as interleukin-5 (IL-5) and immunoglobulin E (IgE).^[45]^[2] Key histological findings include glandular hyperplasia, which contributes to the structural disorganization of the polypoid tissue, alongside loss of ciliated epithelium due to chronic mucosal damage and impaired mucociliary clearance. Submucosal fibrosis is commonly present, ranging from partial to extensive, reflecting ongoing remodeling from persistent inflammation. In benign nasal polyps, there is a notable absence of cellular atypia, distinguishing them from neoplastic lesions.^[45]^[2] Special stains enhance diagnostic precision in specific scenarios: hematoxylin and eosin (H&E) staining highlights the eosinophilic infiltrate and may reveal Charcot-Leyden crystals as indicators of severe eosinophilia, while Grocott's methenamine silver (GMS) is used to detect fungal elements in cases suggestive of allergic fungal rhinosinusitis. Congo red staining is employed for rare variants involving amyloid deposition, confirming apple-green birefringence under polarized light in localized amyloidosis mimicking polyps.^[45]^[2]^[46] Histopathological evaluation is particularly indicated for unilateral or atypical polyps to rule out malignancy, such as squamous cell carcinoma or inverted papilloma, or granulomatous conditions, ensuring accurate diagnosis through biopsy confirmation. This analysis also aids in verifying endotypes, such as eosinophilic CRSwNP, guiding targeted therapies.^[45]^[2]

Differential diagnosis

Nasal polyps must be differentiated from various neoplastic conditions that can present with similar sinonasal masses. Inverted papilloma, a benign but locally aggressive tumor, often appears as a unilateral, irregular mass originating from the lateral nasal wall, potentially leading to bony remodeling on imaging. Squamous cell carcinoma, a malignant neoplasm, typically manifests unilaterally with irregular borders, tissue invasion, and possible necrosis, distinguishing it from the bilateral, smooth appearance of inflammatory polyps.^[2] Infectious etiologies can mimic nasal polyps through localized inflammation and mass-like swelling. Allergic fungal rhinosinusitis involves eosinophilic mucin with fungal elements, presenting with thick, peanut-butter-like secretions and often unilateral opacification on imaging, unlike the edematous, watery polyps in chronic rhinosinusitis. Bacterial abscesses, such as those complicating acute bacterial rhinosinusitis, form pus-filled collections that may protrude into the nasal cavity, characterized by acute symptoms and fever absent in typical polypoid disease.^[47]^[48] Inflammatory conditions overlapping with polypoid changes require careful exclusion. Allergic fungal rhinosinusitis (AFRS), as noted, features type I hypersensitivity to fungi with nasal polyposis but is differentiated by positive fungal cultures and allergic mucin on histopathology. Granulomatous diseases, such as granulomatosis with polyangiitis (formerly Wegener's granulomatosis), present with ulcerative lesions, crusting, and saddle-nose deformity due to vasculitis, contrasting the non-ulcerative, polypoid edema.^[47]^[49] Other non-polypoid structural abnormalities can simulate obstruction from polyps. Hypertrophied turbinates cause mucosal swelling and blockage, often bilateral and responsive to decongestants, without the pedunculated growth of true polyps. Nasal septal deviation leads to asymmetric airflow obstruction without mass formation, identifiable on physical exam. In children, choanal atresia presents as congenital posterior nasal obstruction mimicking polypoid blockage, confirmed by inability to pass a catheter. Imaging or histopathology may briefly aid in distinguishing these mimics from benign nasal polyps by revealing structural anomalies or specific inflammatory patterns.^[50]^[50]^[50]

Treatment

Medical therapy

Medical therapy serves as the cornerstone of initial management for nasal polyps, aiming to reduce inflammation, alleviate symptoms such as nasal obstruction and congestion, and potentially shrink polyp size without invasive procedures.^[2] Intranasal corticosteroids are recommended as first-line treatment for chronic rhinosinusitis with nasal polyposis (CRSwNP), with evidence from clinical guidelines supporting their efficacy in improving nasal endoscopy scores and quality of life.01484-1/fulltext) Intranasal corticosteroid sprays, such as fluticasone propionate or mometasone furoate, are typically administered once or twice daily for several weeks to months, directly targeting local inflammation in the nasal mucosa.^[2] These agents, including formulations like budesonide, have demonstrated significant polyp size reduction in clinical trials when used consistently. High-volume saline irrigations are often combined with intranasal steroids to enhance clearance of mucus and allergens, improving treatment outcomes over steroids alone.^[2] For patients with severe or refractory symptoms, short courses of oral systemic corticosteroids provide rapid symptom relief and polyp shrinkage.^[51] A common regimen involves prednisone at 0.5 mg/kg daily (typically 40 mg for adults) for 5 days, followed by a taper to 20 mg daily for another 5 days, limiting duration to minimize side effects like hyperglycemia or osteoporosis.^[51] Such bursts can be repeated 3-4 times per year if needed, but long-term use is avoided due to risks.^[52] Adjunctive therapies address contributing factors: antihistamines, such as loratadine or cetirizine, are useful for patients with an allergic component, reducing histamine-mediated inflammation.^[42] Antibiotics, like macrolides (e.g., clarithromycin) or doxycycline, are reserved for acute bacterial superinfections or exacerbations, with some evidence for anti-inflammatory effects in CRSwNP.^[2] In patients with aspirin-exacerbated respiratory disease (AERD), aspirin desensitization followed by daily low-dose therapy (e.g., 325 mg) is a targeted approach to prevent polyp recurrence and improve sinonasal symptoms.^[53] This procedure involves gradual aspirin dosing under medical supervision, leading to sustained benefits in nasal polyp scores and reduced need for interventions.01779-X/fulltext) If medical therapy fails to control symptoms after 3-6 months, surgical options may be considered.^[2]

Surgical interventions

Surgical interventions for nasal polyps are typically reserved for cases where medical therapy has failed to provide adequate symptom relief or when significant complications arise, such as severe nasal obstruction or recurrent sinus infections. These procedures aim to remove polypoid tissue and restore normal sinus drainage and ventilation, thereby improving quality of life and reducing the frequency of exacerbations. The primary surgical approaches include functional endoscopic sinus surgery (FESS) and polypectomy, both of which are performed under general or local anesthesia using endoscopic visualization to minimize tissue trauma.^[54] Functional endoscopic sinus surgery (FESS) is the gold standard for managing chronic rhinosinusitis with nasal polyps (CRSwNP), involving the use of a rigid endoscope inserted through the nostrils to excise polyps and widen the natural sinus ostia without external incisions. This minimally invasive technique targets diseased tissue while preserving surrounding structures, allowing for improved mucociliary clearance and better penetration of topical medications postoperatively. Comprehensive FESS, which addresses all involved sinuses, has been shown to significantly improve patient-reported outcomes, such as Sino-Nasal Outcome Test (SNOT-22) scores, compared to more limited approaches.^[55]^[54] Polypectomy, a simpler procedure, focuses on the direct removal of accessible nasal polyps using endoscopic instruments, often performed in an office setting for smaller or anteriorly located polyps or in the operating room for more extensive disease. It provides rapid symptomatic relief by alleviating obstruction but is generally less comprehensive than FESS, as it does not routinely address underlying sinus pathology. While effective in the short term, polypectomy alone is associated with higher rates of polyp regrowth due to its limited scope.^[54] Indications for surgical intervention include persistent symptoms of CRSwNP lasting more than 12 weeks despite maximal medical therapy, such as intranasal corticosteroids for at least 6 weeks, antibiotics for bacterial superinfection, and saline irrigations. Surgery is particularly warranted in cases of severe nasal obstruction leading to anosmia, recurrent acute exacerbations, or anatomical complications like frontal or sphenoid sinus involvement, confirmed by nasal endoscopy and computed tomography (CT) imaging showing ostial obstruction or mucosal thickening. Preoperative CT scans play a crucial role in surgical planning by delineating polyp extent and sinus anatomy.^[55]^[54] Complications of these procedures are generally low due to their endoscopic nature, with major events such as cerebrospinal fluid (CSF) leak or orbital injury occurring in less than 1% of cases and minor issues like postoperative bleeding or crusting in under 5%. Bleeding is the most common immediate complication, often managed with nasal packing, while rare but serious risks include meningitis or vision changes from orbital penetration. Recurrence rates following surgery range from 20% to 60%, influenced by factors like disease severity, asthma comorbidity, and the extent of initial resection; revision surgery is required in approximately 20% of patients, particularly those with aspirin-exacerbated respiratory disease.^[56]^[57]

Biologic agents

Biologic agents represent a targeted class of therapies for severe chronic rhinosinusitis with nasal polyps (CRSwNP), modulating key inflammatory pathways to achieve symptom control and polyp reduction in patients unresponsive to standard treatments.^[58] These monoclonal antibodies inhibit specific cytokines or immunoglobulins involved in type 2 inflammation, offering a steroid-sparing alternative with subcutaneous administration.^[59] As of 2025, four agents—dupilumab, omalizumab, mepolizumab, and tezepelumab—have received U.S. Food and Drug Administration (FDA) approval for CRSwNP, demonstrating efficacy in reducing nasal polyp burden and improving quality of life through phase 3 trials and real-world evidence.^[60]^[6] Dupilumab, a human monoclonal antibody that blocks the shared receptor component for interleukin-4 (IL-4) and IL-13, is administered as a 300 mg subcutaneous injection every two weeks.^[61] The FDA approved dupilumab in 2019 for adults with CRSwNP and expanded approval in 2024 to adolescents aged 12 to 17 years as an add-on maintenance therapy.^[62] Phase 3 trials, including SINUS-24 and SINUS-52, showed significant reductions in nasal polyp score (NPS) by approximately 1.9 to 2.1 points compared to placebo at week 24, alongside improvements in nasal congestion and sinus opacification.^[63] Data presented at the 2025 American College of Allergy, Asthma & Immunology (ACAAI) annual meeting from a pivotal phase 3 trial further confirmed substantial NPS reductions and symptom relief in patients with comorbid conditions like allergic fungal rhinosinusitis.^[64] Omalizumab, an anti-immunoglobulin E (IgE) antibody, is indicated for allergic CRSwNP in adults aged 18 years and older, with dosing ranging from 75 mg to 600 mg subcutaneously every two or four weeks, determined by body weight and serum IgE levels—typically administered monthly in practice.^[65] FDA approval for CRSwNP was granted in 2020 based on the phase 3 POLYP 1 and POLYP 2 trials, which demonstrated a mean NPS reduction of 0.9 to 1.1 points versus placebo at week 24.^[66] In allergic subsets, omalizumab effectively mitigates IgE-mediated inflammation, leading to sustained improvements in total symptom scores and reduced need for rescue medications.^[67] Mepolizumab, a humanized monoclonal antibody targeting IL-5 to deplete eosinophils, is given as 100 mg subcutaneously every four weeks and was FDA-approved in 2021 for adults with recurrent CRSwNP.^[60] The phase 3 SYNAPSE trial established its efficacy, showing a 0.7-point NPS reduction at week 52 compared to placebo, with benefits emerging as early as week 4 in real-world 2025 studies.^[68] These analyses, involving diverse patient cohorts, reported NPS improvements of 1.2 to 1.5 points by week 16, particularly in eosinophilic-dominant cases, alongside reductions in exacerbation frequency.^[69] Tezepelumab (Tezspire), a monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), is administered as a 210 mg subcutaneous injection every four weeks following a loading dose. The FDA approved tezepelumab on October 17, 2025, for add-on maintenance treatment of CRSwNP in adults and adolescents aged 12 years and older. Phase 3 trials demonstrated significant reductions in nasal polyp score and improvements in nasal congestion and sense of smell compared to placebo.^[6]^[70] Biologic agents are primarily indicated for severe, refractory CRSwNP characterized by recurrent polyps, persistent symptoms despite intranasal corticosteroids and/or prior surgery, and evidence of type 2 inflammation such as elevated eosinophils or IgE.^[71] Patient selection often involves endoscopic evaluation and biomarker assessment to match the agent to the endotype, with biologics used as add-on therapy for those with inadequate response to conventional medical management.^[72] Monitoring includes regular assessment for injection-site reactions, which occur in 10-20% of cases and are typically mild and self-resolving, alongside ophthalmologic exams for dupilumab due to rare conjunctivitis risks.^[73] Cost-effectiveness remains a consideration, with annual treatment costs exceeding $30,000 per patient; however, 2025 pharmacoeconomic models indicate favorable incremental cost-effectiveness ratios (under $100,000 per quality-adjusted life year gained) when factoring reduced surgery and steroid use in refractory populations.^[74] These therapies may also be employed post-surgery to help prevent polyp recurrence in high-risk individuals.^[75]

Epidemiology

Prevalence

Nasal polyps, most commonly occurring as part of chronic rhinosinusitis with nasal polyps (CRSwNP), affect approximately 1-4% of the adult population worldwide.^[76] The global pooled prevalence of CRSwNP is estimated at 0.65% (95% CI, 0.56-0.75), based on data from over 237 million participants across 28 studies in 20 countries.^[77] Within the broader category of chronic rhinosinusitis (CRS), which has a global prevalence of 8.71%, nasal polyps are present in 25-30% of cases.^[77]^[33] Regional variations in prevalence are notable, with higher rates observed in Western countries—reaching up to 4.3% in some European populations—compared to lower estimates of 1-2% in Asian countries.^[76] For instance, prevalence in France is 2.1%, in Sweden 2.7%, and in the United States around 1.1%, while in South Korea it is approximately 0.4% overall for CRSwNP.^[76]^[78] These differences may reflect variations in diagnostic criteria, environmental factors, and inflammatory endotypes, with Western regions showing a higher proportion of type 2 inflammation.^[79] Incidence trends for CRSwNP demonstrate stability among females but a slight decrease among males, as reported in a 2025 population-based study.^[80] This sex-specific pattern highlights evolving epidemiological dynamics, potentially influenced by changes in risk exposure or healthcare access. The growing recognition of CRSwNP has also driven market expansion for treatments, with the global nasal polyps market projected to reach USD 128.7 million by 2035, largely due to increased uptake of biologic therapies.^[81]

Demographic patterns

Nasal polyps are rare in children, occurring in less than 2% of cases overall, with an estimated prevalence of approximately 0.1% in the pediatric population.^[82] In contrast, the condition peaks in incidence after the age of 40 years, with the average age at diagnosis ranging from 40 to 60 years among adults.^[76] Among children, nasal polyps are often solitary, particularly antrochoanal polyps, which arise unilaterally from the maxillary sinus and extend into the nasal cavity.^[83] In adults, nasal polyps exhibit a male predominance, with a sex ratio of approximately 1.5-2:1 favoring males.^[84] However, this disparity diminishes in cases associated with aspirin intolerance, where rates are more equal between sexes.^[85] Regarding ethnicity, nasal polyps occur at higher rates among Caucasians compared to other groups.^[86] The condition is also linked to atopy across various ethnic populations, including associations with allergic fungal rhinosinusitis in South Asian, Middle Eastern, and African groups.^[87] Comorbidity patterns further highlight demographic relevance, with nasal polyps affecting 20-30% of patients with asthma, particularly those over 40 years old.^[88] In patients with cystic fibrosis, the prevalence reaches up to 50%.^[5]

Prognosis

Recurrence

Nasal polyps in chronic rhinosinusitis with nasal polyps (CRSwNP) frequently recur following surgical intervention, with rates varying widely based on follow-up duration, patient characteristics, and maintenance therapy. Without ongoing medical management, recurrence rates after functional endoscopic sinus surgery (FESS) range from 12% to 77% over follow-up periods of up to 12 years, reflecting the underlying inflammatory drivers of the disease.^[89] In contrast, real-world data from 2025 indicate that adjunctive biologic therapies can significantly delay and reduce these rates, particularly in sequential treatment approaches combining surgery with agents like dupilumab.^[90]^[91] Several predictors increase the likelihood of polyp regrowth post-treatment. The eosinophilic endotype, characterized by tissue eosinophilia and type 2 inflammation, is a strong risk factor, with recurrence rates up to 72.7% in affected patients.^[89] Comorbid conditions such as aspirin-exacerbated respiratory disease (AERD) and asthma elevate odds ratios for recurrence to 1.6-2.9, while smoking and non-adherence to postoperative therapy further exacerbate risk.^[92]^[89]^[93] Effective long-term management requires vigilant monitoring to detect early regrowth. Serial nasal endoscopy, using scores like Lund-Kennedy or Postoperative Endoscopy Score (POSE), is recommended at 3-6 months post-surgery and periodically thereafter.^[89] Patient-reported outcomes, such as Sino-Nasal Outcome Test (SNOT-22) scores, should be assessed every 6-12 months to track symptom progression and guide interventions.^[89] Prevention of recurrence centers on sustained medical therapy following surgery to control inflammation. Intranasal corticosteroids and biologic agents, such as dupilumab or omalizumab, are key in high-risk patients, significantly lowering regrowth by targeting eosinophilic pathways. Emerging biologics like tezepelumab have demonstrated significant reductions in polyp size as of early 2025.^[89]^[94] Adherence to these regimens, including steroid-eluting implants where appropriate, is essential for maintaining remission.^[93]

Complications

Untreated nasal polyps can lead to several disease-related complications due to persistent obstruction and inflammation in the sinonasal tract. Chronic sinusitis often develops or worsens as polyps block sinus drainage, resulting in recurrent infections and prolonged mucosal inflammation.^[2] Obstructive sleep apnea may arise from nasal airway narrowing, exacerbating breathing difficulties during sleep and contributing to daytime fatigue.^[95] Otitis media, including frequent ear infections, can occur secondary to eustachian tube dysfunction caused by polyp-induced pressure changes.^[95] Additionally, asthma exacerbation is a common sequela, particularly in patients with comorbid aspirin-exacerbated respiratory disease, as nasal inflammation triggers lower airway hyperreactivity.^[1] Treatment interventions for nasal polyps also carry risks of complications. Surgical procedures, such as functional endoscopic sinus surgery, may result in adhesions (synechiae) due to postoperative scarring, potentially requiring revision operations to restore sinus patency.^[96] Orbital injury, including hematoma or penetration, occurs in less than 0.5% of cases but can lead to vision-threatening outcomes if not promptly managed.^[97] For biologic therapies like dupilumab, conjunctivitis affects approximately 2% of patients treated for chronic rhinosinusitis with nasal polyps in clinical trials.^[61] Rare complications from nasal polyps include mucocele formation, where obstructed sinuses expand into cyst-like structures, potentially eroding adjacent bone.^[98] Intracranial extension is an uncommon but serious issue, often stemming from untreated mucoceles or severe sinusitis, leading to abscesses or meningitis.^[99] Malignancy transformation within nasal polyps is extremely rare, though longstanding polyps may occasionally harbor or be associated with sinonasal carcinomas.^[100] Nasal polyps significantly impair quality of life, contributing to depression through chronic symptoms and social isolation.^[101] Reduced productivity is common, with affected individuals reporting limitations in daily activities and work performance. According to 2024 surveys, about 25% of patients experience notable emotional impact, including heightened anxiety and diminished well-being.^[102] Effective management of these complications can improve long-term prognosis by mitigating progression and enhancing symptom control.^[103]

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