Nasal Polyps in Malaysia: Symptoms, Causes & Treatment | aihealz
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Nasal Polyps.Care & specialists in Malaysia
In Malaysia, nasal Polyps is managed by ents. Nasal polyps are soft, pale, fluid-filled outgrowths of the sinus and nasal lining driven by years of type-2 (eosinophilic) inflammation. They affect roughly 1-4% of adults globally and almost always arise on both sides of the nose at once — a unilateral polyp is treated as a red flag for tumor until proven otherwise.
aliases · Nasal Polyps (chronic sinus inflammation with polyp growth)· नाक की पॉलिप (Naak ki Polyp)· Pólipos nasales· Polypes nasaux· reviewed May 12, 2026
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Reviewed by AIHealz Medical Editorial Board · ENTLast reviewed May 12, 2026
Nasal polyps (ICD-10: J33) are non-cancerous, edematous swellings of the sinonasal mucosa that herniate into the nasal cavity, most often originating from the ethmoid sinuses and the middle meatus. Histologically the lesions are loose stromal tissue heavily infiltrated with eosinophils, mast cells, and CD4 T cells skewed toward type-2 cytokines IL-4, IL-5, and IL-13. They are the visible endpoint of chronic rhinosinusitis with nasal polyposis (CRSwNP), which sits within the broader umbrella of chronic rhinosinusitis (CRS). Polyps are graded endoscopically using the Lildholdt or Lund-Mackay scoring systems, and severity is increasingly classified by inflammatory endotype rather than appearance alone — over 80% of cases in Western populations are eosinophilic, while non-eosinophilic polyps predominate in parts of East Asia.
key facts
Prevalence
1-4% of adults globally (EPOS 2020); ~13% of patients with chronic rhinosinusitis carry visible polyps
Demographics
Men affected roughly 2x more than women; rare under age 20
Avg. age
Peak onset age 40-60; aspirin-exacerbated subtype clusters at 30-40
Global cases
Estimated 80-200 million people worldwide based on prevalence and adult population
Specialist
ENT
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How you might notice it
The key symptoms of Nasal Polyps are: Persistent bilateral nasal obstruction that does not clear with decongestant sprays and worsens over months — the most common presenting complaint in over 90% of CRSwNP patients., Reduction or complete loss of the sense of smell (hyposmia or anosmia), often the symptom that bothers patients most and the slowest to recover after treatment., Loss or distortion of taste, which follows the loss of smell because flavor recognition depends largely on retronasal olfaction., Postnasal drip with thick, often discoloured mucus that triggers throat-clearing, chronic cough, and morning sore throat., Dull facial pressure or fullness across the cheeks, forehead, and bridge of the nose, sometimes mistaken for migraine or tension headache., Mouth-breathing, snoring, and disturbed sleep, with daytime fatigue out of proportion to the nasal symptoms., Recurrent acute sinus infections layered on top of the chronic congestion — three or more antibiotic courses in a year is a typical history..
01Persistent bilateral nasal obstruction that does not clear with decongestant sprays and worsens over months — the most common presenting complaint in over 90% of CRSwNP patients.
02Reduction or complete loss of the sense of smell (hyposmia or anosmia), often the symptom that bothers patients most and the slowest to recover after treatment.
03Loss or distortion of taste, which follows the loss of smell because flavor recognition depends largely on retronasal olfaction.
04Postnasal drip with thick, often discoloured mucus that triggers throat-clearing, chronic cough, and morning sore throat.
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How it’s diagnosed
diagnosis
Diagnosis of nasal polyps rests on a focused history, endoscopic examination, and selective imaging rather than a single test. The 2020 European Position Paper on Rhinosinusitis (EPOS 2020) and the 2023 AAO-HNS Clinical Practice Guideline update both require two or more cardiac sinonasal symptoms — nasal obstruction, anterior or posterior nasal discharge, facial pressure, and reduced sense of smell — lasting 12 weeks or longer, plus objective evidence of inflammation. The objective evidence is nasal endoscopy demonstrating polyps in the middle meatus or CT findings of opacified sinuses with characteristic ethmoid mucosal thickening. Anterior rhinoscopy alone misses smaller polyps and is no longer considered sufficient; flexible or rigid endoscopy is the standard of care. The Lund-Mackay CT score quantifies the extent of sinus opacification and guides surgical planning. Smell testing (UPSIT or Sniffin' Sticks) is routinely added because olfactory loss is both a strong diagnostic clue and a sensitive outcome measure. Allergy testing (skin-prick or specific IgE) and a check for asthma should be done in every adult with polyps. Biopsy is reserved for unilateral polyps, asymmetric disease, vascular or fleshy lesions, or any feature suggesting inverted papilloma, sinonasal malignancy, or granulomatosis with polyangiitis — these red-flag presentations need an ENT review rather than empirical medical therapy. In children, every polyp should trigger a sweat chloride test for cystic fibrosis. Once a CRSwNP diagnosis is established, blood eosinophils, total IgE, and questionnaires such as SNOT-22 and an asthma control test stratify disease severity and guide the choice between topical therapy alone, surgery, and biologic treatment.
Key tests
01
Nasal endoscopy (rigid or flexible)Direct visualization of the middle meatus and sinus drainage pathways. Confirms the presence, size, and bilateral distribution of polyps, grades severity with the Lildholdt or Meltzer scale, and detects red-flag features such as unilateral disease, friable tissue, or bleeding.
Functional endoscopic sinus surgery (FESS) with polypectomySmith 2013 prospective cohort: clinically meaningful quality-of-life improvement at 12 months in approximately 80% of patients. Polyp recurrence around 40% by 18 months in unselected CRSwNP and over 80% by 5 years in untreated AERD; both reduced sharply by ongoing topical steroids and biologics.
Reboot (full-house) FESSSingle-center series report polyp-free rates of 60-70% at 2 years compared with 30-40% after standard FESS in matched severe disease.
Endoscopic medial maxillectomy (for antrochoanal polyp or recurrent maxillary disease)Antrochoanal polyp: recurrence under 10% with complete stalk removal versus 25-30% with limited approaches (Frosini 2009).
Office-based polypectomy with microdebrider under local anestheticSymptomatic improvement in 60-70% of selected patients at 6 months; typically followed by intensive topical therapy.
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Causes & risk factors
known causes
Type-2 (eosinophilic) inflammation of the sinonasal mucosa
The central driver in Western CRSwNP. Cytokines IL-4, IL-5, and IL-13 from Th2 cells and innate lymphoid cells recruit eosinophils, expand mast cells, and remodel the epithelium into edematous polypoid tissue. Successful biologics all target this pathway.
Aspirin-exacerbated respiratory disease (AERD)
Dysregulated arachidonic acid metabolism shifts production from prostaglandin E2 toward cysteinyl leukotrienes. Patients have severe polyposis, asthma, and respiratory reactions to COX-1 inhibitors. Polyps regrow rapidly after surgery without ongoing aspirin desensitization or biologic therapy.
Allergic and non-allergic chronic rhinitis
Chronic mucosal inflammation from allergens (dust mite, mold, pollen, animal dander) or irritants primes the lining for polypoid change. Allergic rhinitis is present in 50-80% of polyp patients, though it is a cofactor rather than a sufficient cause.
Cystic fibrosis and CFTR dysfunction
Defective chloride transport produces viscous mucus, impaired mucociliary clearance, and chronic neutrophilic inflammation. Up to 50% of patients with cystic fibrosis develop nasal polyps, often in childhood.
Bacterial dysbiosis and Staphylococcus aureus superantigens
Colonization of the sinus mucosa with Staphylococcus aureus that secretes enterotoxin superantigens amplifies local IgE production and eosinophilic inflammation, particularly in severe and recurrent disease.
Fungal colonization and allergic fungal rhinosinusitis (AFRS)
A specific subtype in which non-invasive fungal hyphae provoke a strong IgE-mediated reaction, eosinophilic mucin, and bony erosion. Often unilateral or asymmetric, with high recurrence rates after surgery alone.
Primary ciliary dyskinesia and other mucociliary disorders
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Living with it
01Use daily intranasal corticosteroid spray or budesonide irrigation indefinitely after the first polyp diagnosis — long-term topical therapy is the single most effective measure to prevent regrowth
02Stop smoking and avoid second-hand smoke — current smoking measurably increases polyp recurrence and reduces response to medical therapy
03Treat concurrent allergic rhinitis with antihistamines and, where appropriate, allergen immunotherapy to reduce the chronic inflammatory baseline
04Avoid aspirin and other COX-1 NSAIDs (ibuprofen, naproxen, diclofenac) unless aspirin tolerance has been formally confirmed — patients with undiagnosed AERD can deteriorate suddenly
05Vaccinate against influenza and pneumococcus to reduce acute exacerbations and antibiotic courses
06Optimize asthma control with inhaled steroids and bronchodilators — upper and lower airway disease move together and good asthma control protects the sinuses
recommended foods
•Anti-inflammatory Mediterranean-style eating pattern rich in olive oil, vegetables, and oily fish — observational data link this pattern to lower CRS symptom scores
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When to seek help
why see an ent
An ENT specialist should be involved when nasal symptoms persist beyond 12 weeks despite intranasal steroids, when polyps are visible on examination, when there is unilateral disease or bleeding, when oral steroids are needed more than once or twice a year, or when smell loss is severe. Allergists and pulmonologists co-manage patients with concurrent severe asthma, AERD, or where biologic therapy is being considered. Pediatric polyps almost always justify ENT plus cystic fibrosis screening.
01Persistent loss of smell, with measurable impact on appetite, mood, and safety (inability to detect smoke, gas leaks, or spoiled food)
02Obstructive sleep-disordered breathing and snoring from chronic nasal obstruction, with daytime fatigue and reduced cognitive performance
03Recurrent acute bacterial sinusitis, sometimes complicated by orbital cellulitis, subperiosteal abscess, or rarely intracranial extension
04Asthma deterioration in patients with the unified airway phenotype; uncontrolled polyposis is a recognized driver of severe asthma exacerbation
05Cumulative oral corticosteroid exposure leading to osteoporosis, hypertension, weight gain, cataracts, and adrenal suppression in patients given repeated courses
Eosinophilic CRSwNP (type-2 high)The dominant Western phenotype. Tissue eosinophil counts above 10 per high-power field, frequent asthma comorbidity, high recurrence after surgery, and excellent response to biologics targeting IL-4Rα, IL-5, or IgE.
Non-eosinophilic CRSwNP (type-2 low)Predominantly neutrophilic, more common in East Asian populations and in cystic fibrosis-related polyposis. Lower recurrence after surgery but historically poorer steroid response; less likely to benefit from current biologics.
Aspirin-exacerbated respiratory disease (AERD / Samter triad)Severe asthma plus nasal polyposis plus respiratory reactions to aspirin and other COX-1 NSAIDs. Affects 7-15% of CRSwNP patients; polyps regrow aggressively after surgery without ongoing aspirin desensitization or biologic therapy.
Antrochoanal polyp (Killian polyp)A solitary polyp arising from the maxillary sinus and extending through the natural ostium into the nasopharynx. Typically unilateral, more common in adolescents and young adults, not driven by type-2 inflammation, and cured by complete surgical removal.
Cystic fibrosis-related nasal polyposisAffects 30-50% of children and adults with cystic fibrosis. Polyps tend to be neutrophilic, often present before age 10, and may regress on CFTR modulator therapy such as elexacaftor-tezacaftor-ivacaftor.
Living with Nasal Polyps
Timeline
After a short oral steroid course, smell and nasal patency typically improve within 3-7 days and benefit lasts 3-6 months. After FESS, the nose feels worse for 7-14 days due to swelling and crusting; saline rinses begin on day 1 or 2 and continue for life. Most patients are back to office work within 7-10 days, with strenuous exercise and air travel deferred 2 weeks. Endoscopic appearance settles by week 6-8, and the benefit of surgery peaks at month 3-6. Biologics begin to reduce polyp size and improve smell by week 4-8 and reach maximum effect by month 6; therapy is continued indefinitely with periodic reassessment.
Lifestyle
01Use isotonic or hypertonic saline rinses 1-2 times daily to clear mucus and crusts and improve topical steroid delivery
02Sleep with the head of the bed elevated by 15-20 cm to reduce overnight congestion and improve sleep quality
03Identify and reduce indoor allergen exposure (dust mite covers, HEPA filters, animal dander control) if allergy testing is positive
04Avoid prolonged exposure to wood dust, chlorine fumes, and other respiratory irritants; wear a fitted mask when occupational exposure is unavoidable
05Maintain hydration to keep mucus thin — 2 liters of water daily unless restricted for other reasons
06Limit alcohol intake, particularly red wine in AERD where sulfite-rich beverages can trigger upper and lower airway symptoms
07Track symptoms with a short weekly diary (smell, congestion, sleep, asthma) — patterns help guide treatment escalation
Complementary approaches
Allergen-specific immunotherapySubcutaneous or sublingual immunotherapy for documented allergic rhinitis can reduce upper airway inflammation and improve patient-reported nasal symptoms. Direct effect on polyp size is modest; best regarded as adjunct in selected allergic patients.
Xylitol nasal irrigationSmall randomized trials (Weissman 2011) suggest improved SNOT-20 scores when xylitol is added to saline rinses. Cheap, safe, and reasonable as an adjunct, though not a substitute for steroid or biologic therapy.
Vitamin D repletionCorrecting deficiency is associated with modest reductions in polyp size and recurrence in observational and small interventional studies (Mulligan 2018). Cheap and safe; check 25-hydroxyvitamin D once and treat to sufficiency.
Choosing a doctor
Look for an otolaryngologist with rhinology fellowship training or substantial CRSwNP volume, comfort with both office-based endoscopy and full FESS, and access to image-guided navigation for revision cases. Ask whether the practice routinely uses high-volume budesonide irrigations, whether biologics are prescribed in-house or referred to allergy, and how aspirin desensitization is handled. Continuity matters — CRSwNP is a lifelong disease and outcomes correlate strongly with consistent follow-up.
Asthma + Lung UK — Nasal polyps →Plain-English UK patient resource with practical guidance on living with polyps and accessing specialist care.
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Frequently asked
What are nasal polyps?▾▴
Nasal polyps are soft, pale, painless growths of inflamed lining tissue that hang into the nasal cavity, almost always on both sides at once. They are not tumors and are not cancerous, but they reflect chronic eosinophilic inflammation in the sinuses that needs ongoing treatment. Polyps cause persistent nasal blockage, loss of smell, postnasal drip, and facial pressure, and they tend to grow back if the underlying inflammation is not controlled.
What are the main symptoms of nasal polyps?▾▴
The main symptoms are persistent nasal blockage that does not respond to decongestants, reduced or absent sense of smell, postnasal drip, facial pressure, snoring, and frequent sinus infections. Symptoms typically build over months on both sides of the nose. Symptoms confined to one side, nosebleeds, or sudden facial pain are red flags and need urgent ENT review.
What causes nasal polyps?▾▴
Nasal polyps are caused by chronic type-2 (eosinophilic) inflammation of the sinus lining. Contributors include asthma, aspirin-exacerbated respiratory disease, allergic rhinitis, cystic fibrosis, fungal sensitization, Staphylococcus aureus superantigens, and genetic susceptibility. They are not contagious and are not caused by hygiene or diet.
How are nasal polyps diagnosed?▾▴
Diagnosis combines history of sinonasal symptoms for at least 12 weeks with nasal endoscopy showing polyps in the middle meatus and a CT scan of the sinuses to map the disease. Smell testing, allergy evaluation, and asthma assessment are added in every adult. Pediatric polyps need a cystic fibrosis sweat test, and unilateral polyps need biopsy to exclude tumor.
Are nasal polyps cancerous?▾▴
Bilateral inflammatory nasal polyps are benign and do not become cancer. However, a unilateral nasal polyp can sometimes be an inverted papilloma, a sinonasal cancer, or another tumor that mimics a polyp. Any polyp limited to one side, any unusual bleeding, or any friable lesion must be biopsied promptly. This is the single most important rule in nasal polyp practice.
Will nasal polyps go away on their own?▾▴
Nasal polyps rarely disappear without treatment because the underlying inflammation persists. Small polyps can fluctuate in size with seasons, infections, and steroid use, but established polyps generally enlarge if untreated. Daily intranasal corticosteroid spray, saline irrigation, and biologic therapy when indicated all shrink polyps and reduce recurrence.
Will my sense of smell come back?▾▴
Smell recovery is the slowest part of treatment and the symptom patients value most. After steroid courses, around 60-70% of patients regain some smell within weeks. After surgery plus continuing topical therapy, full or near-full recovery is reported in 30-50% of patients at 6-12 months. Dupilumab measurably improves olfaction in about 60% of severe CRSwNP patients in trials.
Do nasal polyps require surgery?▾▴
Surgery is offered when symptoms persist after 12 weeks of optimized medical therapy or when polyps are large and obstructing. Functional endoscopic sinus surgery (FESS) removes the polyps and opens the sinus ostia so steroid rinses can reach the diseased mucosa afterward. Many patients now avoid surgery entirely by adding a biologic to topical therapy.
How long does it take to recover from FESS?▾▴
Most patients return to office work within 7-10 days after FESS. Saline rinses start on day 1-2 and continue for life. Strenuous exercise, swimming, and air travel are deferred for about 2 weeks. The nose feels congested and crusted for the first 2-4 weeks; benefit peaks at 3-6 months as the mucosa heals.
Do nasal polyps grow back after surgery?▾▴
Polyps return in about 40% of patients within 18 months of FESS alone. Recurrence is higher in aspirin-exacerbated respiratory disease (over 80% at 5 years), in heavy smokers, and in patients who stop topical steroids. Continued intranasal corticosteroid sprays or budesonide rinses, and biologic therapy in severe cases, substantially reduce recurrence.
What is dupilumab and is it effective for nasal polyps?▾▴
Dupilumab is a monoclonal antibody that blocks the IL-4 and IL-13 signaling driving eosinophilic polyp inflammation. In the SINUS-24 and SINUS-52 trials (NEJM 2019) it halved nasal polyp scores at 24 weeks, restored smell in roughly 60% of patients, and cut the need for surgery and oral steroids dramatically. It is given as a subcutaneous injection every 2 weeks.
What is aspirin-exacerbated respiratory disease (AERD)?▾▴
AERD, sometimes called Samter triad, is a combination of severe asthma, nasal polyposis, and respiratory reactions to aspirin and other COX-1 NSAIDs such as ibuprofen and naproxen. It accounts for 7-15% of CRSwNP patients and behaves more aggressively than usual polyp disease. Aspirin desensitization or biologic therapy is needed to control polyp regrowth.
Can I take ibuprofen or aspirin if I have nasal polyps?▾▴
Most polyp patients tolerate NSAIDs, but anyone with asthma, severe polyposis, or a previous bad reaction to aspirin should avoid aspirin, ibuprofen, naproxen, and diclofenac until AERD has been formally excluded. AERD reactions can be severe and include acute asthma. Paracetamol (acetaminophen) is usually safe; check with your clinician before any new NSAID.
Are nasal polyps linked to asthma?▾▴
Yes — 40-65% of patients with nasal polyps also have asthma, and 7-15% have AERD. Both conditions share type-2 inflammation in the airway. Polyp control often improves asthma control and vice versa, which is why biologic therapy targets both simultaneously and pulmonologists and ENT specialists often co-manage these patients.
Are nasal polyps caused by allergies?▾▴
Allergic rhinitis is present in 50-80% of polyp patients and adds to inflammation but is not the sole cause. People with severe inhalant allergies can have years of nasal symptoms without polyps, and many patients with polyps have no allergies at all. Allergy treatment is part of overall control but does not by itself dissolve established polyps.
Can children get nasal polyps?▾▴
Nasal polyps are uncommon in children. When they occur, cystic fibrosis is the underlying cause in over 90% of cases, with primary ciliary dyskinesia accounting for most of the rest. Every pediatric nasal polyp warrants a sweat chloride test and a referral to ENT and pediatric pulmonology, even if the child appears otherwise well.
Are nasal polyps hereditary?▾▴
There is a genetic component. First-degree relatives of patients with CRSwNP have roughly a 4-fold higher risk than the general population, and several gene variants in immune pathways have been linked to the eosinophilic phenotype. Inheritance is multifactorial — there is no single gene, and lifestyle and environment shape whether the disease develops.
How much does nasal polyp treatment cost?▾▴
Generic intranasal steroid sprays and saline irrigations cost a few dollars to tens of dollars per month worldwide. A short oral steroid course costs little. FESS performed in a US hospital ranges roughly USD 8,000-20,000 self-pay, far less under most insurance plans and far less again in India and other emerging markets. Biologics such as dupilumab, omalizumab, and mepolizumab cost USD 25,000-40,000 per year at US list prices, often covered by insurance for severe disease.
Can diet or supplements shrink nasal polyps?▾▴
Diet alone does not shrink established polyps. A Mediterranean-style anti-inflammatory eating pattern, adequate vitamin D, and omega-3 oily fish appear to reduce overall airway inflammation in observational studies and are reasonable to adopt. Aspirin and NSAID-containing herbal preparations should be avoided in AERD. Diet is supportive — not a substitute for steroids, biologics, or surgery.
When should I see a doctor for nasal symptoms?▾▴
See a clinician if nasal blockage, smell loss, or postnasal drip last more than 12 weeks, if you have one-sided symptoms or nosebleeds, if oral steroid courses have been needed more than once a year, or if asthma is worsening alongside the nasal symptoms. Sudden severe facial pain with fever, vision change, or eye swelling needs same-day care.
05Dull facial pressure or fullness across the cheeks, forehead, and bridge of the nose, sometimes mistaken for migraine or tension headache.
06Mouth-breathing, snoring, and disturbed sleep, with daytime fatigue out of proportion to the nasal symptoms.
07Recurrent acute sinus infections layered on top of the chronic congestion — three or more antibiotic courses in a year is a typical history.
08A nasal voice and reduced ability to taste hot drinks or detect smoke and gas leaks, which raises real safety concerns for some patients.
09Bleeding from one nostril, unilateral obstruction, or facial pain on a single side — when these are present rather than the bilateral pattern above, urgent ENT review is needed to rule out tumor.
10Asthma symptoms (wheezing, chest tightness, increased inhaler use) that worsen in parallel with the nasal symptoms in patients with concurrent lower airway disease.
early warning signs
•Gradual fading of the ability to smell coffee, perfume, or cooked food over weeks to months, before nasal obstruction is obvious
•Persistent low-grade postnasal drip and throat-clearing for more than 12 weeks without an obvious infection
•Worsening asthma control or new aspirin or NSAID sensitivity in an adult — both can precede visible polyps by years
•A child with cystic fibrosis developing nasal congestion or audible mouth-breathing — pediatric polyps almost always justify a cystic fibrosis sweat test
● emergency signs
•Sudden visual disturbance, double vision, eye swelling, or proptosis — possible orbital extension or complication of acute sinusitis on a polyp background
•Severe one-sided facial pain with fever, neck stiffness, or altered mental state — suspected intracranial complication of sinus infection
•Unilateral nasal bleeding, a friable mass, or a polyp that looks vascular or fleshy on endoscopy — must be biopsied to exclude inverted papilloma or sinonasal malignancy
•Sudden severe asthma attack after taking aspirin or an NSAID — features of AERD; immediate emergency care and lifelong NSAID avoidance until formal evaluation
CT scan of the paranasal sinuses (non-contrast)
Maps the extent of mucosal disease, calculates the Lund-Mackay score, identifies bony anatomic variants relevant to surgery (Onodi cells, dehiscent skull base, optic nerve course), and screens for fungal hyperdensities, bone erosion, and tumour features.
03
Quantitative smell testing (UPSIT, Sniffin' Sticks, or B-SIT)Objectively documents olfactory loss, distinguishes hyposmia from anosmia, and tracks treatment response. Olfactory recovery is the symptom patients value most and trial endpoints emphasize.
04
Allergy evaluation (skin-prick testing or specific IgE)Identifies inhalant allergen sensitization that may benefit from environmental control or allergen immunotherapy and informs the choice of biologic when total IgE and allergy status matter (omalizumab).
05
Blood eosinophil count and total serum IgEStratifies type-2 inflammation. Eosinophils above 300 cells/µL and elevated IgE both predict response to type-2 biologics; tissue eosinophilia on histology is the strongest predictor when available.
06
Sweat chloride test (for any pediatric polyp or suspected CF)Screens for cystic fibrosis, which underlies polyposis in over 90% of children and a meaningful fraction of young adults with severe recurrence.
07
Tissue biopsy and histologyReserved for unilateral, vascular, or atypical polyps. Distinguishes inflammatory polyp from inverted papilloma, juvenile angiofibroma, sinonasal lymphoma, granulomatosis with polyangiitis, and rare malignancies. Also quantifies tissue eosinophils per high-power field.
08
Aspirin challenge or desensitization protocolConfirms AERD when history is suggestive and offers a route to therapeutic aspirin desensitization. Performed in specialist centers under close supervision.
Outlook
CRSwNP is a chronic disease — like asthma or eczema, it is controlled rather than cured. With continuous intranasal or irrigation steroid therapy, around 60% of patients maintain acceptable symptom control without surgery. After FESS, roughly 80% of patients report meaningful quality-of-life improvement at 12 months, but polyps recur in about 40% within 18 months without ongoing topical therapy and in over 80% of AERD patients by 5 years. Biologics have shifted the trajectory: dupilumab, omalizumab, and mepolizumab reduce repeat surgery, restore smell in a meaningful proportion of patients, and cut oral steroid exposure substantially. Smell recovery is the most patient-relevant outcome and the slowest — full return is reported in 30-50% of treated patients at 6-12 months. Untreated severe polyposis is rarely life-threatening but causes durable loss of smell, sleep disturbance, repeated antibiotic exposure, and a measurable reduction in work productivity. The strongest predictors of poor long-term outcome are AERD, severe asthma, current smoking, very high eosinophilia, and missed follow-up.
Defective ciliary function impairs sinus clearance, traps secretions, and creates a chronic inflammatory environment that predisposes to polyposis, especially in young patients with concurrent bronchiectasis.
Genetic susceptibility
Heritability is meaningful: first-degree relatives of CRSwNP patients carry roughly a 4-fold increased risk. Genome-wide association studies have linked polymorphisms in IL-1RL1, TSLP, and HLA loci to the eosinophilic phenotype.
risk factors
Coexisting asthmamodifiable
Asthma is present in 40-65% of CRSwNP patients and predicts more severe disease, higher recurrence after surgery, and stronger benefit from biologics targeting IL-4Rα or IL-5.
Aspirin or NSAID sensitivity (AERD)non-modifiable
Patients with AERD have polyp recurrence rates after surgery alone exceeding 80% at 5 years, compared with around 40% in non-AERD CRSwNP — the single strongest clinical predictor of recurrence.
Allergic rhinitis or chronic non-allergic rhinitisenvironmental
Chronic mucosal inflammation from inhalant allergens primes polypoid remodelling. Allergic rhinitis is present in 50-80% of polyp patients across cohorts.
Male sexnon-modifiable
Men develop CRSwNP roughly 2x more often than women, with a more pronounced gap in eosinophilic subtypes.
Age 40-60non-modifiable
Most adult-onset cases present in middle age; the disease is rare under age 20 and pediatric polyps almost always reflect cystic fibrosis or primary ciliary dyskinesia.
Cystic fibrosis or known CFTR variant carriergenetic
30-50% of patients with cystic fibrosis develop polyposis; sweat chloride testing is warranted for any pediatric polyp.
Smoking and chronic irritant exposuremodifiable
Current smoking is associated with more severe symptoms, higher endoscopic scores, and reduced response to topical steroids; cessation measurably improves outcomes after surgery.
Occupational exposure to wood dust, textile dust, and metal fumesenvironmental
Chronic occupational irritant exposure raises both polyp prevalence and recurrence risk; relevant in carpentry, textile work, welding, and farming.
Family history of CRSwNPgenetic
First-degree relatives carry roughly a 4-fold higher risk; familial clusters are over-represented among aspirin-sensitive patients.
Vitamin D deficiencymodifiable
Low serum 25-hydroxyvitamin D correlates with polyp size and recurrence in several observational cohorts; correction has modest benefit in trials but is reasonable in deficient patients.
•Omega-3-rich oily fish (salmon, mackerel, sardines) 2-3 times weekly — modest reductions in eosinophilic airway inflammation in airway disease cohorts
•Adequate vitamin D from sunlight, fortified foods, or supplements if serum 25-OH vitamin D is below 30 ng/mL
•Foods rich in quercetin and natural anti-inflammatory polyphenols (apples, onions, berries, leafy greens)
•Plenty of water to maintain mucociliary clearance — at least 2 liters daily unless contraindicated
foods to avoid
•Aspirin, ibuprofen, naproxen, and diclofenac in any patient with suspected or confirmed AERD until formal evaluation
•Excessive alcohol, particularly red wine and beer with sulfites and biogenic amines, which trigger nasal and asthma symptoms in AERD
•Highly processed foods rich in trans fats and refined sugars — associated with worse symptom scores in observational airway studies
•Known food allergens for the individual patient, identified by history rather than blanket elimination diets
06
Surgical complications of FESS including bleeding, CSF leak (around 0.2%), orbital injury (under 0.5%), and synechiae or scarring needing revision; risk is reduced in high-volume rhinology centers
07Missed sinonasal malignancy or inverted papilloma in patients with unilateral disease who are managed as routine polyposis without endoscopy or imaging
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Daily management
01Perform a saline rinse first, then dose intranasal steroid spray or budesonide irrigation, at the same times daily — adherence is the single strongest predictor of disease control
02Track smell informally each week (coffee, citrus, soap) and note the trend — falling smell is often the earliest sign of recurrence
03Refill steroid sprays, biologic prefilled syringes, and asthma inhalers before they run out — gaps in therapy reliably precede flares
04Carry a written list of NSAID-containing medications to avoid if AERD is diagnosed, and ensure pharmacy, dental, and surgical records flag the diagnosis
05Schedule a 6-12 monthly review with the ENT clinician and an annual smell test to monitor disease control objectively
Exercise
Regular aerobic exercise (brisk walking, swimming, cycling) for 150 minutes per week supports immune regulation and weight management and is safe in stable CRSwNP. Patients with concurrent asthma should have a personalized asthma action plan and pre-exercise short-acting bronchodilator if prescribed. Avoid heavy exertion in air-quality-warning conditions, and rinse nasal passages with saline after swimming in chlorinated pools or freshwater lakes.