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Explain nasal polyp etiology and clinical features like donkey

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nasal polyp clinical appearance endoscopy

This clinical comparison features two images illustrating differential findings in the nasal cavity via anterior rhinoscopy and endoscopy. Image A shows a child's nose with a markedly hypertrophic right inferior turbinate, appearing as a fleshy, smooth, pinkish mass firmly attached to the lateral nasal wall; the external nares show signs of atopic dermatitis with dry, peeling skin. Image B provides a close-up endoscopic view of a nasal polyp (NP). The polyp is characterized by a yellowish, translucent, and gelatinous appearance with a rounded, grape-like morphology, distinct from the surrounding mucosa. This comparison is educational for differentiating benign inflammatory masses like nasal polyps from edematous turbinate hypertrophy commonly seen in pediatric patients with allergic rhinitis. Key diagnostic features include the polyp's glistening, wet surface reflections versus the solid, uniform texture of the hypertrophic turbinate. Medical specialty: Otolaryngology (ENT). Target audience: Medical students and practitioners.

This clinical comparison features two images illustrating differential findings in the nasal cavity via anterior rhinoscopy and endoscopy. Image A shows a child's nose with a markedly hypertrophic right inferior turbinate, appearing as a fleshy, smooth, pinkish mass firmly attached to the lateral nasal wall; the external nares show signs of atopic dermatitis with dry, peeling skin. Image B provides a close-up endoscopic view of a nasal polyp (NP). The polyp is characterized by a yellowish, translucent, and gelatinous appearance with a rounded, grape-like morphology, distinct from the surrounding mucosa. This comparison is educational for differentiating benign inflammatory masses like nasal polyps from edematous turbinate hypertrophy commonly seen in pediatric patients with allergic rhinitis. Key diagnostic features include the polyp's glistening, wet surface reflections versus the solid, uniform texture of the hypertrophic turbinate. Medical specialty: Otolaryngology (ENT). Target audience: Medical students and practitioners.

A comparison of endoscopic images from the nasal cavity and ear canal illustrating therapeutic response in a patient with eosinophilic chronic rhinosinusitis (ECRS) and eosinophilic otitis media (EOM). Panels A-C show findings after 13 months of mepolizumab (anti-IL-5) treatment. (A) Endoscopy of the left olfactory cleft reveals a persistent nasal polyp (arrowheads). (B) The nasal cavity and middle turbinate appear edematous, coated with a whitish exudate (arrowheads), with visible discharge from the maxillary sinus ostium (arrow). (C) Otoscopy shows the ear canal and eardrum obscured by copious dried exudate. Panels D-F show the same sites after 1 month of dupilumab (anti-IL-4Ṛ) treatment. (D) The olfactory cleft is clear with no polyps visible. (E) The nasal mucosa and middle turbinate (arrowhead) appear normal with resolution of inflammation and discharge. (F) The ear canal and eardrum have a normal, clear appearance. The series demonstrates the superior efficacy of dual IL-4/IL-13 inhibition over IL-5 inhibition in resolving inflammatory exudates and polyposis in this clinical scenario.

A comparison of endoscopic images from the nasal cavity and ear canal illustrating therapeutic response in a patient with eosinophilic chronic rhinosinusitis (ECRS) and eosinophilic otitis media (EOM). Panels A-C show findings after 13 months of mepolizumab (anti-IL-5) treatment. (A) Endoscopy of the left olfactory cleft reveals a persistent nasal polyp (arrowheads). (B) The nasal cavity and middle turbinate appear edematous, coated with a whitish exudate (arrowheads), with visible discharge from the maxillary sinus ostium (arrow). (C) Otoscopy shows the ear canal and eardrum obscured by copious dried exudate. Panels D-F show the same sites after 1 month of dupilumab (anti-IL-4Ṛ) treatment. (D) The olfactory cleft is clear with no polyps visible. (E) The nasal mucosa and middle turbinate (arrowhead) appear normal with resolution of inflammation and discharge. (F) The ear canal and eardrum have a normal, clear appearance. The series demonstrates the superior efficacy of dual IL-4/IL-13 inhibition over IL-5 inhibition in resolving inflammatory exudates and polyposis in this clinical scenario.

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I now have excellent content from Cummings Otolaryngology. Let me compose the full answer using the "explain like a donkey" style (simple, fun, plain language with analogies) while keeping the medical accuracy from my sources.

Nasal Polyps - Etiology and Clinical Features (Explained Like You're a Donkey)

Hee-haw! Let me tell you about those weird lumpy grapes that grow in your nose.

What ARE These Things?

A nasal polyp is a soft, fleshy lump that grows from the lining of your nose or sinuses. Imagine your nose is a cozy stable. The walls of the stable are lined with soft, wet tissue. Now imagine that tissue gets so inflamed and waterlogged for so long that it puffs up, fills with fluid, and droops down like a soggy grape. That's a nasal polyp - translucent, yellowish, gelatinous, grape-like in appearance, hanging there, blocking things up. Not a tumor. Not dangerous by itself. Just very, very annoying.

ETIOLOGY - Why Does Your Nose Grow Grapes?

1. The Main Driver: Chronic Inflammation (Type 2)

The lining of your nose is like a bouncer at a club. Its job is to keep out bacteria, fungi, allergens, and toxins. When the bouncer gets overstimulated for months to years, it throws a massive inflammatory party that never ends.
In most people in the Western world, this inflammation is Type 2 (Th2-skewed) - meaning the immune system overproduces a set of "alarm chemicals" called cytokines, especially:
  • IL-4, IL-5, IL-13 - these are the main troublemakers
  • IgE - the allergy antibody that makes mast cells and eosinophils show up
This recruits hordes of eosinophils (a white blood cell that acts like an overenthusiastic donkey kicking everything in sight). The eosinophils damage the tissue, fluid leaks in, edema builds, and - pop - a polyp is born.
(Source: Cummings Otolaryngology Head and Neck Surgery, CRS pathogenesis section)

2. The Trigger Suspects

Think of these as the different things that let the wrong donkeys into the stable:

A. Allergic Rhinitis (Hay Fever)

Allergens breach the mucosal barrier, activate dendritic cells and Th2 lymphocytes, generate IgE-secreting plasma cells. On re-exposure, mast cells degranulate and release more type 2 cytokines, recruiting eosinophils. AR doesn't cause polyps directly but it keeps the nose inflamed, swells the sinus outflow tracts, causes mucociliary stasis, and sets up a perfect environment for polyps to form. - Cummings Otolaryngology

B. Staphylococcus aureus - The Sneaky Bacteria

S. aureus produces superantigens - toxins that behave like fake emergency broadcasts. They non-specifically activate huge swarms of T cells (up to 20% at once, versus the normal 0.001%) and trigger massive IgE production locally in polyp tissue. S. aureus also forms biofilms on mucosal surfaces - sticky colonies that shelter the bacteria from antibiotics and keep the inflammation smoldering. Recent evidence even suggests S. aureus can initiate type 2 responses through TLR2 independently of its superantigenic toxins. - Cummings Otolaryngology, p.824-825

C. Viral Infections

Repeated viral upper respiratory infections damage the epithelial barrier of the nose. This creates gaps the immune system then overreacts to. Viruses may also predispose to CRS by early-life sensitization, similar to how early infections have been linked to childhood asthma. - Cummings Otolaryngology, p.825

D. Allergens and Environmental Toxins

Cigarette smoke causes reactive oxygen species, damages cilia (the tiny sweeping hairs in the nose), promotes biofilm formation, and induces pro-inflammatory cytokines. This contributes to the chronic inflammation that underlies polyp development. - Cummings Otolaryngology, p.825

E. B Cells and Immunoglobulins - The Local Antibody Factory

Nasal polyp tissue is packed with plasma cells, structures resembling germinal centers, and high levels of locally produced IgA, IgM, IgG, and IgE. A cytokine called BAFF (B-cell activating factor) drives B-cell proliferation and switching, particularly to IgA, which is a potent eosinophil degranulator - meaning it causes more tissue damage in the polyp. Autoantibodies (IgA and IgG anti-nuclear) are also elevated in recalcitrant disease, hinting at a possible autoimmune component. - Cummings Otolaryngology, p.825

F. T Regulatory Cell Dysfunction (Treg Failure)

In a normal nose, Tregs (the peacekeepers) suppress excessive inflammation. In CRS with nasal polyps, Treg activity is reduced - partly linked to low vitamin D levels. Without peacekeepers, the Th2 donkeys run wild, sustaining the inflammatory response indefinitely. - Cummings Otolaryngology

G. Geographic / Ethnic Variation

Western patients: mostly Th2/eosinophilic polyps, often with comorbid asthma. Asian patients: historically more Th1/Th17 pattern with neutrophilic infiltrate, less eosinophilia, lower asthma rate - though this pattern is gradually shifting to match Western patterns. - Cummings Otolaryngology

H. Special Associations

AssociationNotes
AsthmaUp to 30-50% of nasal polyp patients have asthma
Samter's TriadNasal polyps + asthma + aspirin sensitivity - the full triple-threat
Cystic FibrosisPolyps in CF are driven by a Th1/Th17 neutrophilic pattern (different mechanism)
Allergic Fungal RhinosinusitisFungal antigens drive intense type 2 inflammation

CLINICAL FEATURES - What Does the Donkey With Polyps Actually Experience?

Here is what happens when the grapes take over:

1. Nasal Obstruction / Blockage

The #1 complaint. The polyps physically block the nasal passage like a potato in a pipe. The more and bigger the polyps, the worse the blockage. Bilateral obstruction is typical. Breathing through the nose becomes like trying to breathe through a hay-filled muzzle. Mouth breathing follows.

2. Anosmia / Hyposmia (Loss of Smell)

The olfactory cleft (the part of the nose where smell receptors sit, right at the top) gets blocked by polyps. No airflow to the smell receptors = no smell. This is one of the most bothersome symptoms. Loss of taste often follows (taste is mostly smell). About half of patients report improvement with topical steroids, but it's often incomplete.

3. Nasal Discharge / Rhinorrhoea

Watery or mucoid discharge, often bilateral and chronic. Post-nasal drip (mucus draining down the back of the throat) is also common.

4. Facial Pressure / Headache

Polyps block sinus drainage, mucus accumulates, pressure builds in the sinuses - particularly the ethmoid and maxillary sinuses. Patients feel a dull pressure or heaviness over the cheeks, forehead, or bridge of the nose.

5. Voice Change (Hyponasality)

The nasal passages contribute to voice resonance. Block them up and the voice goes flat and nasal-sounding, like a donkey with a stuffed nose. Classic "nasal quality" speech.

6. Appearance on Examination

  • On anterior rhinoscopy: glistening, grey/pale or yellowish-translucent, smooth, grape-like masses visible in the nasal cavity
  • Classically arise from the middle meatus (the area between the middle and inferior turbinates)
  • They are insensate (no pain when probed - a key feature that distinguishes them from turbinate hypertrophy, which is painful to touch)
  • Mobile, soft, non-tender, non-vascular (won't bleed on gentle probing unlike other masses)
  • Endoscopically: rounded, gelatinous, wet-surfaced polyps in the olfactory cleft and middle meatus

7. Recurrence After Treatment

Polyps come back. That's the donkey-in-the-mud feature of this disease. Even after surgery, they regrow, especially in patients with eosinophilic disease, aspirin sensitivity, or asthma.

Quick Summary Table

FeatureDetail
Core causeChronic Th2-skewed eosinophilic inflammation of the sinonasal mucosa
Key cytokinesIL-4, IL-5, IL-13, IgE
Key cellsEosinophils, mast cells, Th2 lymphocytes, plasma cells
Bacteria involvedS. aureus (superantigens + biofilms)
Top symptomBilateral nasal obstruction
Hallmark exam findingGrey/translucent, grape-like, insensate masses from middle meatus
Key associationsAsthma, aspirin sensitivity (Samter's triad), CF, allergic fungal sinusitis
Smell lossVery common (olfactory cleft blockage)
RecurrenceVery high - especially in eosinophilic type
Here's what they look like on rhinoscopy (A = turbinate hypertrophy for comparison, B = actual nasal polyp):
Nasal polyp vs turbinate hypertrophy - anterior rhinoscopy and endoscopy
Note the yellowish, translucent, grape-like polyp (B) with its glistening wet surface - versus the solid pinkish turbinate (A).
Sources:

Give answer for nasal polyp for ent subject from standard textbook

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nasal polyp endoscopy clinical photograph

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nasal polyp gross appearance pale gelatinous grape

I now have all the content I need from both Scott-Brown's and Cummings Otolaryngology. Let me compile the comprehensive, standard ENT textbook-style answer.

Nasal Polyps - ENT Standard Textbook Answer

Sources: Scott-Brown's Otorhinolaryngology Head & Neck Surgery (Vol 1, Chapter 95) | Cummings Otolaryngology Head and Neck Surgery (Chapter 41)

Definition

Nasal polyps are oedematous, grape-like protrusions of the sinonasal mucosa, most often originating in the upper part of the nose around the osteomeatal complex on the lateral wall. The surface epithelium is smooth and consists of pale, translucent tissue - distinguishing them from the more vascular mucosa of the nasal cavity. They represent a phenotypic manifestation of chronic rhinosinusitis with nasal polyps (CRSwNP).

Epidemiology

ParameterData
Annual incidence1-20 per 1000 population
Adult prevalence1-4%
Children~0.1%
Sex ratioMore common in males (2-4:1)
AgeDeclines after 60 years
RaceNo racial predilection (in general population)
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1085)

Pathogenesis

Polyps arise in the presence of inflammation that results from a dysregulated interaction between the sinus epithelium and the lymphoid system. Histologically, they consist of:
  • Loose oedematous connective tissue stroma
  • Inflammatory cells (predominantly eosinophils)
  • Fluid accumulation
  • Covered by pseudostratified, columnar, ciliated epithelium
Mechanistic basis: The oedematous connective tissue stroma ruptures and herniates through the basement membrane to form a polyp. (Scott-Brown's, p.1086)

Inflammatory Endotype (Key)

Approximately 80% of nasal polyps in Western countries are characterized by:
  • A robust T-helper 2 (Th2) response
  • Eosinophilic infiltration
  • Decreased T regulatory (Treg) function
  • Abundance of IL-5 cytokine
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1086)
The full type 2 cytokine profile includes IL-4, IL-5, IL-9, IL-13, derived from Th2 cells and type 2 innate lymphoid cells (ILC2). Epithelial cells secrete IL-25, IL-33, and TSLP as "alarmins" that amplify this response. (Cummings Otolaryngology, p.831)
Coronal CT scan showing complete sinus opacification by nasal polyps (Figure 95.1 - Scott-Brown's)
Fig 95.1 - Coronal CT showing complete opacification of sinuses secondary to nasal polyps. (Scott-Brown's)
Histopathology of nasal polyp - H&E stain showing pseudostratified ciliated epithelium over oedematous stroma with scattered inflammatory cells (Figure 95.2 - Scott-Brown's)
Fig 95.2 - Histopathology of a simple inflammatory nasal polyp (x400): pseudostratified ciliated epithelium over oedematous loose stroma with scattered inflammatory cells. (Scott-Brown's)

Etiology / Predisposing Factors

The exact cause remains unknown. Multiple environmental and host factors interact to trigger chronic sinonasal inflammation. The following have been implicated:

1. Allergy (Allergic Rhinitis)

  • Prevalence of allergy in nasal polyp patients ranges from 10% to 64% in different studies
  • Only 0.4-4.5% of patients with allergic rhinitis actually have nasal polyps - similar to the general population - suggesting allergy is not directly causative
  • Elevated serum IgE and positive skin prick tests to inhalant allergens are found in the majority of polyp patients
  • Importantly, local tissue IgE in polyps is often polyclonal and independent of total serum IgE or allergy skin prick test results
  • Mucosal polyclonal IgE can induce mast cell degranulation independently of serum IgE levels
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1086)

2. Bacteria - Staphylococcus aureus Superantigens

  • The main bacterial species implicated in polyp exacerbation is Staphylococcus aureus
  • 42.5% of S. aureus strains isolated from nasal polyp patients harbour at least one classic enterotoxin gene
  • These toxins behave as superantigens: unlike conventional antigens, they do not need antigen processing
  • Superantigens activate up to 20% of the body's T cells (vs. only 0.001-0.0001% for regular antigens)
  • This results in massive cytokine secretion, increased eosinophilic inflammation, and formation of IgE antibodies
  • In Western CRSwNP this manifests as severe eosinophilic disease; this effect is NOT seen in Asian CRSwNP patients (who have predominantly Th1/Th17 patterns)
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1086; Cummings Otolaryngology, p.829)

3. Bacterial Biofilms

  • Bacteria enclose themselves within a self-developed matrix of polysaccharides, rendering them inaccessible to antibiotics and host immune responses
  • Nasal polyp cases with biofilm presence are associated with a more severe disease form and worse postoperative outcome
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1086)

4. Fungi (Controversial)

  • Fungi (particularly Alternaria) are detectable in the nasal cavity of all patients - those with CRS and controls
  • The fungal hypothesis proposed an exaggerated host response to airborne fungi as the underlying cause
  • Current evidence does NOT support fungi as a uniquely important or universal agent driving CRS
  • However, fungi play a definite role in Allergic Fungal Rhinosinusitis (AFRS), a specific subtype characterized by type 1 hypersensitivity, type 2 cytokine expression, and nasal polyps
(Cummings Otolaryngology, p.824)

5. Epithelial Barrier Dysfunction

  • The mechanical barrier (mucociliary clearance + tight junctions between epithelial cells) is the first line of defence
  • Genetic and acquired defects in mucociliary flow with increased mucus viscosity are associated with a high incidence of CRS
  • Intrinsic protective anti-protease activity is reduced in some forms of CRS with type 2 inflammation
  • A permeable epithelial barrier allows environmental antigens access to the immune system, initiating and perpetuating the inflammatory cycle
(Cummings Otolaryngology, p.826)

6. Viruses

  • Viral upper respiratory infections disrupt the epithelial barrier
  • Recurrent viral infections secondary to allergic rhinitis may lead to acquired ostiomeatal obstruction and mucociliary stasis
  • Early-life viral infections may predispose to subsequent CRS development, analogous to early-onset asthma
(Cummings Otolaryngology, p.825)

7. Environmental Toxins

  • Cigarette smoke has the strongest epidemiologic association with CRS, acting through reactive oxygen/nitrogen species, mucociliary dysfunction, biofilm promotion, and pro-inflammatory cytokine induction
(Cummings Otolaryngology, p.825)

Associated Diseases

Asthma

  • Prevalence of CRSwNP is ~7% in asthmatic patients vs. 4% in general population
  • 30-71% of nasal polyp patients have asthma
  • There is a direct association between asthma severity and nasal polyp presence
  • Patients with late-onset asthma: 10-15% develop nasal polyps, generally developing asthma first, then polyps within 9-13 years
  • Asthma and nasal polyps share: eosinophilia, mucus cell hyperplasia, oedema, thickened basal membrane, and increased cysteine leukotrienes
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1087)

Samter's Triad / AERD (Aspirin-Exacerbated Respiratory Disease)

The classic triad of:
  1. Bronchial asthma
  2. Nasal polyposis
  3. Aspirin sensitivity (NSAIDs intolerance)
  • First described by Widal in 1922; formally recognized by Samter in 1967
  • Prevalence: up to 0.3% in general population; 5-10% of adult asthmatics
  • Prevalence of nasal polyps + asthma + aspirin sensitivity increases after 40 years of age
  • These patients are typically non-atopic
  • Polyps with aspirin-induced asthma develop faster - about 2 years from symptom onset (vs. 9-13 years in non-aspirin asthma)
  • CRSwNP prevalence in AERD: 30-60%
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1087)

Cystic Fibrosis

  • Nasal polyps in CF are driven by a Th1/Th17 neutrophilic pattern - a different pathophysiological mechanism from the typical Western eosinophilic polyp
  • Treated differently as the underlying endotype is distinct

Other Associations

  • Allergic Fungal Rhinosinusitis (AFRS)
  • Primary Ciliary Dyskinesia
  • Eosinophilic Granulomatosis with Polyangiitis (EGPA, formerly Churg-Strauss)

Clinical Presentation

Clinical presentation is variable and depends on the extent of polyp disease. Small polyps may be asymptomatic and found incidentally during rhinoscopy.
In general, patients present with symptoms persisting over months to years, progressing from mild to severe:
SymptomNotes
Nasal obstructionBilateral; the hallmark and most common symptom. Persistent and progressive.
Watery rhinorrhoeaEarly symptom; progresses to thick post-nasal discharge
Hyposmia / AnosmiaBlockage of the olfactory cleft. Very common. Associated taste disturbance.
Post-nasal dripThick discharge draining posteriorly
Headache / facial pressureFrom sinus obstruction and pressure build-up; occasionally
Mouth breathingFrom massive polyps obstructing nasal cavity or nasopharynx
Obstructive sleep symptomsWith large/massive polyps
Hyponasal voiceFrom loss of nasal resonance
Epistaxis is NOT associated with benign nasal polyps - its presence should raise suspicion of a more serious underlying pathology (e.g. inverted papilloma, malignancy, angiofibroma).
With massive polyposis, rarely:
  • Proptosis
  • Hypertelorism
  • Diplopia (from alteration of craniofacial structure)
Despite potentially extending into the intracranial cavity, the slow-growing nature of massive polyposis means it does not typically cause neurological symptoms or pain.
(Scott-Brown's Otorhinolaryngology, Vol 1, p.1085)

Examination Findings

Anterior Rhinoscopy

  • Smooth, pale, translucent, grape-like masses visible in the nasal cavity
  • Typically arise from the middle meatus (osteomeatal complex region)
  • Bilateral in most cases (unilateral polyps should prompt exclusion of other pathologies)
  • Insensate on probing (no pain - distinguishes from turbinate hypertrophy, which is painful and bleeds)
  • Soft, mobile, non-tender, non-vascular (do not bleed on gentle probing)

Nasal Endoscopy

  • Polyps in the middle meatus and olfactory cleft
  • Translucent, yellowish or greyish, gelatinous, wet-surfaced masses
  • Mucopurulent discharge from middle meatus may be present
  • Oedema of middle meatus mucosa

Differential Diagnosis of Nasal Masses

ConditionKey Differentiating Feature
Turbinate hypertrophyAttached to lateral wall, painful/bleeds on probing, does not move
Antrochoanal polypUnilateral, origin from maxillary antrum, extends to choana
Inverted papillomaUnilateral, bleeds easily, tendency for malignant transformation
Nasal encephaloceleMidline, pulsatile, increases with crying/Valsalva, intracranial connection
Juvenile angiofibromaYoung males only, bleeds profusely, origin from sphenopalatine foramen
MalignancyUnilateral, hard, bleeds, with pain and facial swelling

Grading of Nasal Polyps (Mackay & Lund Scoring)

GradeDescription
0No polyps
1Polyps confined to middle meatus
2Polyps below inferior border of middle turbinate
3Polyps reaching inferior turbinate or medial wall
4Complete obstruction of nasal cavity

Investigations

InvestigationPurpose
Nasal endoscopyGold standard for diagnosis; grading; site of origin
CT sinuses (coronal)Extent of disease, surgical planning; shows sinus opacification
MRIDifferentiates polyp from tumour; soft tissue detail
Allergy testingIgE levels, skin prick tests - identify atopic contributors
SpirometryAssess concomitant asthma
Sweat chloride / CFTR geneRule out cystic fibrosis, especially in children
Aspirin challengeConfirm AERD/Samter's triad
HistopathologyExclude malignancy; confirm eosinophilic vs. neutrophilic pattern

Summary Box

  • Nasal polyps = oedematous grape-like protrusions from osteomeatal complex
  • Core mechanism: chronic Th2-eosinophilic inflammation (in 80% of Western cases)
  • Exact cause unknown; bacteria (S. aureus superantigens), allergy, epithelial barrier defects all implicated
  • Key symptoms: bilateral obstruction + anosmia + rhinorrhoea
  • Hallmark exam sign: pale, insensate, non-bleeding, mobile masses from middle meatus
  • Epistaxis = NOT a feature; its presence demands further workup
  • Key associations: asthma (30-71%), Samter's triad (AERD), AFRS, cystic fibrosis
  • Bilateral = rule; unilateral = investigate for other pathology
References:
  • Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol 1, Chapter 95 (Nasal Polyps, pp.1085-1088)
  • Cummings Otolaryngology Head and Neck Surgery, Chapter 41 (Etiology and Pathogenesis of CRS, pp.824-831)
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