Epidemiology of nasal polyposis

Introduction:

Lot of developments have taken place in the field of epidemiology of nasal polypi. Before dwelling into them it will be better to analyse the

conclusions of various studies in this subject. These conclusions are:

1. The prevalance of nasal polypi in general population is about 1-3%.
2. Studies have demonstrated that the link between nasal polyp and allergic rhinitis is very weak.
3. Cohort studies of recent times have demonstrated a strong association between asthma and nasal polyposis
4. The incidence of nasal polyposis increases progressively with age. Common age group of occurence being 30 – 60 years
5. Nasal polpi in children should prompt investigations to rule out cystic fibrosis
6. Incidence of aspirin intolerance is rather high in patients with nasal polypi
7. Genetic predisposition to nasal polypi is rather unclear
8. Allergic fungal rhinosinusitis have been categorically proved to be a factor in nasal polyposis

Classification of chronic rhinosinusitis:

Chronic rhinosinusitis has been classified into:

1. Chronic sinusitis without nasal polypi
2. Chronic sinusitis with nasal polypi

Chronic rhinosinusitis without nasal polypi are commonly seen in TH1 mediated inflammation (activated T helper cells). TH1 lymphocytes are

potent inducers of inflammation. This type of inflammation is also seen in antrochoanal polyp. Hence it is mandatory to differentiate these

two conditions. The process of differentiation is rather easy because antrochoanal polyp has the following unique features:

1. They are unilateral
2. They present posteriorly

Chronic rhinosinusitis with nasal polypi are caused by TH2 mediated inflammation. This type of inflammation is commonly seen in patients

with bronchial asthma.

At this juncture let us briefly review TH1 and TH2 immune responses.

TH1 and TH2 are polarized responses of body's T – helper cells when faced with pathogens. Under normal conditions both these types of

reponses should be fully functional to enable our immune mechanism to get rid of the pathogen. Disease begin to develop if one or the other

type of immune mechansim becomes predominant. TH2 becomes predominant in patients with bronchial asthma and nasal polyposis where

as TH1 is predominant in patients with chronic rhinosinusitis without nasal polypi. The T lymphocytes produce cytokines which are

responsibe for the immunological mechanism of the body. Basically the cytokines produced fall into two categories:

1. Cytokines secreted by T – helper cells type I. These are inflammatory mediators and hence known as proinflammatory cytokines.
2. Cytokines secreted by T – helper cells type II. These inflammatory mediators are known for their anti inflammatory response. They are also know to evoke allergic response.

Co morbid conditions associated with nasal polyposis:

1. Allergic rhinitis
2. Generalized atopic status
3. Bronchial asthma

Role of nasal allergy in the pathogenesis of nasal polypi:

Studies have demonstrated that there is no significant increase in the incidence of nasal polypi in patients with allergic rhinitis. Infact the

incidence of nasal polypi in this group is almost the same as that of general population.

Role of Asthma in the pathogenesis of nasal polypi:

Studies conducted (cohort) have clearly demonstrated that the incidence of nasal polypi is more in patients belonging to this group. It should be

borne in mind that Asthma is mediated by TH2 type of inflammation.

Role of Atopy:

Studies have demonstrated that atopy was more prevalent in patients with chronic rhinosinusitis without nasal polypi thus effectively ruling out

atopy as a contributing factor for nasal polyposis.

Age & its relationship to nasal polypi:

Studies have demonstrated that the incidence of nasal polypi increases with age. The incidence reaches the peak at 50 years of age. Asthmatics

over the age of 40 are four times more prone to develop nasal polypi than others.

Genetic predisposition:

Studies have demonstrated that nearly 15% of patients with nasal polyposis have a positive family history. This could be taken to be a pointer

for genetic predisposition. But large cohart studies performed have not been able to clearly pin point genetic predisposition in these patients.

Allergic fungal rhinosinusitis:

Patients with AFRS have a strong predisposition towards extensive nasal polyposis. It can hence be considered as the pathophysiologic

etiological factor in some patients with nasal polyposis.

Diagnostic pointers for diagnosis of AFRS:

1. Type I hypersensitivity to demataceous fungi
2. CT scan findings – inspissated mucous secretions with calcification
3. Eosinophilic mucous containing charcot Leyden crystals
4. Positive fungal elements isolated from sinus contents

Racial differences in nasal polypi patients:

Nasal polypi due to AFRS is known to affect patients with low socio economic status. In caucasians Nasal polypi demonstrate strong

eosinophilic component while in Asian population neutrophilic pattern predominates. The exact reason for this variation is yet to be elucidated.