Welcome to drtbalu's Otolaryngology online






 





Epidemiology of Nasal polyp

By

Dr T Balasubramanian

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 polypi and allergic rhinitis is rather weak
3. Cohort studies of recent times have demonstrated that there is a strong association between asthma and nasal polyp
4. The incidence of nasal polyposis increases with age.  Common affected age group being 30 - 60 years
5. Nasal polypi in children should prompt investigations for cystic fibrosis
6. Incidence of aspirin hypersensitivity is high in patients with nasal polypi
7. Genetic predisposition towards development of nasal polypi is rather unclear
8. Allergic fungal sinusitis has been categorically proved to be a factor in the etiology of nasal polyp

Classification of chronic rhinosinusitis:


Chronic rhinosinusitis has been classified into:

1. Chronic rhinosinusitis without nasal polypi

2. Chronic rhinosinusitis 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 are 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 known 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 (cohart) 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 predisoposition 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 Demateceous fungi

2. CT scan findings - inspissated mucous secretions with calcification

3. Eosinophilic secretions 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.








Copyright drtbalu 2010


Search Query