Indian J Otolaryngol Head Neck Surg
(January 2014) 66(Suppl 1):S16–S21; DOI 10.1007/s12070-011-0427-z
R E V IE W A R TI C L E
Nasal Polyposis: Current Trends
Renu Rajguru
Received: 26 July 2011 / Accepted: 14 December 2011 / Published online: 29 December 2011
Association of Otolaryngologists of India 2011
Abstract Nasal polyps (NP) are one of the most common
inflammatory mass lesions of the nose, affecting up to 4%
of the population. They present with nasal obstruction,
anosmia, rhinorrhoea, post nasal drip, and less commonly
facial pain. Their etiology remains unclear, but they are
known to have associations with allergy, asthma, infection,
fungus, cystic fibrosis, and aspirin sensitivity. However, the
underlying mechanisms interlinking these pathologic con-
ditions to NP formation remain unclear. Also strong
genetic factors are implicated in the pathogenesis of NP,
but genetic and molecular alterations required for its
development and progression are still unclear. Manage-
ment of NP involves a combination of medical therapy and
surgery. There is good evidence for the use of corticoste-
roids (systemic and topical) both as primary treatment and
as postoperative prophylaxis against recurrence, but the
prolonged course of the disease and adverse effects of
systemic steroids limits their use. Hence several new drugs
are under trial. Surgical treatment has been refined signif-
icantly over the past 20 years with the advent of endo-
scopic sinus surgery and, in general, is reserved for cases
refractory to medical treatment. Recurrence of the polyp-
osis is common with severe disease recurring in up to 10%
of patients. Over the last two decades, increasing insights
in the pathophysiology of nasal polyposis opens perspec-
tive for new pharmacological treatment options, with
eosinophilic inflammation, IgE, fungi and Staphylococcus
aureus as potential targets. A better understanding of the
pathophysiology underlying the persistent inflammatory
state in NP is necessary to ultimately develop novel
R. Rajguru (&)
Institute of Aerospace Medicine, Vimanpura, Near Hal Airport,
Bangalore 560017, Karnataka, India
e-mail: renurajguru@yahoo.com
123
pharmacotherapeutic approaches. In this paper we present
the newer treatment options available for better control and
possibly cure of the disease.
Keywords Nasal polyps Pathophysiology
New pharmacological options Surgery
Introduction
Nasal polyposis is an unpleasant disease for a patient,
which severely effects his quality of life. Despite its easy
diagnosis, it is a challenge for otorhinologists, because of
its poorly understood etiopathogenesis, poor impact of
therapeutic intervention and frequent recurrences. It is a
multifactorial condition which is often associated with
many diseases and pathogenic disorders, such as allergy,
infection, allergic fungal sinusitis, cystic fibrosis, asthma,
and aspirin intolerance. However, the underlying mecha-
nisms interlinking these pathologic conditions to NP for-
mation remain unclear. Although the exact etiology of
nasal polyposis is still not revealed, insights in the patho-
genesis have largely expanded over the last years.
Increasing insights in the pathophysiology of nasal polyp-
osis opens perspective for new pharmacological treatment
options, with eosinophilic inflammation, IgE, fungi and
Staphylococcus aureus as potential targets. This paper aims
to summarize current trends in all aspects of management
of NP.
Pathogenesis
NPs are outgrowths of nasal mucosa which are smooth,
semi translucent, gelatinous and pale, mainly situated in the
Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S17
S18 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
middle meatus, originating number of genetic treatment of NPs. present in sinonasal
from mucous membrane association studies found a mucosa of healthy
of the ostiomeatal significant correlation subjects too, but they act
complex, probably between certain human R as antigens in mucosa of
because of release of pro- leukocyte antigen (HLA) o sensitized individuals,
inflammatory cytokines alleles and NP. The risk of l resulting in recruitment of
from epithelial cells as a developing NP can be as e inflammatory cells—
result of contact between high as namely eosinophils—and
two surfaces of mucosa 5.53 times in subjects with o release of major basic
at this narrow region. Air HLA-DQA1*0201- f protein (MBP), which
turbulence and pressure DQB1*0201 haplotype finally causes mucosal
differential may also have [1]. The development and F damage and
an influence. Various persistence of mucosal u superinfection by
n
other important factors inflammation in NPs have migration of other
g
like genetic factors, been reported to be inflammatory cells into
u
bacteria, fungi, biofilm associated with numerous s that location [5]. This
formation, etc. have been genes and potential single fungal antigen is derived
implicated, and have been nucleotide poly- Among the possible from the germinating
discussed in subsequent morphisms. A recent study etiologies, fungi have fungal spores and hyphae.
paragraphs. Histo- showed that in NP tissues, gained wide attention in This inflammatory
morphological 192 genes were recent years. Though reaction is different from
characterization of polyp upregulated by at least fungal particles are the one seen in response to
tissue reveals frequent twofold, and 156 genes a fungus ball which is
epithelial damage, a were downregulated by at more of an irritative
thickened basement least 50% in NP tissues as inflammation, like a
membrane, and com- pared to sphenoid foreign body reaction, i.e.,
oedematous to sometimes sinuses mucosa [2]. It has giant cells, and not an
fibro- tic stromal tissue, also been pos- tulated that eosinophilic inflammation,
with a reduced number of an abnormal mucosal which is present in nasal
vessels and glands, but immune response underlies polyposis [6]. Aspergillus
virtually no neural disease pathogenesis [3]. and Alternaria are
structure. Polyps show an There are a number of commonest fungi species
increased number of mast genes which are involved implicated in the
cells, eosinophils, T in epithelial barrier pathogenesis of nasal
lympho- cytes, cytokines, maintenance and repair in polyposis [7].
chemokines, interleukins, the inflammatory state of
TNF-a and adhesion NP. For example, carbonic
molecules. anhy- drase (CA) is a zinc R
metalloenzyme that o
participate in the l
Role of biological processes of e
Genetic various fluid transporting
Factors in epithelia, including ion o
Pathogen and water transport. A f
esis decreased expression level
of CA was found to be B
During the past two associated with impaired i
decades, many studies elec- trolyte and water o
have been per- formed to transport across the f
determine differential i
epithelial cell, which will
gene expression profiles l
result in oedema of NP
between NP and normal m
tissue [4]. Identifying the s
nasal tissues, in order to causal genes and variants
identify susceptible genes in NP is important to the Microorganisms like
that are associated with path towards improved
NP-related traits. A bacteria and fungi exist in
prevention, diagnosis and
 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S19
two main forms in the nt of
sinonasal cavities: as free- Sinon
floating planktonic asal
replicating cells and in Polyp
biofilms. Biofilms are osis
defined as organized
communities of Therapy for NP involves
collaborating a combination of
microorganisms that are observation, medical, and
attached to an inert or surgical treatments
living surface contained in depending on individual
a self-produced polymeric case assessment. The aims
matrix primarily of treatment are to
composed of eliminate or significantly
exopolysaccharides, reduce the size of the NP
nucleic acids, and proteins resulting in relief of nasal
[8]. The structural nature obstruction, improvement
of biofilms and the in sinus drainage, restora-
characteristics of sessile tion of olfaction and taste.
cells produce resistance Treatment of Surgical
against antimicrobial proce- dures alone is
agents, resulting in an insufficient to treat the
environment that affords underlying inflammation
protection against adverse of the nasal mucosa.
conditions and the host’s Supplementary medical
defenses [9]. The bacteria treatment is always
in these biofilms, while necessary to prevent
protected from host recurrence.
defenses and antibiotics,
actively metabolize and
produce endotoxins and
other virulence factors.
This may perpetu- ate an
inflammatory host
response, even in the
absence of culturable
planktonic bacteria and
lead to chronic inflam-
mation [10]. Traditional
antimicrobial treatments
that tar- get single
microbial cells within
biofilms will never be able
to eliminate them.
Therefore, antibiofilm
therapies that target the
entire biofilm as a
complex multicellular
organism or prevent
unique, biofilm-specific
processes are needed to
fight biofilm infections.

Mana
geme
S20 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S21
M (medical polypectomy). of polyp growth. So short- increased prevalence. The
e Simple saline nasal term oral cortico- steroid germs release enterotoxins,
d douching to help cleanse therapy combined with which act as superantigens
i the nose prior to topical montelukast in a daily and induce a topical
c medications is beneficial dosage of 10 mg as multiclonal IgE formation
a as it improves nasal mu- maintenance therapy in as well as a severe,
l cociliary clearance. controlling symptoms of possibly steroidinsensitive
Corticosteroids should be severe sinonasal polyposis eosinophilic inflammation
M used with caution in ‘at- has been proven very [15]. Recently, S. aureus
a effective. Also, an
risk groups’ particularly could be demonstrated to
n additional 3 months of
patients with diabetes, reside intraepithelially, and
a
uncontrolled hypertension, montelukast therapy com- potentially to release
g
and peptic ulcer disease. bined with intranasal and superantigens into the
e
m inhaled corticosteroids tissue from within the
e produces subjective and epithelial cells. An
n Rol objective improvements in immune defect, either in
t e nasal symptoms and the innate or adaptive
of function as well as immunity, might be
Intranasal glucocorticoids Le significant improvements responsible for this
constitute presently the uk in lung function in patients phenomenon. Folli- cle-
best treatment of NP. They otri with nasal polyposis [14]. like structures and
ene lymphocyte
decrease polyp size,
s
improve nasal airway accumulations, specifi-
An Role of S. aureus
patency, improve cally binding enterotoxins,
tag and Concept of
symptoms of rhinitis like oni can be found within the
rhinor- rhoea, sneezing Superantigens polyp tissues, giving rise
sts
and nasal blockage, delay to local IgE formation. The
the recurrence of polyps Evidence accumulates that superantigen- induced
Leukotrienes (LTs) and
after surgery and postpone S. aureus colonizes immune response also
prostaglandins are
the need for a new surgery chronic rhi- nosinusitis leads to a modulation of
products of ara- chidonic
[11]. The unusually wide with, but not without the severity of the
acid metabolism, and are
range of GC actions can polyps, with significantly eosinophilic inflammation,
key mediators in acute and
be explained by GC chronic inflammatory and may be linked to lower
receptors present in three diseases of the airways. airway co-morbidity in
cell compart- ments: Leuko- triene levels have polyp patients. IgE
nucleus, cytoplasm, and been shown to be elevated antibodies to enterotoxins
plasma membrane. Both in patients with sinonasal can be found in the
topical and systemic polyposis and sinusitis. majority of aspirin-sensi-
glucocorticoids may affect Recent studies have tive polyp tissues,
the eosino- phil function shown, an objective associated with a
by both directly reducing alleviation, or at least substantial increase in
eosinophil viability and stabilization, of sinonasal eosinophilic cationic
function or indirectly polyposis after use of protein (ECP) and IL-5
reducing the secretion of short-term oral corticoste- [16].
chemo- tactic cytokines by roid therapy combined
nasal mucosa and polyp with the LT synthesis
epithelial cells [12]. inhibitor zileuton or the R
Systemic steroids are LT receptor antagonist o
reserved for advanced or l
zafirlukast and
refrac- tory cases e
montelukast as
particularly when allergy is maintenance therapy [13].
present and it results in o
These improve- ments are
relatively rapid short-term f
probably based on the
dramatic improvement, control of NP
nasal symptoms and A
inflammation and possibly
endoscopic findings n
 S22 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
t S. aureus derived Topical steroid sprays and
i enterotoxins acting as
b superantigens, massive
i IgE formation takes place
o within the airways.
t Because of the
i multiclonality, a range of
c
allergens could possibly
s
maintain a constant
degranu- lation of mast
Based on the concept of
cells present in the polyp
S. aureus intraepithelial
tissue, which may
coloni- zation, studies
contribute to disease
have been done to support
severity. Omalizumab
the use of anti- biotics
counteracts these
along with corticosteroids
interactions by reducing
to treat patients with NP.
serum levels of free IgE.
Recent studies have shown
Therapy targeted at IgE
that oral doxycycline (200
also interferes with its
mg on the first day,
binding to the low-affinity
followed by 100 mg
receptors inhibiting the
once daily) for
amplification of the Th2-
20 days has shown a
type response [18]. The
significantly decreased
high costs of treatment
NP size, reduced levels of
with omalizumab, the
myeloperoxidase, ECP,
high frequency of NP, as
and matrix
well as the current lack of
metalloproteinase 9 in
data concerning safety in
nasal secretions [17].
long-term appli- cation of
omalizumab has to be
borne in mind and further
R
studies have to be
o
l conducted [19].
e

o R
f o
l
e
A
n
t o
i f

I C
g M
E C

T F
h o
e a
r m
a
p Recurrence of nasal
y polyposis after endoscopic
sinus sur- gery can be
Based on the concept of difficult to manage.
Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S23
S24 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
irrigations may not o absorption. Therefore, was administered for 1
provide adequate l furosemide can cause a month twice a year.
treatment and sys- temic e chem- ical gradient Examination of patients
steroid therapy is limited between the submucosa every 6 months (complete
by side effects. Steroid- o and the luminal surface of ear, nose, and throat
infused f the respiratory epithelium examination, active
carboxymethylcellulose I and lead to an increased anterior rhinomanometry,
(CMC) foam as a treat- n absorption of sodium and AR, and nasal endoscopy)
ment for recurrence of t water. This would revealed that 17.5% of
r effectively dehydrate the
chronic rhinosinusitis with patients treated with
a surface of the respiratory
nasal polyposis after furosemide had relapses,
n
endoscopic sinus surgery epithelial cell [23]. compared with 24.2% in
a
has been tried. Four Furosemide also has a the mo- metasone group
s
milliliter of CMC foam a protective effect with its and 30.0% in the untreated
hydrated with l ability to alter group [25]. Also the
triamcinolone, F prostaglandin (PG) severity of recurrence is
40 mg/ml is placed u synthesis by the airway much less. As there are no
endoscopically into the r epithelium. It has shown to long- term term side
ethmoid cavi- ties o cause a marked reduction effects, furosemide can be
bilaterally. Statistically s in both basal and ara- used as a valid therapeutic
significant endoscopic e chidonic acid stimulated tool for the prevention of
results were obtained m production of PGE2 and CHS–NP as an alter-
regarding improvement in i PGF2 alpha [24]. In the native to the use of topical
d recent studies, furosemide corticosteroids, which have
symptoms and endoscopic
e is diluted in physiological
findings in patients with some clinical adverse
recurrent sinonasal solution (2 ml furosemide effects on the nasal
The best therapeutic and 2 ml isotonic sodium
polyposis after endoscopic mucosa like epistaxis and
approach to relapse of chloride solution)
sinus surgery [20]. septal perforation.
nasal polyposis is to administered as nasal puffs
interfere with the early (2 puffs per day per nostril,
phase of NP development. each puff corresponding to
T Role of
a A key element in this 50 lg) for every alternate Amphote
m context is the edematous month for the first 2 years ricin-B
o infiltrate. Manipu- lation (total treatment, NASAL
x of this target may be 6 months/year). During the Wash
i effective in preventing next 3 years, treatment is
f relapses after surgery. given for 1 month and then With the discovery of the
e According to this interrupted for 2 months possible role of fungi in
n hypothesis, the genesis of (total treat- ment, 4 nasal pol- yposis,
nasal polyposis and their months/year). After 5 antifungal medical therapy
Possible future relapse is the development years of treatment, has been an appealing and
perspectives in sinonasal of edema secondary to furosemide promising alternative in
polyposis include increased plasma and maintaining treatment
inhibition of human mast water absorption into the following FESS to reduce
cell proliferation by lamina propria of the NP recurrence and its
tamoxifen. A study by tissue [22]. The topical use severity in polyposis
Duffy et al. [21] suggests of furosemide, a loop patients [26, 27].
that tamoxifen might be diuretic and inhibitor of Amphotericin B is a
useful in the treatment of the potassium and sodium natural polyene anti-
mast cell-mediated chloride cotransporter fungal agent which binds
diseases. Further studies channels, at the basolat- to ergosterol, a component
are needed to prove its eral surface of the of cell walls of most fungi,
efficacy. respiratory epithelial cell leading to formation of ion
may result in a decrease in channels and cell death; it
sodium absorption and an may also act secondarily
R ultimate decrease in water through oxidative damage
 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S25
to fungal cell membranes dose of 100 mg/ml can be
through creation of free used [29].
radicals from its own
oxidation [28]. It is
hypothesized that topical S
intranasal application of u
Amphotericin B can r
decrease the fungal load in g
the sinonasal region, i
thereby decreasing the c
local eosinophilic a
l
inflammatory reaction to
fungal antigens seen in
M
many chronic rhino-
a
sinusitis with or without
n
nasal polyposis patients a
[29, 30]. Amphotericin B g
is poorly absor- bed e
through the gut when m
ingested orally, therefore e
there is little or no n
potential for systemic t
exposure to the drug when
administered by the topical Surgical therapy is
intranasal route [31]. Direct reserved for cases
muco- administration of refractory to medical
intranasal amphotericin B treatment. In general,
is found to reduce the patients are treated
inflammatory mucosal medically in the
thickening by CT scan, the
disease stage by
endoscopy, and an
intranasal marker of
eosinophilic inflammation,
EDN [32]. Patients are
instructed to apply
20 ml amphotericin B
solution (250 mg/ml
dissolved in sterile water)
to each nostril twice a day
by using a bulb syr- inge
and pointing the tip toward
the middle meatus region
after bending their heads
laterally to the side being
irrigated. As exposure to
light and room temperature
reduces the antifungal
potency in reconstituted
amphotericin B in a time-
dependent manner, so a
higher concentration of
amphotericin B (250 mg/
ml) is used, but if it is
possible for patients to
refrigerate the solution, a
S26 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
primary care setting before
consideration of surgical
pro- cedures by an
otolaryngologist.
Endoscopic sinus surgery
is now the mainstay of
treatment for NP [33, 34],
though no single surgical
technique has proved to be
entirely curative and the
recurrence rate is around
5–10% [35, 36]. Con-
current use of micro
debrider enables accurate
removal of NP whilst
preserving normal
anatomical structures such
as the turbinates.
Thorough knowledge of
sinus anatomy, combined
with preoperative imaging
helps to avoid major
complications such as
blindness and CSF
rhinorrhoea. Also the use
of computer-aided
surgery (CAS)
technology, which allows
a direct comparison of
the intraoperative
anatomy with
preoperative imaging
information furthers the
operative accuracy. After a
registration and calibration
process, the surgeon may
point to a specific
structure with the CAS
instrument and then view
the location of the
instrument tip on the CT
image [37, 38]. The use of
CAS systems may allow
for more precise
dissections and greater
rates of sinus patency
outcomes and fewer
complications [39]. It is
important postoperatively
to regularly douche the
nasal cavity with saline to
prevent crusting and
adhesions [40]. Topical
intranasal steroids are also
a routine part of after
surgery care to prevent
S27
recurrence [41]. n down-regulate the
e antimicrobial immune
. function of human
sinonasal epithelial cells.
C Am J Rhinol 22(2):115–
o 121
4. Kim TH, Lee HM, Lee SH,
n
R Kim HK, Lee JH, Oh KH
c (2008) Down-regulation of
e
l carbonic anhydrase
f
u isoenzymes in nasal
e polyps. Laryngoscope
s
r 118(10):1856–1861
i
e 5. Davis LJ, Kita H (2004)
o Pathogenesis of chronic
n
n rhinosinusitis: role of
c
airborne fungi and bacteria.
e
With improvement in the Immunol Allergy Clin
s North Am 24:59–73
management protocols and 6. Inoue Y, Matsuwaki Y,
fur- ther research, nasal 1. Fajardo-Dolci G, Solorio- Shin SH et al (2005)
polyposis would no longer Abreu J, Romero-Alvarez Nonpathogenic,
remain a challenge for JC, Zavaleta- Villa B, environmental fungi induce
Cerezo-Camacho O, activation and
otorhinolaryngologists. Jimenez-Lucio R et al degranulation of human
Future studies are needed (2006) DQA1 and DQB1 eosinophils. J Immunol
to identify the key factors association and nasal 175:5439–5447
polyposis. Otolaryngol
underlying the devel- 7. Weschta M, Rimek D,
Head Neck Surg Formanek M, Polzehl D,
opment or formation of 135(2):243–247 Riechelmann H (2003)
NP and to investigate the 2. Liu Z, Kim J, Sypek JP, Local production of
interac- tions between Wang IM, Horton H, Aspergillus fumigatus
Oppenheim FG et al specific immunoglobulin
genetic, local and
(2004) Gene expression E in
environmental factors that profiles in human nasal nasal polyps.
influence the complex polyp tissues studied by Laryngoscope
traits of this disease. means of DNA 1
microarray. J Allergy Clin 1
Identifying the causal
Immunol 3
factors and variants in NP 114(4):783–790 :
is important to the path 3. Ramanathan M Jr, Lee 1
towards improved WK, Spannhake EW, 7
Lane AP (2008) Th2 9
prevention, diagnosis and 8
cytokines associated with
treatment of NPs. chronic rhinosinusitis with –
polyps 1
C 8
o 0
n 2
f 8. Gilbert P, Maira-Litran T,
l McBain AJ, Rickard AH,
i Whyte FW (2002) The
c physiology and collective
t recalcitrance of microbial
biofilm communities. Adv
Microb Physiol 46:202–
o
256
f
9. Foreman A, Psaltis AJ, Tan
LW, Wormald PJ (2009)
i Charac- terization of
n bacterial and fungal
t biofilms in chronic rhino-
e sinusitis. Am J Rhinol
r Allergy 23(6):556–561
e 10. Kilty SJ, Desrosiers MY
s (2008) The role of bacterial
t biofilms and the
pathophysiology of chronic
N rhinosinusitis. Curr Allergy
o Asthma Rep 8(3):227–233
 S28 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
11. Pujols L, Alobid I, Benitez 17. Van Zele T, Gevaert P,
P, Martinez-Anto´ n A, Roca- Holtappels G, Beule A,
Ferrer J, Wormald PJ, Mayr S,
Fokkens WJ, Mullol J, Hens G, Hellings P, Ebbens
Picado C (2008) FA, Fokkens W, Van
Regulation of gluco- Cauwenberge P, Bachert C
corticoid receptor in (2010) Oral steroids and
nasal polyps by systemic doxycycline: two different
and intranasal approaches to treat nasal
glucocorticoids. Allergy polyps. J Allergy Clin
63:1377–1386 Immunol 125(5):1069–
12. Grzanka A, Misiołek M, 1076
Golusin´ ski W, Jarza˛b J 18. Incorvaia C, Mauro M,
(2011) Molec- Riario-Sforza GG, Frati F,
ular mechanisms of Tarantini F, Caserini M
glucocorticoids action: (2008) Current and future
implications for treatment applications of the anti-IgE
of rhinosinusitis and nasal antibody omalizumab.
polyposis. Eur Arch Biologics 2(1):67–73
Otorhinolaryngol 19. Holgate ST, Djukanovid R,
268(2):247–253 Casale T, Bousquet J
13. Modrzynski M, Zavisza (2005) Anti-
E, Rapiejko P (2002) immunoglobulin E
Zafirlukast in treatment of treatment with omalizumab
nasal polyposis in patients in allergic dis- eases: an
with aspirin intolerant update on anti-
bronchial asthma- inflammatory activity and
preliminary report. Pol clinical effi- cacy. Clin
Merkur Lekarski Exp Allergy 35(4):408–
1 416
2 20. Pletcher SD, Goldberg AN
( (2010) Treatment of
6 recurrent sino- nasal
9 polyposis with steroid-
) infused
: carboxymethylcellulose
2 foam. Am J Rhinol
2 Allergy 24(6):451–453
4 21. Duffy SM, Lawley WJ,
– Kaur D, Yang W, Bradding
2 P (2003) Inhibition of
2 human mast cell
7 proliferation and survival
14. Zhang N, Gevaert P, Van by tamoxifen in association
Zele T, Perez-Novo C, with ion channel
Patou J, Hol- tappels G, modulation. J Allergy Clin
Van Cauwenberge P, Immunol 112:965–972
Bachert C (2005) An
update on the impact of
Staphylococcus aureus
enterotoxins in chronic
sinusitis with nasal
polyposis. Rhinology
43:162–168
15. Kutting B, Nieschalk M,
Brehler K (2000) A new
concept for treatment of
sinonasal polyposis.
Allergy 55:1091–1092
16. Zhang N, Gevaert P, van
Zele T, Perez-Novo C, Patou J,
Hol-
tappels G, van
Cauwenberge P, Bachert C
(2005) An update on the
impact of Staphylococcus
aureus enterotoxins in
chronic sinusitis with nasal
polyposis. Rhinology
43(3):162–168
Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21 S29
S30 Indian J Otolaryngol Head Neck Surg (January 2014) 66(Suppl 1):S16–S21
22. Bernstein JM (2001) The epithelial cells in culture. pharmacology of 31. Ricchetti A, Landis BN,
molecular biology of nasal Am J Respir Cell Mol antifungal compounds. Giger R, Zheng C, Lacroix JS
polyposis. Biol 10(4):378–383 Infect Dis Clin North Am (2002/
C 25. Passa`li D, Bernstein JM, 17:159–191 2003) Effect of local
u Passa`li FM, Damiani V, 30. Ponikau JU, Sherris DA, antifungal treatment on
r Passa`li GC, Weaver A, Kita H (2005) nasal polyposis.
r Bellussi L (2003) Treatment of Otorhinoloaryngologia
Treatment of recurrent chronic rhinosinusitis with 12(2):48–51
chronic hyperplastic intranasal amphotericin B: 32. Wise GJ, Kozinn PJ,
A
sinusitis with nasal a ran- domized, placebo- Goldberg P (1982)
l
polyposis. Arch controlled, double-blind Amphotericin B as a
l
Otolaryngol Head Neck pilot trial. J Allergy Clin urologic irrigant in the
e
Surg Immunol 15:125–131 management of
r
g 1 noninvasive candiduria. J
y 2 Urol 128:82–84
9 33. Telmesani LM (2009)
: Prevalence of allergic
A 6 fungal sinusitis among
s 5 patients with nasal polyps.
t 6 Ann Saudi Med 29(3):212–
h – 214
m 6 34. Poetker DM, Mendolia-
a 5 Loffredo S, Smith TL (2007)
9 Outcomes
R 26. Passa`li D, Mezzedimi C, of endoscopic sinus
e Passa`li GC, Bellussi L surgery for chronic
p (2000) Efficacy of rhinosinusitis associated
inhalation form of with sinonasal polyposis.
1 furosemide to prevent Am J Rhinol 21:84–88
: postsurgical relapses 35. Bhattacharyya N (2007)
2 of rhinosinusal Influence of polyps on
6 polyposis. J outcomes after endoscopic
2 Otorhinolaryngol sinus surgery.
– 62:307–310 Laryngoscope 117:1834–
2 27. Shin SH, Ye MK (2004) 1838
6 Effects of topical 36. Wynn R, Har-El G
7 amphotericin B on (2007) Recurrence rates
23. Passa`li D, Bellussi L, expression of cytokines after endoscopic sinus
Lauriello M, Ferrara A, in nasal polyps. Acta surgery for massive
Bernstein JM (1996) Otolaryngol sinus polyposis.
Medical therapy for 1 Laryngoscope
prevention of relapsing 2 114:811–813
nasal polyp- 4 37. Anon JB (1998)
osis: a pilot study on the ( Computer-aided endoscopic
use of furosemide by 1 sinus surgery.
inhalation. Am J 0 Laryngoscope 108:949–961
R ) 38. Olson G, Citardi MJ
h : (2000) Image-guided
i 1 functional endoscopic sinus
n 1 surgery. Otolaryngol Head
o 7 Neck Surg 123:188–194
l 4 39. Al-Swiahb JN, Al-
– Dousary SH (2010)
1 Computer-aided endo-
1 1 scopic sinus surgery: a
0 7 retrospective comparative
: 7 study. Ann Saudi Med
1 28. Kern BE, Sherris D, 30(2):149–152
8 Stergiou AM, Katz LM, 40. Talbot AR, Herr TM,
7 Rosenblatt LC, Ponikau JU Parsons DS (1997) Mucocilliary
– (2007) Diagnosis and clearance
1 treatment of chronic and buffered hypertonic
9 rhinosi- nusitis: focus on saline solution.
2 intranasal Amphotericin B. Laryngoscope
24. Levasseur-Acker GM, Ther Clin Risk Manag 107:500–503
Molimard M, Regnard J, 3(2):319–325 41. Newton RJ, Ah-See KW
Naline E, Freche C, 29. Groll AH, Gea- (2008) A review of nasal
Lockhart A (1994) Effect Banacloche JC, polyposis.
of furosemide on Glasmacher A et al Ther Clin Risk Manag
prostaglandin synthesis by (2003) Clinical 4(2):507–512
human nasal and bronchial