otolaryngologia polska 66 (2012) 373378

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Review/Praca pogladowa

Current view on nasal polyps management in Samters triad

patients
Wspo czesne spojrzenie na postepowanie z polipami nosa u pacjento w
z triada Samtera
Katarzyna Mro wka-Kata *, Eugeniusz Czecior, Dariusz Kata, Grzegorz Namysowski,
Judyta Dziechciarz-Werbowska, Pawe Sowa
Katedra i Oddzia Kliniczny Laryngologii w Zabrzu, S laskiego Uniwersytetu Medycznego w Katowicach, Poland
Ordynator: prof. dr hab. n. med. Grzegorz Namysowski

article info

abstract

Article history:

The nasal polyps associated with Samters triad are often very extensive, difficult to treat,

Received: 30.03.2012

with great tendency to recurrence. In this paper the current opinion on nasal polyps

Accepted: 26.06.2012

management in aspirin triad patients was presented. Pathogenesis: Opinions on pathoge-

Available online: 01.07.2012

nesis of these disease was remembered as well as its epidemiology. Diagnostic methods:
The available diagnostic methods were presented. Treatment options: The available pre-

Keywords:
 Samters triad
 Nasal polyps

servative treatment options was analyzed including aspirin desensitization. The role of
surgical treatment, functional endoscopic sinus surgery was analyzed.
2012 Polish Otorhinolaryngology - Head and Neck Surgery Society. Published by

 Treatment

Introduction
The triad of nasal polyps, aspirin intolerance and asthma was
first described by Widal at al. in 1922 and again by Samter in
1968 what gave the name of this clinical entity. Asthma
usually occurs first, followed by aspirin intolerance, and then
nasal polyps. In many cases, only two parts of the triad are
present [1, 2].
The exact mechanism of the disease in unknown but it is
considered to be due, at least in part, to a disturbance of
eicosanoid biosynthesis. Eicosanoids are rapidly synthesized
and released products of arachidonic acid (AA) metabolism
mainly via the cyclooxygenase (CO) and lipooxygenase (LO)
pathway and, to a small extend, via the epoxygenase pathway

Elsevier Urban & Partner Sp. z o.o. All rights reserved.

(EO). The conversion of AA to prostaglandin (PGs) and

thromboxanes (TXs) involves the CO pathway. The conversion
of AA to leukotriens (LTs) and hydroxyeicosatetranoic acid
(HETEs) is via the LO pathway. Aspirin competes with AA by
irreversibly binding to the cyclooxygenase active site, thereby
shifting AA to the LO pathway. The inhibition of cyclooxygenases by aspirin results in the diversion of arachidonic
acid products toward the lipo-oxygenase pathway, resulting in
overproduction of leukotriens and other mediators, and
a reduction of anti-inflammatory prostaglandins [14]. However, in some scientists opinion, increased production of LTs
apparently does not depend on the acetylosalicic acid (ASA)
effect alone. Even in the absence of ASA, the baseline AA
metabolic rate of peripheral blood monocytes of patients with
ASA-sensitive respiratory disease is higher than those of

* Corresponding author at: Katedra i Oddzia Kliniczny Laryngologii SUM, ul. M. Skodowskiej-Curie 10, 41-800 Zabrze, Poland.
Tel.: +48 032 271 74 20; fax: +48 032 271 74 20.
E-mail address: mrowkakata@wp.pl (K. Mrowka-Kata).
0030-6657/$ see front matter 2012 Polish Otorhinolaryngology - Head and Neck Surgery Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.

http://dx.doi.org/10.1016/j.otpol.2012.06.017

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otolaryngologia polska 66 (2012) 373378

normal controls [58]. Jurgens et al. found that monocytes of

ASA-sensitive patients produce larger amounts of both TXs
and LTs compared to normal individuals. This indicates
a generalized acceleration in the AA metabolic rate through
both the CO and LO pathways in these patients. They also
found subsequent ingestion of ASA resulted in a significant
decrease in TX and a significant increase in cysteinyl LT
release and that this was clinically associated with bronchospasm [9]. Thus ASA inhibited CO, shunted AA through the LO
pathway, and resulted in the hypersecretion of cysteinyl LTs.
These LO products are potent bronchoconstrictors and also
increase vascular permeability, resulting in the airway edema
and secretions associated with acute asthmatic attacks as well
as the nasal symptoms seen in the Aspirin Triad (AT)
syndrome. This is thought to cause an exacerbation of asthma
and formation of nasal polyps [4, 5, 810]. The HLA allele
DPB1*0301 may represent the aspirin exacerbated respiratory
diseases (AERD) phenotype, and that patients with this
allele displayed typical clinical characteristics of Samters
triad with lowered FEV1 levels and increased prevalence
of rhinosinusitis with nasal polyps [5, 1012]. Another
potential AERD genetic biomarkers include leucotriene C4
synthase (LTC4S), ALOX5, CYSLT, PGE2, TBXA2R, TBX2,
MS4A2, IL10-1082A > G, ACE-262A > T, CRTH2-466T > C, together with the four-locus single nucleotide polymorphism (SNP)
set B2ADR46A > G, CCR3-520T > G, CysLTR1-634C > T and
FCER1B-109 > C [5, 1317].
This disease represents the most aggressive form of nasal
polyps. Nasal polyps occur in 3696% of patients with aspirin
intolerance. Conversely, of all patients with nasal polyps 12.8%
have aspirin intolerance [3, 4].
Thus, the upper and lower respiratory disease of aspirin
triad patients involves a number of complex mechanisms
operating at the level of their respiratory mucosa. This results
in mast cell activation, eosinophilia, and the production of
chronic inflammatory mediators that worsens with ASA
ingestion. These mechanisms appear to be distinct from
those seen in other patients with chronic rhinosinusitis with
nasal polyps (CRS/NP) but without ASA-sensitivity [25].
Patients with Samters triad generally tend to have more
severe symptoms of nasal polyposis and asthma, as well as
rhinosinusitis, than do patients without the triad. When their
chronic sinusitis fails to respond to aggressive medical
management, surgical intervention is indicated and has been
found in a number of studies to reduce the severity of the
asthma, but their postoperative course is often complicated by
a recurrence of nasal polyps [35].
The aim of the study was to present actual tendencies in the
management with nasal polyps in the course of Samters triad.

Epidemology
According to Varghese at al. the presence of nasal polyps in
aspirin sensitivity patients may be as high as 1422% and the
chronic rhinosinusitis from 0.7 to 2.6% [18].
Jenkins et al. found that nasal polyps prevalence rates are
21% and 5% for asthmatic adults and children, respectively,
when examining primarily unblended oral provocation tests
in a systematic review of 66 articles on aspirin exacerbated

asthma (AEA). The prevalence was dependent on the method

used to diagnose AEA, with patients histories alone giving
a much lower prevalence rate of 2.7% in adults and 2% in
children [19].
A database study from Poland in which 12,971 adults were
randomly selected showed a prevalence of AEA of 0.6% in the
general population and 4.3% of subjects with a known
diagnosis of asthma. With nasal polyps patients, aspirin
sensitivity may be as high as 1422%, and with chronic
rhinosinusitis, it is 0.72.6% [20].
Aspirin intolerance may be widely underdiagnosed in the
European network of aspirin induced asthma, 18% of
participants were unwary of aspirin sensitivity before undergoing unblended aspirin provocation tests [3, 4, 21].
Rhinorrhea and nasal congestion are usually the first
symptoms of AEA and are commonly refractory to pharmacologic therapy. It becomes perennial and more difficult to
treat and then becomes associated with anosmia, recurrent
and chronic sinusitis, and nasal polyposis [3, 4, 21, 22].

Diagnosis
Taking the medical history is of primary importance during
the first visit to the doctor, who must attempt to establish
the link between salicylate contact and the occurrence of the
symptoms. This is only successful if they occur at close
intervals. The doctor must therefore ask whether asthma, skin
symptoms, swelling of the nasal mucosa, gastrointestinal
symptoms or the (very rare) cardiovascular shock have
occurred immediately after salicylate consumption. Polyps
in the nose and nasal sinuses occur later and grow slowly; the
decisive clue is than provided by rapid and repeated
recurrence after operative removal.
The accepted diagnostic gold standard is the exposure on
aspirin or provocation test. However, these can only confirm
or exclude the suspicion for rapid reaction such as asthma.
Long-term developments such as polyps cannot be adequately
followed. Acetylsalicylic acid is normally administered orally
or nasally. Emergency precaution should be taken, as there
may be violent reaction, such as asthma. This includes
possibility of observation in hospital and follow-up care. This
diagnostic measure requires the proper equipment and is
demanding for the personnel [35, 23].
Diagnosis can also be based on imagine techniques,
including computed tomography (CT) for polyps and tests of
lung functions to measure obstruction after exposure or
provocation. Triad patients usually have a more extensive
sinus involvement at initial presentation and are twice as
likely as nontriad patients to report a history of previous
nasal surgery. CT scans evaluation and the number of
previous nasal surgeries have often been cited as a useful
prognostic indicators. As evidenced, the mean radiologic
grades of triad patients are significantly higher than those of
nontriad patients. Of note is that the anterior and posterior
ethmoid sinuses are the most extensively involved sinuses
in both groups of patients, but more so in the triad patients
[2427]. As Richtsmeier explained, the pathogenesis of
maxillary and frontal sinusitis shows a central role of
the anterior ethmoidal complex. The higher radiologic

otolaryngologia polska 66 (2012) 373378

grades of the ethmoid sinuses in the triad would explain

the grater level of triad patients involvement of the
frontal and maxillary sinuses in that same group [28]. The
nontriad patients, who have a much lower degree of
ethmoid involvement, also have a lower degree of frontal
and maxillary involvement [2628].
Functional ex vivo tests are based on the detection of
indicators in the patients tissues exposed to the test
substances. The following systems are currently commercially
available.
Measurement of the released quantity of LT from prepared
basophils. This corresponds to the LOX-dependent metabolic pathways.
Measurement of the lysozyme associated membrane
proteine CD 63 by flow cytometry. This has been reported
to occur on degranulating basophiles. The measurement of
enriched basophiles is a less suitable approach to diagnose
salicylate intolerance.
An extended functional eicosanoid test (FET) can be used to
measure the eicosanoids LT and PG released after exposure
to salicylates or other substances. This gives a more
quantitative measurement of the metabolic pathway of
LOX and COX under both normal conditions equivalent to
the disease, together with the dependence on symptoms
such as polyposis, rhinitis, and others [2932].
The newer functional tests are useful for unclear cases and
when there is no close correlation in time between the
symptoms and exposure or provocation on aspirin. These
tests are absolutely indispensable when exposure or provocation is unacceptable because of the circumstances and the
patients expected reaction, or because of contraindications
such as infection or bronchial asthma [2932].

Differential diagnosis
In the differential diagnosis all types of chronic rhinosinusitis
(chronic rhinosinusitis without nasal polyps and chronic
rhinosinusitis with nasal polyps) should be taken under
consideration. Especially, correlation between chronic rhinosinusitis and presence of allergy should be considered in these
cases [35].

Treatment
Prevention
The most reliable form of prophylaxis and therapy is to
interrupt treatment. It is particularly important to avoid
COX-1 inhibitors. However, some patients react with the
same symptoms to very high dosages of paracetamol, used
as a substitute. In these cases, low-dose buprenorphine or
tramadol, other non-steroid anti-inflammatory drugs (NSAID)
must be prescribed [35, 33, 34].
NSAID that are highly selective for COX-2, for example,
celecoxib and rofecoxib, do not cause acute exacerbation of
asthma in AEA [3, 4, 35].

375

If highly sensitive patients interrupt treatment they must

also avoid cosmetics and food with high salicylate content,
particularly spices and industrially processed food [35, 34].

Drug treatment
The guidelines used to treat and manage AEA are no different
from those used to treat moderate to severe persistent aspirin
tolerate asthma (ATA). Individuals with AEA occasionally
require systemic corticosteroids in addition to their regular
maintenance therapy.
The most active drugs are corticosteroids, as one of their
activities to inhibit the catalysis of the formation of arachidonic acid by phospholipases, the precursor of the responsible
eicosanoids. Steroids treatment can be topical or systemic
[3, 4, 3335].
Leukotriene inhibitors, such as zileuton, which inhibits
5-LO, and leukotriene receptor antagonists, such as montelukast and zafirlukast, are used to treat AEA. However, ATA
and AEA subjects on leukotriene inhibitors have similar
clinical outcomes, and urinary LTE4 cannot be used to
determine responses to these medications [3638]. AEA
subjects with the C allele appear to have a better response
with leukotriene receptor antagonists [3638].

Surgical treatment
Little has been reported in the literature about the prevalence
of Samters triad among patients who are treated with
functional endoscopic sinus surgery (FESS). In the paper of
Kim and Kountakis the prevalence of these patients among all
undergoing FESS was: 4.8% among all patients undergoing
FESS 9.4% for patients with nasal polyps, 16.9% for patients
with asthma, and 25.6% for patients with both nasal polyps
and asthma [39].
Surgical treatment of severe sinusitis in aspirin triad
patients does not worsen their asthma and has been helpful
in decreasing steroid dependence and improving asthma and
sinus symptoms.
Although numerous publications have focused on the
overall outcome of FESS, very few have explicitly studied the
impact of Samters triad on the success of these procedure.
In one of the few studies looking at Samters triad, Schaitkin
et al. recorded a 91% symptomatic improvement at a 4-year
follow-up of non-aspirin triad patients having undergone
FESS. Eighteen percent of these patients were completely
symptom free. Triad patients reported only an 82% improvement, with 0% reporting complete resolution of symptom.
Furthermore, 36% of ASA triad patients required revision
surgery during the follow-up period versus 23% for non-ASA
triad patients [40]. McFadden et al. reported that if antral
and sphenoid disease is present in a triad patient, a more
radical approach such as Caldwell-Luc surgery is indicated
rather than a FESS [40, 41].
Despite the use of these surgical procedures recurrences
are common, and up to 60% of patients require further
polypectomy over a 5-year period. Furthermore, patients with
Samters triad have more aggressive disease and require over
seven times as many revision endoscopic surgeries as
nontriad patients [40, 41].

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otolaryngologia polska 66 (2012) 373378

Surgery for nasal polyposis associated with AEA results in

an 80% subjective improvement rate with a 40% chance or
more of recurrence of nasal polyps and persistence of nasal
symptoms [42]. Mild to marked improvement in quality of life
was reported in individuals with AEA following sinus surgery
in a Japanese study [39]. McFadden and colleagues also
reported improvements in quality of life and pulmonary
function tests (PFTs) and a reduction in systemic and topical
corticosteroid requirements [41]. Simple polypectomy alone
does not seem to be as useful as FESS owing to the excessive
amount of polypoid tissue burden in AEA [4347].
As the frequency of revision functional endoscopic sinus
surgery it is higher in patient with aspirin sensitivity and
asthma, Palikhe et al. suggest in their paper that endoscopic
sinus surgery should be selected for severe chronic sinusitis
with multiply nasal polyps and nasal passage obstruction [48].
Despite these findings, evidence suggests that sinonasal
symptoms are significantly improved in the postoperative
period following functional endoscopic sinus surgery in
patients with aspirin-exacerbated respiratory disease, although
the benefit of surgery may be short lived. With regard to
improvement also olfaction following functional endoscopic
sinus surgery, aspirin-exacerbated respiratory disease (AERD)
is a significant predictor of a worse outcome in comparison
with patients with allergic rhinitis and nasal polyps [4953].
When aspirin sensitivity is diagnosed, additional effort should
be made to educate patients about nonsurgical management
options and the long-term postoperative prognosis. Postoperative, aggressive medical management is necessarily to
control the mucosal disease in an attempt to prevent or delay
polyp recurrence. The gold standard for medical therapy is the
use of intranasal corticosteroids. In some cases, with additional
indications, oral corticosteroids can be used with limitations.
Patients can also use mucolythics and perform nasal saline
douches to remove the thick eosinophilic debris from the
sinonasal cavities. After surgery for nasal polyps patients
usually continue with topical corticosteroids, antihistamine
and antileucotriens tablets. Some of them may also require
short course of oral steroids [46, 50, 51, 5456].

Biological methods
Inactivation or desensitization is a possible biological
approach. The term desensitization is widely used in the
USA, but is somewhat misleading, as it implies the specific
suppression of immunological genuine allergies [57]. The
treatment is based on the administration of increasing
quantities of acetylosalicylic acid. There is no fix scheme.
The first dose is usually 5 mg per day. The single doses are
then increased up to 100300 mg, which must than be taken
once daily on a long term basis. Depending on the procedure
and the patients tolerance, this can last from a few days to
two weeks [58, 59]. In about 80% of cases, improvement in
nasal respiration, sense of smell and freedom from recurrent
polyps are retained for two to three years. The effect can last
for up two weeks after salicylate has stopped. There are no
consequences if a single dose is omitted or forgotten. If there
are longer interruptions (as may be necessary before
operations), the treatment must be restarted. It is better to

perform the initial phase of treatment in hospital, as there

a some risk of adverse reactions such as asthma or
gastrointerstinal symptoms, particularly in the phase of dose
increase. This deactivation is only justified and permissible
in patients with established salicylate intolerance [6063].
It has been suggested that aspirin desensitization
followed by aspirin therapy should be considered when the
symptoms of aspirin exacerbated respiratory disease
persist despite the optimal use of conventional treatments,
or when a patient requires treatment with aspirin or nonsteroidal anti-inflammatory drugs for an alternative
clinical indications [64, 65]. Suitable patients include the
following:
Moderate or severe asthma and/or intractable nasal symptoms that are uncontrolled with topical corticosteroids and
leucotriens-modifying drugs.
Severe extensive, nasal polyps.
Requirements for daily or frequent courses of systemic
corticosteroids to control nasal symptoms and/or asthma.
Additional medical indications for aspirins such as atherosclerotic cardiovascular disease.
Medical indication for other COX-1 enzyme inhibiting
medications such as arthritic pain refractory to other
anti-inflammatory drugs [64, 65].
Topical lysine-aspirin, administered endonasally, has shown
encouraging results in the nasal polyposis in aspirin-exacerbated respiratory disease (AERD) management. The effect of
intranasal lysine-aspirin administration on resistant nasal
polyps of asthmatics, aspirin-intolerant patients, together
with routine therapy, was examined in a well-structured buy
small prospective study [66, 67].

Conclusions
The nasal polyps associated with Samters triad are often
very extensive, difficult to treat, with great tendency to
recurrence. Their treatment include preservative treatment
options like salicylate avoiding, using selective COX-2
inhibitors, antileukotriens preparates, in some cases glicocorticosteriod preparates as well as aspirin desensitization.
The second treatment option is surgical treatment, mainly
functional endoscopic sinus surgery. According to the
significant frequency of this diseases appearance and often
its underdiagnosis we postulate that doctors of different
specializations laryngologists, allergologists should be
familiar with all symptoms of this diseases like presented
in this paper nasal polyps.

Authors contributions/Wkad autorow

According to order.

Conflict of interest/Konflikt interesu

None declared.

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